Mitokondriesykdommer (mitokondrielle sykdommer) (legehandboka.no) (f rambu.no) (frambu.no) (frambu.no) (unn.no)

Mitochondria, Cell Energy, ATP Synthase | Learn Science at ... (nature.com)

Mitochondria (illustration) (U.S. National Library of Medicine) (qiagen.com)

Mitokondrie ...dei er sete for tilverting av energi (oksidasjon av pyruvat og feittsyrer til karbondioksid og NADH som gir elektronar til ATP-syntesen) (Norsk medisinsk ordbok) (youtube.com) (socialstyrelsen.se)

Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9)

Hyperlactatemia, metabolic acidosis, and peripheral neuropathy are adverse effects of linezolid,2,3 which could be related to the drug's capacity for interference with mitochondrial function.4 (NEJM 2005;353:2305-2306)

Steroids cause "catastrophic" brain damage (netdoctor.co.uk 3.10.2006)

Parasitt-RNA i genterapi mot mitokondriesykdom? (Tidsskr Nor Lægeforen 2007; 127: 11 (4.1.2007))

Antidepressiva linket til forverring av hvit substans hos eldre (Reuters Health 17.3.2008)

Kan fysiske symptomer ved depresjon skyldes lav energiproduksjon (medicalnewstoday.com 28.3.2008)

- Dette er første gang at en undersøkelse viser at mitokondrier er nødvendige for cellulær aldring. (- Mitokondrier får nerver til å gro.) (- Teknologi fra hydrogenbiler kan forklare hvorfor livet oppstod.)

Eradicating mitochondria from cells may reverse aging
medicalnewstoday.com 5.2.2016
For første gang har forskere vist at mitokondriene - cellenes "kraftstasjoner" - er avgjørende for aldring, dette etter å ha påvist at fjerning av mitokondrier fra menneskelige celler reduserte nivåer av markører for cellulær aldring, hvilket trigger en prosess med foryngelse. (For the first time, scientists have shown that mitochondria - the "powerhouses" of cells - are crucial for aging, after finding that removing mitochondria from human cells reduced levels of markers for cellular aging, triggering a process of rejuvenation.)

Studieleder Dr. João Passos ved Institutt for Aging ved Newcastle University i Storbritannia og hans team uttalte at resultatene baner vei for nye strategier for å reversere aldringsprosessen. (Study leader Dr. João Passos, of the Institute for Aging at Newcastle University in the UK, and his team say their findings pave the way for new strategies to reverse the aging process.)

Resultatene er publisert i The Embo Journal. (They publish their findings in The Embo Journal.)

(Anm: Mitochondria are required for proageing features of the senescent phenotype. The EMBO Journal 2016 (Published online 04.02.2016 ).)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitochondrial Toxicity of Tobacco Smoke and Air Pollution. Toxicology. 2017 Aug 21. pii: S0300-483X(17)30229-9.)

- Cellulær stress «resetter levetiden betraktelig». Overraskende resultater fra en nylig studie viser at stress på en celle kan reversere tegn på cellulær aldring. Resultatene kan åpne dører for mer vellykkede måter å redusere aldringsprosessen.

(Anm: Cellular stress 'resets lifespan profoundly'. Surprising results from a recent study show that stressing a cell can reverse signs of cellular aging. The findings might open doors to more successful ways to slow the aging process. Although the desire to stave off aging has a whiff of vanity about it, it's not all about reducing wrinkles and covering gray hair; getting older comes with a range of diseases that grow steadily more prevalent as our population ages. Those interested in senescence are keen to understand the molecular pathways involved in aging in the hope that associated disease processes will also be unlocked. Molecular bioscientists from Northwestern University in Evanston, IL, recently gained a new and surprising insight into cellular aging. Their findings are published this week in the journal Cell Reports. This new study focused on the transparent nematode Caenorhabditis elegans. This species is often used as a model for human aging and disease; its cellular properties and biochemical environment are similar to our own.  (…) 'It's like magic'. These surprising findings fly in the face of the previously held notion that stressing mitochondria has negative effects, as Prof. Morimoto explains. He says, "This has not been seen before." "People have always known that prolonged mitochondrial stress can be deleterious," he explains. "But we discovered that when you stress mitochondria just a little, the mitochondrial stress signal is actually interpreted by the cell and animal as a survival strategy. It makes the animals completely stress-resistant and doubles their lifespan. It's like magic." (...) What they found came as a surprise: under these conditions, mitochondria sent out signals to the protein machinery, preventing it from failing. This, in turn, reduced the buildup of badly packed proteins. (medicalnewstoday.com 8.11.2017).)

(Anm: Rask gåing kan hjelpe eldre kvinner til å leve lenger. Brisk walking may help older women live longer. (…) This was the main finding of a large study — by researchers from Brigham and Women's Hospital in Boston, MA — that measured physical activity in older women as they wore sensitive activity trackers and then followed them for up to 4 years. "Physical inactivity is estimated to cause as many deaths globally each year as smoking," note the researchers in a report on the study that was published recently in the journal Circulation. (medicalnewstoday.com 8.11.2017).)

(Anm: Fysisk trening (aktivitet / løping / jogging). (mintankesmie.no).)

- Gjennombrudd: Forskere reverserer aldring i menneskelige celler.

(Anm: Breakthrough: Scientists reverse aging in human cells. New research published in the journal BMC Cell Biology shows that old human cells can be rejuvenated using chemicals similar to resveratrol, which is a substance found in red wine and dark chocolate. The new study was carried out by researchers at the Universities of Exeter and Brighton, both of which are located in the United Kingdom. (…) The new study builds on previous research from the University of Exeter, which found that so-called splicing factors — which are a type of protein — tend to become inactive as we age. (medicalnewstoday.com 8.11.2017).)

- IMB forskere avslører aldringsprosessens mysterium. Forskere ved Institute of Molecular Biology (IMB) i Mainz har gjort et gjennombrudd i å forstå opprinnelsen til aldringsprosessen.

(Anm: IMB researchers unveil mystery of aging process. esearchers at the Institute of Molecular Biology (IMB) in Mainz have made a breakthrough in understanding the origin of the aging process. They have identified that genes belonging to a process called autophagy, which is one of the cells most critical survival processes, promote health and fitness in young worms but drive the process of aging later in life. This research published in the journal Genes & Development gives some of the first clear evidence for how the aging process arises as a quirk of evolution. These findings may also have broader implications for the treatment of neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's disease where autophagy is implicated. The researchers show that by promoting longevity through shutting down autophagy in old worms there is a strong improvement in neuronal and subsequent whole body health. Getting old is something that happens to everyone and nearly every species on this planet, but the question is: should it? In a recent publication in the journal Genes & Development titled "Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans," Dr. Holger Richly's lab at IMB has found some of the first genetic evidence that may put this question to rest. (news-medical.net 15.11.2017).)

- Teknologi fra hydrogenbiler kan forklare hvorfor livet oppstod.

(Anm: Teknologi fra hydrogenbiler kan forklare hvorfor livet oppstod. (…) I cellene til mennesker og dyr blir energien produsert i det som kalles cellenes kraftverk, mitokondriene. De har et membran, som på mange måter tilsvarer membranet i brenselcellen. (nrk.no 21.3.2014).)

- Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl».

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

(Anm: NeuroAge (uib.no).)

- Linker mitokondriell dynamikk til mitokondriell kvalitetskontroll av protein.

(Anm: Linking mitochondrial dynamics to mitochondrial protein quality control. Abstract Over the last decade, countless discoveries have been made that have expanded our knowledge of mitochondrial biology, and more often than not, these discoveries provided fascinating new insights into the etiology of human disease. For example, advances in mitochondrial genetics exposed the role of mitochondrial mutations in cancer progression, and the discovery of mitophagy highlighted the role of mitochondrial quality control in Parkinson's disease. Additional discoveries underscored the importance of the mTor pathway in aging and disease, and more recently, the mitochondrial unfolded protein response was implicated in the regulation of mammalian lifespan. Some of the most fundamental discoveries though, were made in the context of mitochondrial fusion and fission. The balance between these two opposing forces shapes the mitochondrial population in our cells, and influences mitochondrial function at every level. Here, we highlight the basic biology that underlies mitochondrial fusion and fission, explain how these processes promote human health by solving a problem that is innate to multifarious organelles, and make a novel prediction: that fusion and fission are intimately linked to mitochondrial protein quality control. Curr Opin Genet Dev. 2016 Jun;38:68-74.)

- Cellulær bioenergetikk er svekket hos pasienter med kronisk utmattelsessyndrom (CFS). (Cellular bioenergetics is impaired in patients with chronic fatigue syndrome.) (- Resultatene viste konsekvent lavere målinger av OXPHOS parametere i PBMC som er tatt fra CFS pasienter sammenlignet med sunne kontrollpersoner. Sju nøkkelparametere for OXPHOS ble planlagt: basal respirasjon, ATP-produksjon, protonlekkasje, maksimal respirasjon, reservekapasitet, ikke-mitokondriell respirasjon og koblingseffektivitet.)

(Anm: Cellular bioenergetics is impaired in patients with chronic fatigue syndrome. Abstract Chronic fatigue syndrome (CFS) is a highly debilitating disease of unknown aetiology. Abnormalities in bioenergetic function have been cited as one possible cause for CFS. Preliminary studies were performed to investigate cellular bioenergetic abnormalities in CFS patients. A series of assays were conducted using peripheral blood mononuclear cells (PBMCs) from CFS patients and healthy controls. These experiments investigated cellular patterns in oxidative phosphorylation (OXPHOS) and glycolysis. Results showed consistently lower measures of OXPHOS parameters in PBMCs taken from CFS patients compared with healthy controls. Seven key parameters of OXPHOS were calculated: basal respiration, ATP production, proton leak, maximal respiration, reserve capacity, non-mitochondrial respiration, and coupling efficiency. While many of the parameters differed between the CFS and control cohorts, maximal respiration was determined to be the key parameter in mitochondrial function to differ between CFS and control PBMCs due to the consistency of its impairment in CFS patients found throughout the study (p≤0.003). The lower maximal respiration in CFS PBMCs suggests that when the cells experience physiological stress they are less able to elevate their respiration rate to compensate for the increase in stress and are unable to fulfil cellular energy demands. The metabolic differences discovered highlight the inability of CFS patient PBMCs to fulfil cellular energetic demands both under basal conditions and when mitochondria are stressed during periods of high metabolic demand. PLoS One. 2017 Oct 24;12(10):e0186802. eCollection 2017.)

(Anm: ME: Jeg ble avfeid med at jeg var lat og oppmerksomhetssyk. Hanne lå på et mørkt rom i to år med ME. Hun veide 28 kilo. (kk.no 2.9.2017).)

(Anm: «Å være på kafé og gå turer har hun krefter til, men ikke å jobbe». (…) Om du gikk fra å kunne jobbe 100 prosent til på enkelte dager ikke ha krefter nok til å komme deg opp av sengen?  (aftenposten.no 19.9.2017).)

(Anm: Kronisk tretthetssyndrom/Myalgisk encefalopati (CFS/ME). (mintankesmie.no).)

(Anm: Chronic Fatigue Syndrome Causes and Treatment (webmd.com 1.6.2016).)

(Anm: Nøkkelen til kronisk utmattelsessyndrom sitter i tarmen, ikke hodet. (Key to chronic fatigue syndrome is in your gut, not head.) (mediarelations.cornell.edu 27.6.2016).)

- Våre (mors) mitokondrier og vårt sinn. (- Det meste av energien vi får å bruke er levert av mitokondrier, svært små levende strukturer som sitter inne i våre celler eller sendes frem og tilbake innvendig hvor de trengs. Mitokondrier produserer energi ved å forbrenne hva som gjenstår av måltider etter at vi har fordøyd det, men på bekostning av stadig å tære på seg selv og oss. (- Vi diskuterer hvorfor motvirkning av mitokondriell tæring mht. antioksidant fra kosttilskudd ofte er uklokt, og hvorfor våre mitokondrier, og derfor vi selv, i stedet har nytte av trening, meditasjon, søvn, solskinn og spesielle matvaner.)

(Anm: Våre (mors) mitokondrier og vårt sinn. Abstrakt Det meste av energien vi får å bruke er levert av mitokondrier, svært små levende strukturer som sitter inne i våre celler eller sendes frem og tilbake innvendig hvor de trengs. Mitokondrier produserer energi ved å forbrenne hva som gjenstår av måltider etter at vi har fordøyd det, men på bekostning av stadig å tære på seg selv og oss. Her vurderer vi hvordan mitokondrier utviklet seg fra invaderende bakterier og har beholdt en liten grad av uavhengighet fra oss; hvordan vi arver dem bare fra vår mor; og hvordan de er tungt involvert i læring, minne, kognisjon og nesten alle mentale eller nevrologiske lidelser. Vi diskuterer hvorfor motvirkning av mitokondriell tæring mht. antioksidant fra kosttilskudd ofte er uklokt, og hvorfor våre mitokondrier, og derfor vi selv, i stedet har nytte av trening, meditasjon, søvn, solskinn og spesielle matvaner. Til slutt beskriver vi hvordan mitokondriell funksjonsfeil tvinger rotter til å bli sosialt underordnet andre, hvordan slike forskjeller kan kompenseres av et vitamin, og hvorfor disse funnene er relevante for oss. (Our (Mother's) Mitochondria and Our Mind. Abstract Most of the energy we get to spend is furnished by mitochondria, minuscule living structures sitting inside our cells or dispatched back and forth within them to where they are needed. Mitochondria produce energy by burning down what remains of our meal after we have digested it, but at the cost of constantly corroding themselves and us. Here we review how our mitochondria evolved from invading bacteria and have retained a small amount of independence from us; how we inherit them only from our mother; and how they are heavily implicated in learning, memory, cognition, and virtually every mental or neurological affliction. We discuss why counteracting mitochondrial corrosion with antioxidant supplements is often unwise, and why our mitochondria, and therefore we ourselves, benefit instead from exercise, meditation, sleep, sunshine, and particular eating habits. Finally, we describe how malfunctioning mitochondria force rats to become socially subordinate to others, how such disparity can be evened off by a vitamin, and why these findings are relevant to us.) Perspect Psychol Sci. 2017 Sep 1:1745691617718356. [Epub ahead of print].)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Fathers can influence the sex of their offspring, scientists show. It has traditionally been thought that in mammals only mothers are able to influence the sex of their offspring. But a new study in wild mice led by Dr Aurelio Malo of Oxford University's Department of Zoology has shown that fathers can, in fact, influence sex ratios. The paper is published in the journal Proceedings of the Royal Society B and involves researchers from the UK, Spain and the USA. (medicalnewstoday.com 13.9.2017).)

(Anm: A father effect explains sex-ratio bias. (…) 'The implications are important, as we now have the proof that fathers matter independently of any maternal effects. Scientists can now improve their predictive models of sex ratios at birth, including not only mothers but also fathers. 'Proc Biol Sci. 2017 Aug 30;284(1861). pii: 20171159. doi: 10.1098/rspb.2017.1159.)

- Antipsykotikas (nevroleptikas) hemming av kompleks I i cortex i normale menneskehjerner er en parallell til den ekstrapyramidale giftigheten til antipsykotika (neuroleptika). (…) Våre data støtter hypotesen om at antipsykotika (nevroleptika)-induserte ekstrapyramidale bivirkninger kan skyldes hemming av mitokondriell respiratorisk kjede.

(Anm: Antipsykotikas (nevroleptikas) hemming av kompleks I i cortex i normale menneskehjerner er en parallell til den ekstrapyramidale giftigheten til antipsykotika (nevroleptika). (…) Våre data støtter hypotesen om at antipsykotika (neuroleptika)-induserte ekstrapyramidale bivirkninger kan skyldes hemming av mitokondriell respiratorisk kjede.(Inhibition of complex I by neuroleptics in normal human brain cortex parallels the extrapyramidal toxicity of neuroleptics. (…) Our data support the hypothesis that neuroleptic-induced extrapyramidal side effects may be due to inhibition of the mitochondrial respiratory chain.) Mol Cell Biochem. 1997 Sep;174(1-2):255-9.)

(Anm: Bivirkninger (legemiddelinduserte organskader og sykdommer) (mintankesmie.no).

(Anm: SSRI-preparater og antipsykotika har uheldige effekter på mitokondrier (mintankesmie.no).)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Mitochondrial Dysfunction and Altered Renal Metabolism in Dahl Salt-Sensitive Rats. Kidney Blood Press Res. 2017 Sep 19;42(3):587-597.)

- Mitokondrier i nervesystemet: Fra helse til sykdom, del I.

(Anm: Mitokondrier i nervesystemet: Fra helse til sykdom, del I. (Mitochondria in the nervous system: From Health to Disease, Part I.) (…) Til sist granskes nye måter å redde mitokondriell struktur og funksjon ved akutt og kronisk hjerneskade. ( Finally, novel ways to rescue mitochondrial structure and function in acute and chronic brain injury are explored.) Neurochem Int. 2017 Sep 13. pii: S0197-0186(17)30481-3.)

(Anm: Functional Mitochondria in Health and Disease. The ability to rapidly adapt cellular bioenergetic capabilities to meet rapidly changing environmental conditions is mandatory for normal cellular function and for cancer progression. Any loss of this adaptive response has the potential to compromise cellular function and render the cell more susceptible to external stressors such as oxidative stress, radiation, chemotherapeutic drugs, and hypoxia. Mitochondria play a vital role in bioenergetic and biosynthetic pathways and can rapidly adjust to meet the metabolic needs of the cell. Increased demand is met by mitochondrial biogenesis and fusion of individual mitochondria into dynamic networks, whereas a decrease in demand results in the removal of superfluous mitochondria through fission and mitophagy. (…) Concluding Remarks The ability to adapt cellular bioenergetics capabilities to meet rapidly changing environmental conditions is mandatory for cellular function and for cancer progression. Any compromise in this adaptive response has the potential to compromise cellular function and render the cell more susceptible to external stressors such as oxidative stress, radiation, chemotherapeutic drugs, hypoxia, etc. Front. Endocrinol. 2017 (03 November 2017).)

(Anm: Fluoksetin (Prozac; SSRI) og mitokondriene: En gjennomgang av de toksikologiske aspekter. (- Fluoksetin induserer også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser.) (Fluoxetine and the mitochondria: A review of the toxicological aspects. (Fluoksetin og mitokondriene: En gjennomgang av de toksikologiske aspekter.) Toxicol Lett. 2016 Jul 5. pii: S0378-4274(16)32264-0.)

- Linker mitokondrier og synaptisk overføring: CB1-reseptoren. (- Akutt aktivering av mtCB1 endrer mitokondrisk ATP-generasjon, synaptisk overføring og hukommelse, ytelse.)

(Anm: Linking Mitochondria and Synaptic Transmission: The CB1 Receptor. Abstract CB1 receptors are functionally present within brain mitochondria (mtCB1), although they are usually considered specifically targeted to plasma membrane. Acute activation of mtCB1 alters mitochondrial ATP generation, synaptic transmission, and memory performance. However, the detailed mechanism linking disrupted mitochondrial metabolism and synaptic transmission is still uncharacterized. CB1 receptors are among the most abundant G protein-coupled receptors in the brain and impact on several processes, including fear coping, anxiety, stress, learning, and memory. Mitochondria perform several key physiological processes for neuronal homeostasis, including production of ATP and reactive oxygen species, calcium buffering, metabolism of neurotransmitters, and apoptosis. It is therefore possible that acute activation of mtCB1 impacts on these different mitochondrial functions to modulate synaptic transmission. In reviewing and integrating across the literature in this area, we describe the possible mechanisms involved in the regulation of brain physiology by mtCB1 receptors. Bioessays. 2017 Oct 23. doi: 10.1002/bies.201700126.)

- Alvorlig epilepsi og sirkadisk rytmeprotein linket. Nye funn kan åpne døren til nye behandlinger av epilepsi.

(Anm: Severe epilepsy and circadian rhythm protein linked. New findings may open the door to novel epilepsy treatments. Researchers probing the brain tissue of people with severe forms of epilepsy make a surprising breakthrough: a protein involved in circadian rhythms, called CLOCK, may play a role. Epilepsy is a relatively common brain disorder that causes seizures. It affects around 1.2 percent of people in the United States, and to date, it is not curable. There are drugs available to treat the condition, but side effects can be significant and not all cases of epilepsy respond well. Although certain genetic mutations have been identified that are responsible for inherited forms of epilepsy, these only account for a minority of cases. In most cases, the exact causes are unknown. (medicalnewstoday.com 12.10.2017).)

(Anm: Epilepsi og legemidler (mintankesmie.no).)

- Stor betydning for helsen Forskning tyder på at en dårlig koordinert indre tidtagning øker risikoen for sykdom, for eksempel ved langvarig skiftarbeid.

(Anm: Får nobelpris for oppdagelsen av døgnrytmen. De amerikanske forskerne Jeffrey C. Hall, Michael Rosbash og Michael W. Young tildeles årets nobelpris i medisin eller fysiologi for oppdagelsen av den biologiske klokka. (…) Et selvregulerende urverk i kroppen Årets nobelprisvinnere begynte med å studere et gen som krevdes for bananfluens normale døgnrytme. De viste at genet kodet for et protein som økte om natten men brøt ned til lave nivåer om dagen. De identifiserte flere proteiner og kunne dermed beskrive et selvregulerende urverk i våre celler. Klokken har siden vist seg å fungere med samme prinsipp i andre flercellede organismer, også i menneske. (…) Stor betydning for helsen Forskning tyder på at en dårlig koordinert indre tidtagning øker risikoen for sykdom, for eksempel ved langvarig skiftarbeid. Etter nobelprisvinnernes oppdagelser har cirkadisk biologi utviklet seg til et dynamisk og raskt voksende forskningsfelt, med stor betydning for helsen vår. (nrk.no 2.10.2017).)

(Anm: Interview about the 2017 Nobel Prize in Physiology or Medicine (8 minutes) (nobelprize.org 2017).)

- SSRI-er (lykkepiller) forårsaker en varig serotonerg ubalanse grunnet legemidlenes skadelige endringer mht. serotonin og andre nevrotransmittere, mitokondriell dysfunksjon, avkortet levetid, plutselige dødsfall etc.

(Anm: SSRI-er (lykkepiller) forårsaker en varig serotonerg ubalanse grunnet legemidlenes skadelige endringer mht. serotonin og andre nevrotransmittere, mitokondriell dysfunksjon, avkortet levetid, plutselige dødsfall etc. (- SSRI-er øker nivået av serotonin i deler av hjernen med opptil 700 % (eller mer?), samt reduserer serotonin i blod med opptil 93 %.) (mintankesmie.no).)

(Anm: Effekten av psykostimulerende legemidler på blod-hjerne barrierens funksjon og nevroinflammasjon. (The effects of psychostimulant drugs on blood brain barrier function and neuroinflammation) (Front. Pharmacol. 2012;3:121 (Published online: 29 June 2012).)

- Antidepressiva ökar risken för benbrott hos äldre.

(Anm: Antidepressiva ökar risken för benbrott hos äldre. (…) Den förhöjda risken för höftfraktur gällde alla de vanliga antidepressiva läkemedlen, SSRI-preparat, mirtazapin och SNRI-preparat (selektiva serotonin- och noradrenalinåterupptagshämmare. Sambandet gällde även då det kontrollerats för andra faktorer som ålder, annan medicinering som ökar fallrisken, benskörhet, socioekonomisk status, kroniska sjukdomar och psykiatriska diagnoser.) (lakemedelsvarlden.se 12.1.2017).)

- Hvordan trening forynger celler, forlenger levetiden. Ny forskning gir innsyn i hvordan trening, på cellulært nivå, kan øke muskelhelse og til slutt treningskapasitet, som er "den beste indikator på dødelighet i befolkningen."

(Anm: How exercise rejuvenates cells, extending lifespan. New research provides a window into how, on a cellular level, exercise can improve muscle health and, ultimately, exercise capacity, which is "the best predictor of mortality in the general population." A new study published in the journal Nature Communications describes how exercise helps the body to keep the cells in the muscles healthy and strong. "Whether muscle is healthy or not really determines whether the entire body is healthy or not," says lead researcher Prof. Zhen Yan, of the University of Virginia School of Medicine in Charlottesville. "And exercise capacity, mainly determined by muscle size and function," he adds, "is the best predictor of mortality in the general population." According to the new study, exercise improves muscle health by renewing its cellular powerhouse: the mitochondria. Mitochondria are crucial to the good functioning of our bodies, as well as to our overall health and longevity. These tiny parts of the cell turn the food we eat into energy. Mitochondria transform proteins, fats, and sugars into the fuel that the body needs to live. So, how does exercise affect the mitochondria in the muscles? Exercise promotes mitophagy in mice The answer given by the new study is through "mitophagy." Mitophagy describes the process by which damaged or defective mitochondria are selected and removed, usually after a period of stress. In the case of muscles, mitophagy contributes to keeping skeletal muscle healthy and strong. And to show how exercise induces mitophagy, Prof. Yan and team genetically modified mice to carry a gene that helps to report on the effects of physical activity. This gene is called pMitoTimer. It makes mitochondria fluorescent, allowing the researchers to study mitophagy in vivo, after the mice engaged in 90 minutes of treadmill running. Three to 12 hours after the running session, the researchers observed that mitochondria showed signs of stress. After 6 hours, they saw signs of mitophagy. Prof. Yan explains the effect of exercise on mitochondria through an analogy that includes a vehicle inspection, the purpose of which is to remove defective cars from the streets. "Aerobic exercise removes damaged mitochondria in skeletal muscle. If you do it repeatedly, you keep removing the damaged ones. You have a better muscle with better mitochondrial quality. We clean up the clunkers, now the city, the cell, is full of healthy, functional cars." Prof. Zhen Yan Chemical reaction in mitophagy identified The researchers also identified the molecular mechanism behind the process. The treadmill workout seemed to activate a kinase called AMPK. A kinase is an enzyme that modifies other proteins through a process called phosphorylation. In this biochemical process, phosphate groups are added to proteins. The researchers determined that, in a biochemical chain reaction, AMPK triggers another kinase called Ulk1. Prof. Yan continues the vehicle inspection analogy, saying, "When [it's] turned on, Ulk1 activates other components in the cell to execute the removal of dysfunctional mitochondria." "It's analogous to a 911 call where a tow truck removes the clunkers. However," he says, "we still do not know how these activities are coordinated." To confirm their discovery - that Ulk1 plays a critical role in mitophagy - the team created a mouse model lacking the Ulk1 gene. These mice were also subjected to treadmill exercise, but the ensuing mitophagy was considerably inhibited. Mice that were unable to do mitophagy did not have the benefit of exercise," explains study co-author Joshua Drake, a postdoctoral fellow in Prof. Yan's laboratory. "Even though, from an exercise standpoint, they still were able to run just as far as normal mice, they didn't benefit metabolically with training," he adds.
"These findings provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 signaling in skeletal muscle," the authors conclude. (medicalnewstoday.com 29.9.2017).)

- Ampk fosforylering av Ulk1 er krevet for målretting av mitokondrier til lysosomer i treningsinducert mitofagi. (- Mitokondriell helse er kritisk for skjelettmuskulaturfunksjon og forbedres ved trening gjennom både mitokondriell biogenese og fjerning av skadede / dysfunksjonelle mitokondrier via mitofagi.)

(Anm: Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy. Abstract Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555. Using mice expressing dominant negative and constitutively active Ampk in skeletal muscle, we demonstrate that Ulk1 activation is dependent on Ampk. Furthermore, exercise-induced metabolic adaptation requires Ulk1. These findings provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 signaling in skeletal muscle.Exercise is associated with biogenesis and removal of dysfunctional mitochondria. Here the authors use a mitochondrial reporter gene to demonstrate the occurrence of mitophagy following exercise in mice, and show this is dependent on AMPK and ULK1 signaling. Nat Commun. 2017 Sep 15;8(1):548.)

- Proteinforskning ved University of Kent kan hjelpe i jakten på en kur mot Alzheimers og Parkinsons.

(Anm: Protein research at University of Kent could help in hunt for Alzheimer's and Parkinson's cures. Research carried out at the University of Kent has the potential to influence the future search for treatment of neurodegenerative diseases that are linked to a family of protein molecules known as 'amyloid'. The findings by a team of scientists led by Dr Wei-Feng Xue in the School of Biosciences could lead to a better understanding of the diseases, and suggest potential diagnostics and therapeutics strategies to combat amyloid-associated disease progression and their possible infectivity. Currently, there is a gap in the knowledge of the factors that govern the infectious potential of amyloid in general. In an article published in the journal eLife, Dr Xue's team report on their investigations into why some forms of amyloid are highly infectious - the so-called prion form associated with BSE (Mad Cow Disease) and the human form, CJD (Creutzfeldt Jakob Disease) - while others are less infectious or even inert. (news-medical.net 11.9.2017).)

- Mitokondrielle nano-tunneler. (- Samlingen av individuelle mitokondrier til dynamiske nettverk av kommunikasjonsorganeller via nanotunneller og andre mekanismer har store implikasjoner for organell og cellulær funksjon.)

(Anm: Mitochondrial Nanotunnels. Abstract Insight into the regulation of complex physiological systems emerges from understanding how biological units communicate with each other. Recent findings show that mitochondria communicate at a distance with each other via nanotunnels, thin double-membrane protrusions that connect the matrices of non-adjacent mitochondria. Emerging evidence suggest that mitochondrial nanotunnels are generated by immobilized mitochondria and transport proteins. This review integrates data from the evolutionarily conserved structure and function of intercellular projections in bacteria with recent developments in mitochondrial imaging that permit nanotunnel visualization in eukaryotes. Cell type-specificity, timescales, and the selective size-based diffusion of biomolecules along nanotunnels are also discussed. The joining of individual mitochondria into dynamic networks of communicating organelles via nanotunnels and other mechanisms has major implications for organelle and cellular behaviors. Trends Cell Biol. 2017 Sep 18. pii: S0962-8924(17)30146-0. [Epub ahead of print].)

(Anm: Jakten på leukemi-cellenes hemmelige nano-tunneler. Maria Omsland disputerer fredag 03.02.2017 for ph.d.-graden ved Universitetet i Bergen med avhandlingen: «Investigation of the intercellular structure tunneling nanotube (TNT) in leukemia». Nanotunnelen er en struktur, som blir brukt til kommunikasjon mellom celler. Den ble beskrevet første gang av Rustom og medarbeidere i 2004. Det er en tynn (50-200 nm) tunnel-lignende struktur, som består av filamentøst-aktin (F-aktin) er dekket av plasmamembran og kan koble sammen celler. Den biologiske funksjonen til nanotunnelen, og det molekylære maskineriet bak dannelsen, er fortsatt ikke kartlagt. Det er derimot kjent at denne strukturen kan tillate transport av ulike komponenter mellom celler. (uib.no 26.1.2017).)

(Anm: Peripheral blood mitochondrial DNA content in relation to circulating metabolites and inflammatory markers: A population study. Abstract Mitochondrial DNA (mtDNA) content might undergo significant changes caused by metabolic derangements, oxidative stress and inflammation that lead to development and progression of cardiovascular diseases. (…) We demonstrated that in a general population relative peripheral blood mtDNA content was associated with circulating metabolites indicative of perturbed lipid metabolism and with inflammatory biomarkers. PLoS One. 2017 Jul 13;12(7):e0181036. doi: 10.1371/journal.pone.0181036. eCollection 2017.)

- Forskere fikk gjennombrudd mht. å forstå kraftverket til menneskelige celler. (- Når det gjelder mitokondrier må proteiner krysse grenser til to membraner for å komme inn i dem. "Vi så etter - og var i stand til å ta bilder med enestående detaljer – av ribosomer festet til mitokondrier.)

(Anm: Scientists make breakthrough in understanding the powerhouse of human cells. Scientists have made a breakthrough in understanding how mitochondria - the "powerhouses" of human cells - are made. Mitochondria, which exist within human cells but have their own DNA, need many different proteins to function - but the process of how they get these has never been imaged in detail. Now a study led by Dr Vicki Gold, of the University of Exeter, has shown that some ribosomes - the tiny factories of cells which produce proteins - are attached to mitochondria. This can explain how proteins are pushed into mitochondria whilst they are being made. The findings open new avenues for studying protein targeting and mitochondrial dysfunction, which has been implicated in diseases including cancer and neurodegenerative disorders such as Parkinson's. "Proteins are responsible for nearly all cellular processes. The cell has to make a huge variety of proteins and target them to the precise location where they are needed to function," said Dr Gold, of Exeter's Living Systems Institute. "In the case of mitochondria, proteins have to cross the boundary of two membranes to get inside them. "We looked for - and were able to image at unprecedented detail - ribosomes attached to mitochondria." The images were taken using cutting-edge technology called cryo-electron microscopy. Dr Gold and her colleague Dr Bertram Daum have both come from Germany to set up a cryo-electron microscopy facility at the University of Exeter. Having made the latest discovery by studying healthy cells, Dr Gold now plans to see how the process works in unhealthy cells. "Mitochondria are the energy factories of the cell, so when they don't function properly it can lead to a huge range of health problems," she said. "In many cases these are age-related disorders like Parkinson's disease. "Our findings may help us understand these conditions better, which is an important step towards better treatments." (medicalnewstoday.com 31.8.2017).)

- Mitokondriesykdommer som modell for neurodegenerasjon. (- "Mitokondrier" delvis autonom (uavhengig) sofistikert cellulær organelle involvert i et bredt spekter av kritiske cellulære funksjoner kjent som cellens kraftverk hvor ATP (adenosintrifosfat) - produksjonen finner sted, som er den cellulære energikilden.)

(Anm: Mitokondriesykdommer som modell for neurodegenerasjon. (Mitochondrial Diseases as Model of Neurodegeneration.) Abstrakt "Mitokondrier" delvis autonom (uavhengig) sofistikert cellulær organelle involvert i et bredt spekter av kritiske cellulære funksjoner kjent som cellens kraftverk hvor ATP (adenosintrifosfat) - produksjonen finner sted, som er den cellulære energikilden. (Mitochondrial Diseases as Model of Neurodegeneration.( Abstract "Mitochondria" partially autonomous sophisticated cellular organelle involved in a wide range of crucial cellular functions, well known as the power house of the cell where ATP (adenosine triphosphate) production takes place, that is the cellular source of energy.) Adv Exp Med Biol. 2017;1007:129-155.)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Fluoksetin (Prozac; SSRI) og mitokondriene: En gjennomgang av de toksikologiske aspekter. (- Fluoksetin induserer også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser.) (Fluoxetine and the mitochondria: A review of the toxicological aspects. (Fluoksetin og mitokondriene: En gjennomgang av de toksikologiske aspekter.) Toxicol Lett. 2016 Jul 5. pii: S0378-4274(16)32264-0.)

(Anm: SSRI-er (lykkepiller) forårsaker en varig serotonerg ubalanse grunnet legemidlenes skadelige endringer mht. serotonin og andre nevrotransmittere, mitokondriell dysfunksjon, avkortet levetid, plutselige dødsfall etc. (- SSRI-er øker nivået av serotonin i deler av hjernen med opptil 700 % (eller mer?), samt reduserer serotonin i blod med opptil 93 %.) (mintankesmie.no).)

(Anm: Effekten av psykostimulerende legemidler på blod-hjerne barrierens funksjon og nevroinflammasjon. (The effects of psychostimulant drugs on blood brain barrier function and neuroinflammation) (Front. Pharmacol. 2012;3:121 (Published online: 29 June 2012).)

(Anm: Mitochondrial diseases: Yeast as a model for the study of suppressors. (…) Results support the possibility that a small peptide could correct defects associated with many mt tRNA mutations, suggesting a novel therapy for mitochondrial diseases treatment. The involvement of the mt EF-Tu in cellular heat stress response has also been suggested. Biochim Biophys Acta. 2017 Apr;1864(4):666-673.)

- Dette må du vite for å unngå å bli syk av ris- og pastarestene. - Hovedsynderen er en bakterie som heter Bacillus cereus, sier ekspert. (- Ris og pasta som er lagret over seks timer i romtemperaturer gjøre deg syk.) (- Granum har forsket på Bacillus cereus i mat i over 30 år. Han forklarer at toksinet produseres ved temperaturer mellom 10 og 40 grader, at det dannes raskest ved romtemperatur, og raskere ved lavere enn ved høyere temperaturer: – Toksinet ødelegger mitokondriene i menneskecellene slik at cellen dør. I høye konsentrasjoner vil toksinet kunne gi leversvikt og i verste fall føre til døden.)

(Anm: Dette må du vite for å unngå å bli syk av ris- og pastarestene. - Hovedsynderen er en bakterie som heter Bacillus cereus, sier ekspert. (…) Ifølge Per Einar Granum, som er professor ved Norges miljø- og biovitenskapelige universitet, NMBU, kan ris og pasta som er lagret over seks timer i romtemperaturer gjøre deg syk. Og rester som har ligget i over et døgn i romtemperatur kan i verste fall være dødelige. – Hovedsynderen er en bakterie som heter Bacillus cereus, sier Granum og forklarer at bakterien lever i jorden, og at den på den måten havner i ris, pasta og mel. – Bakterien er lite konkurransedyktig, og så lenge det er andre bakterier tilstede vil den ikke vinne i konkurransen med dem. Problemet oppstår under varmebehandling, når alle andre bakterier dør. Da vil dannede sporer spire, og om maten deretter lagres i temperaturer over 10 grader vil toksinet begynne å dannes. Granum har forsket på Bacillus cereus i mat i over 30 år. Han forklarer at toksinet produseres ved temperaturer mellom 10 og 40 grader, at det dannes raskest ved romtemperatur, og raskere ved lavere enn ved høyere temperaturer: – Toksinet ødelegger mitokondriene i menneskecellene slik at cellen dør. I høye konsentrasjoner vil toksinet kunne gi leversvikt og i verste fall føre til døden. (kk.no 27.9.2017).)

— Behandling med antidepressiva og forverring av hvit substans påvist ved MRI hos eldre. (—  Resultater Bruk av hvilken som helst antidepressiva i løpet av studien ble assosiert med forverring av hvit substans.)

(Anm: Behandling med antidepressiva og forverring av hvit substans påvist ved MRI hos eldre. (…) Resultater — Bruk av hvilken som helst antidepressiva i løpet av studien ble assosiert med forverring av hvit substans.) (Antidepressant Treatment and Worsening White Matter on Serial Cranial Magnetic Resonance Imaging in the Elderly. (…) Results— Use of any antidepressant during the period of study was associated with worsening white matter.) (Stroke 2008; 39: 857-862).)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

- Hvit substans i hjernens kan holde ledetråder til autisme, ADHD.

(Anm: Brain White Matter May Hold Clues to Autism, ADHD. Researchers say there may be a connection between abnormalities in the brain’s white matter and the severity of symptoms in autism and ADHD. There may be a link between white matter in the brain and autism. Researchers at the New York University (NYU) School of Medicine have found a consistent connection between structural abnormalities in the brain’s white matter with the severity of symptoms in people with autism. The study was published earlier this month in JAMA Psychiatry. Researchers say these findings hold true in children with autism spectrum disorder (ASD) as well as, to some degree, in children with attention deficit hyperactivity disorder (ADHD) who have autistic traits. According to the Centers for Disease Control and Prevention (CDC), one in 68 children has some degree of ASD. (medicalnewstoday.com 13.9.2017).)

- Mitokondrier i nervesystemet: Fra helse til sykdom, del I.  (- Til sist granskes nye måter å redde mitokondriell struktur og funksjon ved akutt og kronisk hjerneskade.)

(Anm: Mitochondria in the nervous system: From Health to Disease, Part I. (Mitokondrier i nervesystemet: Fra helse til sykdom,) del I. Abstrakt I denne spesialutgaven om "Mitokondrier i nervesystemet: Fra helse til sykdom" samler redaktører bidrag fra eksperter innen hjernens mitokondrielle forskning for å gi en oppdatert oversikt over mitokondriell funksjon i fysiologi og patologi. Utgaven gir banebrytende vurderinger på klassiske områder av mitokondriell biologi som inkluderer bruk av energisubstrat, kalsiumhåndtering, mitokondrieendoplasmisk retikulumkommunikasjon og celledødsregulering. Ytterligere vurderinger og originale forskningsartikler berører viktige mitokondrielle defekter som er sett på tvers av flere nevrodegenerative tilstander, inkludert fragmentering, tap av respiratorisk kapasitet, kalsiumoverbelastning, forhøyet reaktiv oksygenproduksjon, foruroligende NAD + metabolisme, endret proteinacetylering og kompromittert mitofagi. Linker som anskueliggjøres mellom genetikk mht. nevrodegenerative forstyrrelser og forstyrrelser i mitokondriell funksjon diskuteres, og en ny musemodell av kompleks I-mangel er beskrevet. Endelig utforskes nye måter å redde mitokondriell struktur og funksjon i akutt og kronisk hjerneskade. (Mitochondria in the nervous system: From Health to Disease, Part I.Abstract In Part I of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together contributions from experts in brain mitochondrial research to provide an up-to-date overview of mitochondrial functioning in physiology and pathology. The issue provides cutting edge reviews on classical areas of mitochondrial biology that include energy substrate utilization, calcium handling, mitochondria-endoplasmic reticulum communication, and cell death regulation. Additional reviews and original research articles touch upon key mitochondrial defects seen across multiple neurodegenerative conditions, including fragmentation, loss of respiratory capacity, calcium overload, elevated reactive oxygen species generation, perturbed NAD+ metabolism, altered protein acetylation, and compromised mitophagy. Emerging links between the genetics of neurodegenerative disorders and disruption in mitochondrial function are discussed, and a new mouse model of Complex I deficiency is described. Finally, novel ways to rescue mitochondrial structure and function in acute and chronic brain injury are explored.) Neurochem Int. 2017 Sep 13. pii: S0197-0186(17)30481-3.)

(Anm: Commentary: Nix restores mitophagy and mitochondrial function to protect against PINK1/Parkin-related Parkinson's disease. Front. Mol. Neurosci., 19 September 2017.)

(Anm: Nix is a selective autophagy receptor for mitochondrial clearance. EMBO Rep. 2010 Jan; 11(1): 45–51. Published online 2009 Dec 11.)

- Mitofagi ved Parkinsons sykdom: Patogene og terapeutiske implikasjoner. Nevroner påvirket av Parkinsons sykdom (PD) opplever mitokondriell dysfunksjon og bioenergetiske underskudd som oppstår tidlig og fremmer den sykdomsrelaterte a-synucleinopati.

(Anm: Mitophagy in Parkinson’s Disease: Pathogenic and Therapeutic Implications. Neurons affected in Parkinson’s disease (PD) experience mitochondrial dysfunction and bioenergetic deficits that occur early and promote the disease-related α-synucleinopathy. Emerging findings suggest that the autophagy-lysosome pathway, which removes damaged mitochondria (mitophagy), is also compromised in PD and results in the accumulation of dysfunctional mitochondria. Studies using genetic-modulated or toxin-induced animal and cellular models as well as postmortem human tissue indicate that impaired mitophagy might be a critical factor in the pathogenesis of synaptic dysfunction and the aggregation of misfolded proteins, which in turn impairs mitochondrial homeostasis. Interventions that stimulate mitophagy to maintain mitochondrial health might, therefore, be used as an approach to delay the neurodegenerative processes in PD. Front. Neurol., 04 October 2017).)

- Stadig flere får Alzheimers sykdom: Når kraftverkene i hjernen svikter. (- Basert på de foreløpige resultatene våre, er det grunn til å tro at viktige bidrag til Alzheimers sykdom i stor grad skyldes at mitokondriene ikke fungerer som de skal.)

(Anm: Stadig flere får Alzheimers sykdom: Når kraftverkene i hjernen svikter. Hjernens behov for energi er enormt. Mitokondriene gjør jobben. Men noen ganger går det galt. (…) Av alt blodet hjertet pumper ut i kroppen, ender hele 20 prosent i hjernen, selv om den bare utgjør rundt to prosent av kroppsvekten. (…) Hjernens forbruk i hvile er hele 60 prosent av kroppens glukose. Det er helt enormt! Kraftverkene Hva er det som omsetter all denne glukosen til energi? Det er mitokondriene, kroppens små og iherdige kraftverk. De finnes inne i cellene. I en hudcelle er det ganske få av dem, i en muskelcelle eller en hjernecelle, flere tusen. (...) En hel verden leter nå etter medisiner som effektivt kan bremse eller kurere Alzheimers sykdom. – Jo mer vi vet om de molekylære mekanismene bak sykdommen, dess bedre står vi rustet til å behandle den. Da er det viktig å finne ut når sykdommen oppstår: Hva skyldes sviktende DNA-reparasjon? Og hva skyldes sviktende mitokondrieaktivitet? Basert på de foreløpige resultatene våre, er det grunn til å tro at viktige bidrag til Alzheimers sykdom i stor grad skyldes at mitokondriene ikke fungerer som de skal. Hos de ulike undergruppene av pasienter med sykdomme, kan mitokondriedefekter ha mer eller mindre å si; her er det kanskje mer en defekt i DNA-reparasjon, mens der er det mer mitokondriell dysfunksjon. – Det vi vil med framtidens medisin, og ikke minst med personlig medisin, er jo nettopp å forstå hvordan arvematerialet vårt predisponerer oss for å havne i den ene eller den andre undergruppen. (apollon.uio.no 22.8.2016).)

(Anm: Mitochondria (mitokondrie) (mitokondriesykdommer) (mitokondrielle sykdommer). (mintankesmie.no).)

(Anm: I denne studien oppdaget forskerne at det å ta visse antidepressiva, sedativer, beroligende midler eller antipsykotika økte veteranenes risiko for å utvikle demens sammenlignet med risikoen for veteraner som ikke tok slike legemidler. PTSD and psychoactive drugs linked to increased risk for dementia.) (newmedpagetoday.com 9.5.2017.)

- Alzheimer: Lavt serotoninnivå kan drive utviklingen. En av hypotesene frem til nå har vært at nevrotransmitteren serotonin spiller en nøkkelrolle. (…) Prof. Smith bemerker imidlertid at SSRI-behandling for Alzheimers sykdom ikke har vist seg å være vellykket.

(Anm: Alzheimer: Lavt serotoninnivå kan drive utviklingen. En av hypotesene frem til nå har vært at nevrotransmitteren serotonin spiller en nøkkelrolle. (…) Prof. Smith bemerker imidlertid at SSRI-behandling for Alzheimers sykdom ikke har vist seg å være vellykket. (Alzheimer's: Low serotonin levels may drive development. One of the hypotheses put forth so far has been that the neurotransmitter serotonin plays a key role. In recent years, studies have accumulated evidence that people with Alzheimer's disease have less of this brain chemical, which is known to regulate mood, sleep, appetite, and sexual function, among other things. (…) Prof. Smith notes, however, that SSRI treatment for Alzheimer's disease has not been proven successful. The reason for this, she ventures, might be that SSRIs need to bind to serotonin transporters in order to work, but in patients with Alzheimer's disease, it is precisely these transporters that are missing. She therefore suggests that serotonin receptors - rather than transporters - might be a better therapeutic target. (medicalnewstoday.com 16.8.2017).)

(Anm: Antidepressiva (nytteverdi) (mintankesmie.no).)

(Anm: Dementia and low brain serotonin may be linked: Study finds. Johns Hopkins researchers looked into the brain scans of persons with mild loss of thought and memory and have found that they have significantly low levels of serotonin in their brains. Serotonin is a natural brain chemical that is responsible for several functions including mood, sleep and appetite and also is important for several mental health conditions. (…) This new study on persons with early stages of memory decline showed conclusively that serotonin loss was causing the memory loss rather than the other way round. The study is published in the September issue of the journal Neurobiology of Disease. (…) According to Smith, with this idea in mind, researchers have already tried to treat Alzheimer’s disease and other diseases of cognitive decline with SSRIs but have met with limited success. But these drugs need adequate number of serotonin transporters or SERTs in the brain to work, she noted, and that was missing among those with cognitive decline. That is probably why SSRIs do not show as much success as expected. (medicalnewstoday.com 14.8.2017).)

- Kokain og ecstasy forårsaker DNA-mutasjon: studie

Cocaine and ecstasy cause DNA mutation: study (Kokain og ecstasy forårsaker DNA-mutasjon: studie)
Reuters Health 5.12.2003
- Cocaine and ecstasy not only cause addiction and raise the risk of cancer but also provoke genetic mutations, Italian scientists said on Friday.

"Cocaine and ecstasy have proved to be more dangerous than we had imagined," said Giorgio Bronzetti, chief scientist at the National Center for Research's (CNR) biotechnology department.

"These drugs, on top of their toxicological effects, attack DNA provoking mutations and altering the hereditary material. This is very worrying for the effects it could have on future generations," he said. (...)

(Anm: Kokainbruk og slagrisiko (nhi.no 18.2.2014).)

(Anm: Ecstasy er i likhet med SSRIer (lykkepiller) en såkalt serotoninreopptakshemmer, dvs. ecstasy og SSRIer har enkelte likhetstrekk mht. mulige bivirkninger, bl.a. antikolinerge skadevirkninger, såkalt serotonin syndrom etc. (mintankesmie.no).)

- Mitochondrial complex I bridges a connection between regulation of carbon flexibility and gastrointestinal commensalism in the human fungal pathogen Candida albicans.

(Anm: Mitochondrial complex I bridges a connection between regulation of carbon flexibility and gastrointestinal commensalism in the human fungal pathogen Candida albicans. Abstract Efficient assimilation of alternative carbon sources in glucose-limited host niches is critical for colonization of Candida albicans, a commensal yeast that frequently causes opportunistic infection in human. C. albicans evolved mechanistically to regulate alternative carbon assimilation for the promotion of fungal growth and commensalism in mammalian hosts. However, this highly adaptive mechanism that C. albicans employs to cope with alternative carbon assimilation has yet to be clearly understood. Here we identified a novel role of C. albicans mitochondrial complex I (CI) in regulating assimilation of alternative carbon sources such as mannitol. Our data demonstrate that CI dysfunction by deleting the subunit Nuo2 decreases the level of NAD+, downregulates the NAD+-dependent mannitol dehydrogenase activity, and consequently inhibits hyphal growth and biofilm formation in conditions when the carbon source is mannitol, but not fermentative sugars like glucose. Mannitol-dependent morphogenesis is controlled by a ROS-induced signaling pathway involving Hog1 activation and Brg1 repression. In vivo studies show that nuo2Δ/Δ mutant cells are severely compromised in gastrointestinal colonization and the defect can be rescued by a glucose-rich diet. Thus, our findings unravel a mechanism by which C. albicans regulates carbon flexibility and commensalism. Alternative carbon assimilation might represent a fitness advantage for commensal fungi in successful colonization of host niches. PLoS Pathog. 2017 Jun 1;13(6):e1006414. eCollection 2017 Jun.)

- Mitochondrial complex I deficiency enhances skeletal myogenesis but impairs insulin signaling through SIRT1 inactivation

Mitochondrial complex I deficiency enhances skeletal myogenesis but impairs insulin signaling through SIRT1 inactivation
J Biol Chem. 2014 Jun 3. pii: jbc.M114.560078. [Epub ahead of print]
Abstract To address whether mitochondrial biogenesis is essential for skeletal myogenesis, C2C12 myogenesis was investigated after knockdown of NADH dehydrogenase [ubiquintone] flavoprotein 1 (NDUFV1), which is an oxidative phosphorylation complex I (CI) subunit that is the first subunit to accept electrons from NADH. The NDUFVI knockdown enhanced C2C12 myogenesis by decreasing the NAD+/NADH ratio and subsequently inactivating SIRT1 and SIRT1 activators (pyruvate, SRT1720 and resveratrol) abolished the NDUFV1 knockdown-induced myogenesis enhancement. However, the insulin-elicited activation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) was reduced with an elevated levels of protein tyrosine phosphatase 1B (PTP1B) after NDUFV1 knockdown in C2C12 myotubes. The NDUFV1 knockdown-induced blockage of insulin signaling was released by PTP1B knockdown in C2C12 myotubes and we found that NDUFV1 or SIRT1 knockdown did not affect mitochondria biogenesis during C2C12 myogenesis. Based on these data, we can conclude that CI dysfunction-induced SIRT1 inactivation leads to myogenesis enhancement but blocks insulin signaling without affecting mitochondria biogenesis. (…)

(Anm: In Vivo Assessment of Mitochondrial Dysfunction in Clinical Populations Using Near-Infrared Spectroscopy. (…) Conclusion Recent studies have demonstrated the utility of NIRS in the evaluation of mitochondrial dysfunction in persons with neurological, autoimmune, cardiovascular, and mitochondrial diseases. NIRS provides an affordable, versatile, and noninvasive technique for evaluating mitochondrial oxidative capacity of skeletal muscle in clinical populations. Front. Physiol., 14 September 2017.)

- Suicidalitet og aggresjon under behandling med antidepressiva.

(Anm: Suicidalitet og aggresjon under behandling med antidepressiva. Alkohol og alvorlige skader under behandling med antidepressiva. Suicidality and aggression during antidepressant treatment. Alcohol and serious harms of antidepressant treatment. BMJ 2016;352:i892 (Published 17 February 2016).)

(Anm: Straffesaker (fengselsstraff) (mintankesmie.no).)

- Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking.

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smokng. BMJ Open 2017;7:e016224.)

Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

- Her behandles piger og kvinder, der lider af svimmelhed, hovedpine eller lammelser, der muligvis skyldes vaccinen. 29 procent af dem, hvilket svarer til næsten hver tredje, havde indløst en recept på medicin mod en psykiatrisk lidelse i løbet af fem år inden vaccinationen.

(Anm: Ny forskning viser igen, at piger og kvinder, der søger hjælp til behandling af formodede bivirkninger efter hpv-vaccinen, har oftere end andre været berørt af angst, depression eller anden psykisk sygdom, inden de blev vaccineret. (…) Undersøgelsen lægger sig op ad en undersøgelse fra Statens Serum Institut fra 2016. Den nye undersøgelse bygger på data fra 1496 kvinder, som i 2015 var henvist til et af regionernes fem hpv-centre. Her behandles piger og kvinder, der lider af svimmelhed, hovedpine eller lammelser, der muligvis skyldes vaccinen. 29 procent af dem, hvilket svarer til næsten hver tredje, havde indløst en recept på medicin mod en psykiatrisk lidelse i løbet af fem år inden vaccinationen. De er sammenlignet med 2240 jævnaldrende kvinder, som også er vaccinerede, men som ikke har søgt behandling.) (jyllands-posten.dk 19.9.2017).)

- En dansk undersøkelse viste at omtrent halvdelen av forskrivninger av selektive serotoninreopptakshemmere (SSRI-preparater) gjelder funksjonsfriske mennesker (4).

(Anm: Selektive serotonin- reopptakshemmere – skade ikke dokumentert? (…) En undersøkelse publisert i 1999 viste at ni av ti allmennpraktiserende leger ikke var oppmerksom på serotonergt syndrom (2).  (…) En dansk undersøkelse viste at omtrent halvdelen av forskrivninger av selektive serotoninreopptakshemmere (SSRI-preparater) gjelder funksjonsfriske mennesker (4). Slike preparater fører muligens til en marginal økning i antall selvmord (5). Tidsskr Nor Legeforen 2002 122:731.)

(Anm: Fluoksetin (Prozac; SSRI) og mitokondriene: En gjennomgang av de toksikologiske aspekter. (- Fluoksetin induserer også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser. (...) På den annen side har inntak av fluoxetin blitt assosiert med økt risiko for kreft. Likevel forblir data motstridende og ingen konklusjoner er trukket.) (Fluoxetine and the mitochondria: A review of the toxicological aspects. (Fluoksetin og mitokondriene: En gjennomgang av de toksikologiske aspekter. (...) On the other hand, fluoxetine intake has been associated with increased cancer risk.) Toxicol Lett. 2016 Jul 5. pii: S0378-4274(16)32264-0.)

- Har Mitokondrier et immunsystem?

(Anm: Do Mitochondria Have an Immune System? Abstract The question if mitochondria have some kind of immune system is not trivial. The basis for raising this question is the fact that bacteria, which are progenitors of mitochondria, do have an immune system. The CRISPR system in bacteria based on the principle of RNA interference serves as an organized mechanism for destroying alien nucleic acids, primarily those of viral origin. We have shown that mitochondria are also a target for viral attacks, probably due to a related organization of genomes in these organelles and bacteria. Bioinformatic analysis performed in this study has not given a clear answer if there is a CRISPR-like immune system in mitochondria. However, this does not preclude the possibility of mitochondrial immunity that can be difficult to decipher or that is based on some principles other than those of CRISPR. Biochemistry (Mosc). 2016 Oct;81(10):1229-1236.)

- Mitokondrier: En hovedregulator av makrofag og T-celle-immunitet.

(Anm: Mitochondria: A master regulator in macrophage and T cell immunity. Abstract Orchestrating biological activities of immune cells through metabolic reprogramming reveals a new approach to harnessing immune responses. Increasing evidence reveals that the mitochondrion is a central regulator for modulating metabolic reprogramming and controlling immune cell activation and functions. In addition to supporting bioenergetic demands, the mitochondrion serves as a signaling platform through the generation of reactive oxygen species and metabolites of the tricarboxylic acid cycle to modulate signaling cascades controlling immune cell activation and immune responses. Herein, we discuss the mechanisms through which the mitochondrion acts as a master regulator to fine-tune immune responses elicited by macrophages and T cells. Mitochondrion. 2017 Nov 13. pii: S1567-7249(17)30214-3.)

(Anm: Makrofag, stor «etecelle» (fagocytt) som har viktige renovasjons- og forsvarsfunksjoner i organismen. De dannes fra monocyttene, som er en type hvit blodcelle (se blod). Monocyttene kommer fra benmargen og finnes i blodet. Makrofager finnes i mange organer og vev, men de er særlig tallrike i milt, lever og lunge. De finnes også i bindevevet, spesielt der det pågår en betennelsesprosess. Kilde: Store norske leksikon.)

(Anm: Immunobiology: The Immune System in Health and Disease. 5th edition. Chapter 8T Cell-Mediated Immunity. Once they have completed their development in the , enter the bloodstream and are carried by the circulation. On reaching a peripheral lymphoid organ they leave the blood again to migrate through the lymphoid tissue, returning to the bloodstream to recirculate between blood and peripheral lymphoid tissue until they encounter their specific . Mature recirculating T cells that have not yet encountered their antigens are known as naive T cells. To participate in an , a naive T cell must first encounter antigen, and then be induced to proliferate and differentiate into cells capable of contributing to the removal of the antigen. We will term such cells because they act very rapidly when they encounter their specific antigen on other cells. The cells on which armed effector T cells act will be referred to as their . Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001. Chapter 8, T Cell-Mediated Immunity. Available from: https://www.ncbi.nlm.nih.gov/books/NBK10762/.)

- Type 1 diabetes: Kan endrede blodstamceller føre til en kur? (- "Den hellige gral" for forskere som søker en kur for type 1 diabetes er å finne en måte å forebygge eller stoppe immunforsvarets angrep på betacellene.)

(Anm: Type 1 diabetes: Could modified blood stem cells lead to a cure? Increasing levels of a certain protein in blood stem cells so that the immune system stops attacking insulin cells in the pancreas could be a way to halt type 1 diabetes, according to a new study reported in Science Translational Medicine. (…) The "holy grail" of scientists seeking a cure for type 1 diabetes is to find a way to prevent or stop the immune attack on the beta cells. (…) Now, in the new study, the researchers — who were led by senior investigator Paolo Fiorina, an assistant professor of pediatrics at Harvard Medical School's Boston Children's Hospital — might have discovered why treatments that use the person's own blood stem cells may not always work. "We found that in diabetes," explains Prof. Fiorina, "blood stem cells are defective, promoting inflammation and possibly leading to the onset of disease." The defect that they discovered is that the blood stem cells — that is, the progenitor cells that give rise to mature cells — do not produce enough of a protein called PD-L1 that reigns back attack by T cells. (medicalnewstoday.com 17.11.2017).)

(Anm: Type 1 Diabetes: What Are The Symptoms? (medicinenet.com 2.8.2016).)

(Anm: Type 2 Diabetes Overview (webmd 2.2.2016).)

(Anm: Diabetes: Kender du forskel på type 1 og 2? (netdoktor.dk 6.6.2017).)

(Anm: What is the immune system? (medicalnewstoday.com 17.11.2017).)

(Anm: Diabetes (mintankesmie.no).)

- Norsk forskerbragd: Ditt eget immunforsvar kan utløse kronisk sykdom og ta liv. (- – Når dette immunapparatet overaktiveres, misforstår og går løs på kroppen selv, så blir det kroppens verste fiende, sier han. Da utløses en betennelsesreaksjon eller en blodforgiftning, og pasienten kan i verste fall dø.)

(Anm: Norsk forskerbragd: Ditt eget immunforsvar kan utløse kronisk sykdom og ta liv. Immunforsvaret kan bli kroppens verste fiende, ifølge ny, norsk forskning. Den norske legen Tom Eirik Mollnes høster internasjonal anerkjennelse for å ha bidratt med ny og skremmende kunnskap om kroppens eget immunforsvar. Udetonert bombe – Det er som en udetonert bombe, sier forskeren som tok sin doktorgrad i Oslo. Siden har han samarbeidet med en rekke medisinske miljøer i Norge og Danmark for å dokumentere sin teori om at kroppens eget immunforsvar i gitte situasjoner kan utløse kronisk sykdom og i verste fall ta liv. – Når dette immunapparatet overaktiveres, misforstår og går løs på kroppen selv, så blir det kroppens verste fiende, sier han. Da utløses en betennelsesreaksjon eller en blodforgiftning, og pasienten kan i verste fall dø. (tv2.no 14.11.2017).)

- En pasient på UNN døde av blodforgiftning som følge av et legemiddel mot psykiske lidelser, opplyser Statens helsetilsyn.

(Anm: En pasient på UNN døde av blodforgiftning som følge av et legemiddel mot psykiske lidelser, opplyser Statens helsetilsyn. (- Pasienten døde etter kort tid, og dødsårsaken var nøytropen sepsis (blodforgiftning), heter det i tilsynets rapport. (nrk.no 12.10.2016).)

(Anm: Multiorgansvikt, svikt eller delvis svikt i funksjonen av mer enn to organer. Pasienter med multiorgansvikt finner man på intensivavdelinger og postoperative avdelinger på sykehus. Kilde: Store norske leksikon.).)

(Anm: Mitochondria-meditated pathways of organ failure upon inflammation. (…) Analysis of the literature suggests that further research should be focused on the impact of mtROS on organ failure induced by inflammation and simultaneously providing a new theoretical basis for a targeted therapy of overwhelmed inflammatory response. Redox Biol. 2017 May 25;13:170-181. [Epub ahead of print].)

(Anm: sepsis; alvorleg smittesjukdom med nærvere av sjukdomsbakteriar eller andre smittekim i blodet; «blodforgiftning», gir feber, frostrier, rask puls og pust, leukocytose, mødd allmenntilstand; kan føra til blodtrykksfall med mjølkesyreacidose, oliguri, uklart sensorium m v pga dårleg organgjennombløding, ev til multiorgansvikt (s d) og sjokk; bakterieendotoksin, TNF, IL-1 og andre cytokin, NO m v er utløysingsfaktorar; kan skuldast ein abscess, sårinfeksjon, kateterinfeksjon e a; jf bakteriemi, septikopyemi, septikemi, TSS, septisk sjokk, DIC, endokarditt, urosepsis. Kilde: Norsk medisinsk ordbok.)

(Anm: Sepsis; grunnleggende kliniske observasjoner (hnt.no 5.11.2013).)

(Anm: Drug-resistant bacteria in patients' urine or stools raise risk of drug-resistant sepsis (medicalnewstoday.com 26.4.2017).)

- «Alle» har fått avvik. Ikke ett eneste av akuttmottakene som Helsetilsynet har gjort tilsyn ved, unngikk avvik når det gjelder gjenkjennelse og behandling av sepsis.

(Anm: «Alle» har fått avvik. Ikke ett eneste av akuttmottakene som Helsetilsynet har gjort tilsyn ved, unngikk avvik når det gjelder gjenkjennelse og behandling av sepsis. (…) Rundt 50 prosent av alle pasienter som utvikler sepsis, kommer inn via akuttmottaket. – Pasientene kommer da gjerne med en infeksjon, eller med en uavklart tilstand. (…) Sepsis som oppstår på sengepost ser ikke Fylkesmennene på i dette tilsynet. (sykepleien.no 23.2.2017).)

(Anm: Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body, frequently a response of the immune system to infection. (en.wikipedia.org).)

(Anm: Sepsis. Definisjon: SIRS + påvist/mistenkt infeksjon (f. eks. positiv blodkultur). SIRS- kriteriene er: - Feber > 38 ºC eller hypotermi < 36 ºC - Puls > 90/minutt - Respirasjonsfrekvens > 20/minutt eller hypokapni med pCO2 < 4,3 kPa i blodgass - Leukocytose ≥ 12 × 109/l eller leukopeni < 4 × 109/l eller > 10 % umodne leukocytter. (helsebiblioteket.no - Metodebok for indremedisinere, 2012).)

- Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt.

(Anm: Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt. (The role of mitochondrial dysfunction in sepsis-induced multi-organ failure). (Virulence. 2013 Nov 1;5(1).)

- Diagnostisering av sepsis. Sepsis, også kjent som blodforgiftning, er kroppens hyperaktive respons på en infeksjon som kan føre til betennelse, vevskader, organsvikt etc.

(Anm: Diagnosing Sepsis. Sepsis, also known as blood poisoning, is the body’s hyperactive response to an infection that can lead to inflammation, tissue damage, organ failure etc. It is a very dangerous state in which the immune system stops fighting with the invading agents  and turns to itself. Around one-third of patients who are affected with sepsis die every year. (news-medical.net 7.9.2017).)

- Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon.

(Anm: Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon. Recognizing Sepsis as a Global Health Priority — A WHO Resolution. “Some very important clinical issues, some of them affecting life and death, stay largely in a backwater which is inhabited by academics and professionals and enthusiasts, dealt with very well at the clinical and scientific level but not visible to the public, political leaders, leaders of healthcare systems... The public and political space is the space in which [sepsis] needs to be in order for things to change.” NEJM (June 28, 2017).)

(Anm: Sepsis – den dödliga sjukdomen som glöms bort. Trots att infektionssjukdomen sepsis förekommer oftare än de vanligaste formerna av cancer och att upp emot hälften som drabbas av den allvarligaste formen dör, så har många knappt hört talas om sjukdomen. Sepsis som är den medicinska termen på blodförgiftning, drabbar omkring 40 000 svenskar varje år. (netdoktor.se 7.6.2017).)

- Ny innsikt i hvorfor immunforsvaret ikke oppdager kreft. Studien gransker relasjonen mellom hvordan immunforsvaret ser perifert vev og kreft.

(Anm: New insights into why the immune system fails to see cancer. Study explores relationship between how the immune system sees peripheral tissues and cancers. Cancer hides in plain sight of the immune system. The body's natural tumor surveillance programs should be able to detect and attack rogue cancer cells when they arise, and yet when cancer thrives, it does so because these defense systems have failed. A team of investigators led by Niroshana Anandasabapathy, MD, PhD, at Brigham and Women's Hospital have uncovered a critical strategy that some cancers may be using to cloak themselves - they find evidence of this genetic program across 30 human cancers of the peripheral tissue, including melanoma skin cancer. Their results are published in Cell. "Our study reveals a new immunotherapy target and provides an evolutionary basis for why the immune system may fail to detect cancers arising in tissues," said corresponding author Anandasabapathy, of BWH's Department of Dermatology. "The genetic program we report on helps the immune system balance itself. Parts of this program prevent the immune system from destroying healthy organs or tissues, but might also leave a blind spot for detecting and fighting cancer."(medicalnewstoday.com 3.7.2017).)

(Anm: IFNγ-Dependent Tissue-Immune Homeostasis Is Co-opted in the Tumor Microenvironment. Cell. 2017 Jun 29;170(1):127-141.e15.)

- Fjerning av senescente celler fra ledd kan reversere progresjon av osteoartritt (betennelse i ledd og tilgrensende knokkel).

(Anm: Removing senescent cells from joints could reverse progression of osteoarthritis. In a preclinical study in mice and human cells, researchers report that selectively removing old or 'senescent' cells from joints could stop and even reverse the progression of osteoarthritis. The findings, published April 24 in Nature Medicine, support growing evidence that senescent cells contribute to age-related diseases and demonstrate that using drug therapies to remove them from the joint not only reduces the development of post-traumatic osteoarthritis but creates an environment for new cartilage to grow and repair joints. (news-medical.net 2.5.2017).)

- Mayo Clinic-studie avslører link mellom senescente celler og benskjørhet (osteoporose) hos mus.

(Anm: Mayo Clinic study reveals link between senescent cells and bone loss in mice. Mayo Clinic researchers have reported a causal link between senescent cells - the cells associated with aging and age-related disease - and bone loss in mice. Targeting these cells led to an increase in bone mass and strength. The findings appear online in Nature Medicine. (news-medical.net 21.8.2017).)

- UCI, Italienske forskere begrenser akselerert cellulær aldring (senescens) forårsaket av bruk av metamfetamin.

(Anm: UCI, Italienske forskere begrenser akselerert cellulær aldring (senescens) forårsaket av bruk av metamfetamin. UCI, Italian scientists limit accelerated cellular aging caused by methamphetamine use. Grasp of underlying molecular mechanisms could improve addiction recovery efforts. The ravaged faces of methamphetamine addicts tell a terrible tale - abusing the drug dramatically accelerates aging. Now scientists from UC Irvine and the Italian Institute of Technology have discovered how this occurs at the cellular level and identified methods to limit the process. (medicalnewstoday.com 14.2.2015).)

- Celledød: Er vår helse i fare? (- Når celler brister og dør, blir deres innhold frigitt og forårsaker betennelse.) (- Hver dag dør mer enn 50 milliarder celler i kroppen vår. Dette er ikke tilfeldige hendelser, men en del av en finjustert biologisk mekanisme som kalles programmert celledød.)

(Anm: Celledød: Er vår helse i fare? (Cell death: Is our health at risk?) Når celler brister og dør, blir deres innhold frigitt og forårsaker betennelse. Livet og døden til cellene i kroppen vår er stramt regulert. Dette er viktig for normal funksjon og begrensning av skader. Men celledød kan ha sideeffekter, og hvis det svikter er vår helse risikoutsatt. Hver dag dør mer enn 50 milliarder celler i kroppen vår. Dette er ikke tilfeldige hendelser, men en del av en finjustert biologisk mekanisme som kalles programmert celledød. Multicellære organismer, inkludert mennesker, må holde nøye kontroll på antall celler i kroppen. Dette ville være enkelt hvis cellene aldri delte seg, men på noen steder - som blod, hud og «lining» av tarmsystemet - produseres stadig nye celler. (Cell death: Is our health at risk? When cells burst and die, their contents are released, causing inflammation. The life and death of the cells in our bodies are tightly regulated. This is essential for normal function and limiting damage. But cell death can have side effects, and if it malfunctions, our health is at stake. Every day, more than 50 billion cells die in our bodies. These are not random events, but part of a finely tuned biological mechanism called programmed cell death. Multicellular organisms, including humans, need to keep a tight lid on the number of cells in their bodies. This would be easy if the cells never divided, but some areas - such as the blood, skin, and lining of the gut - are constantly producing new cells.) (medicalnewstoday.com 11.8.2017).)

(Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking. BMJ Open 2017;7:e016224.)

- Eksponering for decabromodiphenyl (BDE-209) gir mitokondriell dysfunksjon i lever hos rotter og celledød.

(Anm: - Eksponering for decabromodiphenyl (BDE-209) gir mitokondriell dysfunksjon i lever hos rotter og celledød. Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death. Abstract Polybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. J Toxicol Environ Health A. 2017 Sep 7:1-16.)

(Anm: Miljø og helse (mintankesmie.no).)

(Anm: Klima, miljø og globalisering (mintankesmie.no).)

(Anm: Miljø og legemiddel (Legemidler er farlig avfall). (mintankesmie.no).)

- Konklusjoner -Treningsinduserte reduksjoner i glykolytisk aktivitet stimulerer fysiologisk hjertereparasjon, og metabolisk fleksibilitet er viktig for å opprettholde mitokondriell helse i hjertet.

(Anm: Exercise-Induced Changes in Glucose Metabolism Promote Physiologic Cardiac Growth. Conclusions -Exercise-induced decreases in glycolytic activity stimulate physiologic cardiac remodeling, and metabolic flexibility is important for maintaining mitochondrial health in the heart. Circulation. 2017 Aug 31. pii: CIRCULATIONAHA.117.028274.)

(Anm: Orale steroider (glukokortikoider) linket til 10 ganger økt risiko for diabetes. (Oral steriods linked with ten-fold increased risk of diabetes. (pulsetoday.co.uk 5.5.2016).)

(Anm: Bivirkninger (legemiddelinduserte organskader og sykdommer) (mintankesmie.no).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking. BMJ Open 2017;7:e016224.)

- Alvorlig hjertesvikt kan være reversibel. Forskere kan ha oppdaget en måte å reversere hjertesvikt på ved å få hjertemuskler til å regenerere seg selv. De oppdaget at siling av en signalvei i mus som hadde utviklet hjertesvikt etter et hjerteinfarkt aktiverte en tidligere ukjent selvhelbredelsesprosess.

(Anm: Severe heart failure may be reversible. Scientists may have discovered a way of reversing heart failure by getting heart muscle to regenerate itself. They found that silencing a signaling pathway in mice that had developed heart failure following a heart attack activated a previously unrecognized self-healing process. In a paper recently published in the journal Nature, the researchers, led by a team from Baylor College of Medicine in Houston, TX, report their findings about the signaling pathway, which is known as Hippo. (medicalnewstoday.com 5.10.2017).)

- Forskere avslører mekanisme som knytter tarmbakterier til hypertensjon (høyt blodtrykk).

(Anm: Forskere avslører mekanisme som knytter tarmbakterier til hypertensjon (høyt blodtrykk). Scientists unravel mechanism that links gut bacteria to hypertension. (...) In a few studies, when gut bacteria were killed off with antibiotics, patients with hypertension saw a drop in blood pressure. And when gut bacteria were transplanted from hypertensive people into normal mice, they developed high blood pressure. The evidence is compelling, but until now, scientists have not identified a mechanism to explain how bacteria increase blood pressure. (news-medical.net 3.10.2017).)

(Anm: Mitochondrial DNA copy number appears to be predictive of sudden cardiac death, heart attacks. The two studies, one on cardiovascular disease published in JAMA Cardiology on Oct. 11 and the other focused on sudden cardiac death and published in the… (news-medical.net 11.10.2017).)

(Anm: Gut colonization linked to development and progress of heart failure. (…) It has long been known that heart failure and gut health are linked. The gut, thus, has a worse blood supply in instances of heart failure; the intestinal wall is thicker and more permeable, whereby bacteria and bacterial components may find their way into the blood. (news-medical.net 11.7.2017).)

- Betennelser endrer mitokondrier til giftige fabrikker. Å lære hvordan å kontrollere betennelser kan ha store implikasjoner for behandlingen av mange sykdommer.

(Anm: Betennelser endrer mitokondrier til giftige fabrikker. Å lære hvordan å kontrollere betennelser kan ha store implikasjoner for behandlingen av mange sykdommer. Banebrytende forskning oppdager hvordan makrofager endrer mitokondriene til giftige kjemisk-produserende betennelsespromotører. (Inflammation turns mitochondria into toxic factories. Learning how to control inflammation could have huge implications for the treatment of many diseases. Breaking research discovers how macrophages turn mitochondria into toxic chemical-producing inflammation-promoters.) (medicalnewstoday.com 25.9.2016).)

- Forskere gjør overraskende funn om hvordan nevroner kommuniserer med hverandre. (…) Neuroner kommuniserer med hverandre ved å frigjøre kjemikalier kalt neurotransmittere, som dopamin og glutamat inn i det lille rommet mellom to nevroner som er kjent som synaps. (- "Våre funn viser for første gang at nevroner kan forandre hvor mye dopamin de frigjør som en funksjon av deres generelle aktivitet. Når denne mekanismen ikke fungerer som den skal, kan det ha store helseeffekter…

- Nylige estimater av den globale byrden av soppsykdom antyder at deres forekomst har blitt drastisk undervurdert, og at dødeligheten kan konkurrere med malaria eller tuberkulose.

(Anm: Mitochondrial Complex I Is a Global Regulator of Secondary Metabolism, Virulence and Azole Sensitivity in Fungi. Abstract Recent estimates of the global burden of fungal disease suggest that that their incidence has been drastically underestimated and that mortality may rival that of malaria or tuberculosis. (...) Evidence presented in this paper suggests that complex I may play a role in the hypoxic response and that one possible mechanism for cell death during azole treatment is a dysfunctional hypoxic response that may be restored by dysregulation of complex I. Both deletion of the 29.9 KD subunit of complex I and azole treatment alone profoundly change expression of gene clusters involved in secondary metabolism and immunotoxin production raising potential concerns about long term azole therapy. PLoS One. 2016 Jul 20;11(7):e0158724. eCollection 2016.)

- Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes.

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: Azoles are a class of five-membered heterocyclic compounds containing a nitrogen atom and at least one other non-carbon atom (i.e. nitrogen, sulfur, or oxygen) as part of the ring.[1] Use as anti-fungal agents. The search for antifungal agents with acceptable toxicity profiles led first to the discovery of ketoconazole, the first azole-based oral treatment of systemic fungal infections, in the early 1980s. Later, triazoles fluconazole and itraconazole, with a broader spectrum of antifungal activity and improved safety profile were developed. In order to overcome limitations such as sub-optimal spectra of activity, drug-drug interactions, toxicity, development of resistance and unfavorable pharmacokinetics, analogues (en.wikipedia.org).)

(Anm: Sykelighet, sykefravær, uførhet og trygd (mintankesmie.no).)

- Atorvastatin (ATV) som vanligvis brukes til å behandle dyslipidemi rapporteres også å ha effekt mot 6-hydroksydopamin (6-OHDA) indusert nevrotoksisitet. I tillegg kan atorvastatin forstyrre mitokondriell funksjon ved å redusere nivået av Q10. Derfor kan den terapeutiske effekten av atorvastatin (20 mg / kg) bli kompromittert. (- De aktuelle resultater gir bevis på at tilskudd av Q10 til ATV viser synergistisk effekt ved å redusere dopamin toksisitet.) (- Det var signifikant reduksjon i mitokondriell kompleks enzymaktivitet og mitokondrielt membranpotensial (MMP).)

(Anm: Abstract Atorvastatin (ATV) generally used to treat dyslipidemia is also reported to have effect against 6-hydroxydopamine (6-OHDA) induced neurotoxicity. Additionally, atorvastatin can interfere with mitochondrial function by reducing the level of Q10. Therefore, the therapeutic effect of atorvastatin (20 mg/kg) could be compromised. In this context, the present study evaluated the effect of ATV supplemented with Q10. 6-OHDA was unilaterally injected into the right striatum of male rats. On day 8 of 6-OHDA infusion, ATV (20 mg/kg), Q10 (200 mg/kg), and their combination were administered per oral for 14 days. On day 21, there was significant loss of striatal dopamine indicating neurotoxicity. The combination of ATV+Q10 showed significant amelioration of dopamine (DA) toxicity compared to individual treatments. Similarly, ATV+Q10 compared to individual treatment significantly decreased the motor deficits induced by 6-OHDA. Further, 6-OHDA induced mitochondrial dysfunction in the substantia nigra pars compacta (SNpc). There was significant decrease in mitochondrial complex enzyme activities and mitochondrial membrane potential (MMP). Treatment with ATV and ATV+Q10 ameliorated mitochondrial dysfunction by increasing complex enzyme activities; however, only ATV+Q10 were able to stabilize MMP and maintained mitochondrial integrity. Moreover, there was significant induction of oxidative stress as observed from increase in lipid peroxidases (LPO) and nitrite (NO), and decrease in super oxide dismutase (SOD). Treatment with ATV+Q10 significantly altered the above effects indicating antioxidant activity. Furthermore, only combination of ATV and Q10 decreased the 6-OHDA induced expression of cytochrome-C, caspase-9 and caspase-3. Therefore, current results provide evidence that supplementation of Q10 with ATV shows synergistic effect in reducing dopamine toxicity. Neurotox Res. 2017 May;31(4):478-492.)

(Anm: Statiner etc. (mot høyt kolesterol) (mintankesmie.no).)

- Studien identifiserer en ny måte å forhindre at en dødelig soppinfeksjon sprer seg til hjernen.

(Anm: Studien identifiserer en ny måte å forhindre at en dødelig soppinfeksjon sprer seg til hjernen. Study identifies a new way to prevent a deadly fungal infection spreading to the brain. (- Det er mange sykdommer, ikke bare kryptokokker, hvor patogener - bakterier, virus, sopp eller parasitter kan forårsake sykdom - som overlever ved bevisst å kapre immunforsvaret på denne måten. (medicalnewstoday.com 21.8.2017).)

(Anm: Effekter av MPTP på serotonerge nevronale systemer og mitokondrie Complex I aktiviteten i den levende hjernen: En PET-studie på bevisste rhesusaper. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys.) J Nucl Med. 2017 Mar 9. pii: jnumed.116.189159.)

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: Pasienter behandlet med antipsykotika (nevroleptika) har signifikant senket platelet complex I aktivitet i mitokondrier i likhet med det som er observert ved idiopatisk Parkinsons sykdom. (...) Antipsykotika (nevroleptika) hemmer kompleks I i elektrontransportkjeden. (Neuroleptic medications inhibit complex I of the electron transport chain. (...) Neuroleptic treated patients have significant depression of platelet complex I activity similar to that seen in idiopathic Parkinson’s disease. Complex I inhibition may be associated with the extrapyramidal side effects of these drugs.) Ann Neurol. 1993;33:512-7).)

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: Sygdom trækker danskere ned i gæld. (…) En sygdom rammer, og al energi bliver lagt i blodprøver og møder med læger. Imens hober gammel gæld sig op, eller ny kommer til. (...) For mange kommer et svigtende helbred til at betyde begyndelsen på en lang og sej kamp mod renter og minus på kontoen. (…) Her angiver de gældsramte oftest sygdom som det, der startede deres pengeproblemer. (…) »Det er jo hårdt at være syg i sig selv, og det er yderligere hårdt, at man kommer ud i nogle situationer, hvor man risikerer, at huset skal sælges på tvangsauktion, eller man ikke har til huslejen«, siger han. »Så man bliver på en måde dobbelt ramt. (politiken.dk 29.4.2017).)

- Mitokondriell aldring og aldersrelatert mitokondriell dysfunksjon. Alderselaterte endringer i mitokondrier er knyttet til redusert i mitokondriell funksjon. Med fremskyndet aldring reduseres mitokondrielt DNA-volum, integritet og funksjonalitet på grunn av akkumulering av mutasjoner og oksidativ skade fremkalt av reaktive oksygensubstanser (ROS). Hos eldre mennesker er mitokondriene preget av redusert funksjon som redusert oksidativ kapasitet, redusert oksidativ fosforylering, redusert ATP-produksjon, betydelig økning i ROS-generasjon og redusert antioksidantforsvar.

(Anm: Mitokondriell aldring og aldersrelatert mitokondriell dysfunksjon. Abstrakt. Alderselaterte endringer i mitokondrier er knyttet til redusert i mitokondriell funksjon. Med fremskyndet aldring reduseres mitokondrielt DNA-volum, integritet og funksjonalitet på grunn av akkumulering av mutasjoner og oksidativ skade fremkalt av reaktive oksygensubstanser (ROS). Hos eldre mennesker er mitokondriene preget av redusert funksjon som redusert oksidativ kapasitet, redusert oksidativ fosforylering, redusert ATP-produksjon, betydelig økning i ROS-generasjon og redusert antioksidantforsvar. (Abstract Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense.) Biomed Res Int. 2014;2014:238463. Epub 2014 Apr 10.)

(Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking. BMJ Open 2017;7:e016224.)

(Anm: SSRI-preparater og antipsykotika har uheldige effekter på mitokondrier (mintankesmie.no).)

(Anm: Legemiddelindusert kreft og andre typer celleskader (mintankesmie.no).)

(Anm: Bivirkninger (legemiddelinduserte organskader og sykdommer) (mintankesmie.no).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking. BMJ Open 2017;7:e016224.)

(Anm: SSRI-preparater og antipsykotika har uheldige effekter på mitokondrier (mintankesmie.no).)

(Anm: Legemiddelindusert kreft og andre typer celleskader (mintankesmie.no).)

(Anm: Bivirkninger (legemiddelinduserte organskader og sykdommer) (mintankesmie.no).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Sovemidler (sovemedisiner) og beroligende midler (mintankesmie.no).)

(Anm: Sovemidler knyttes til dødelighet eller kreft: en matchet kohortstudie. (Hypnotics' association with mortality or cancer: a matched cohort study.)  (...) Målsetting Anslagsvis 6 % -10 % av amerikanske voksne tok et sovemiddel (hypnotika) mot dårlig søvn i 2010. Denne studien underbygger tidligere rapporter som knytter hypnotika (sovemidler) til økt dødelighet. BMJ Open 2012;2:e000850 (27 February).)

(Anm: - Slår sovepiller os ihjel? (- Studiet er det største af sin slags på globalt plan og har også undersøgt sammenhængen mellem brug af antidepressiver og antipsykotika og dødelighed. Også her fandt forskerne en overdødelighed.) (videnskab.dk 21.3.2016).)

- Forskning på cellulær senescens kan føre til nye måter å behandle aldersrelaterte lidelser på.

(Anm: Forskning på cellulær senescens kan føre til nye måter å behandle aldersrelaterte lidelser på. Research into cellular senescence may lead to new ways of treating age-related disorders. (…) In basic research conducted on human cell cultures and on mice, Dr. Krizhanovsky and his team asked, "what, exactly, ties senescent cells to aging?" (medicalnewstoday.com 18.5.2017).)

(Anm: Senescence-associated ultrastructural features of long-term cultures of induced pluripotent stem cells (iPSCs). Aging (Albany NY). 2017 Oct 23.)

(Anm: Senescence promotes chemotherapy side effects and cancer relapse. Standard chemotherapy is a blunt force instrument against cancer - and it's a rare cancer patient who escapes debilitating side effects from systemic treatments that mostly affect dividing cells, both malignant and healthy, throughout the body. Researchers at the Buck Institute and elsewhere now show that chemotherapy triggers a pro-inflammatory stress response termed cellular senescence, promoting the adverse effects of chemotherapy as well as cancer relapse and metastasis. Eliminating the senescent cells in mice prevented the side effects and relapse. The research is published in Cancer Discovery.  (medicalnewstoday.com 18.1.2017).)

(Anm: Mechanisms of Neurotoxic Symptoms as a Result of Breast Cancer and Its Treatment: Considerations on the Contribution of Stress, Inflammation, and Cellular Bioenergetics. (…) SUMMARY: We propose reduced cellular energy (mitochondrial dysfunction) induced by inflammation, oxygen radical production, and stress as a result of cancer and/or cancer treatment as a final mechanism underlying neurotoxic symptoms. Curr Breast Cancer Rep. 2017;9(2):70-81.)

(Anm: Men appear to have worse chemotherapy-induced cardiomyopathy than women, research shows. Men seem to have worse chemotherapy-induced cardiomyopathy than women despite receiving similar cancer treatments, according to research presented today at EuroCMR 2017. (news-medical.net 25.5.2017).)

(Anm: Senescence (/sɪˈnɛsəns/) (from Latin: senescere, meaning "to grow old", from senex) or biological aging (also spelled biological ageing) is the gradual deterioration of function characteristic of most complex lifeforms, arguably found in all biological kingdoms, that on the level of the organism increases mortality after maturation. The word senescence can refer either to cellular senescence or to senescence of the whole organism. It is commonly believed that cellular senescence underlies organismal senescence. The science of biological aging is biogerontology. (en.wikipedia.org).)

(Anm: UCI, Italienske forskere begrenser akselerert cellulær aldring (senescens) forårsaket av bruk av metamfetamin. UCI, Italian scientists limit accelerated cellular aging caused by methamphetamine use. Grasp of underlying molecular mechanisms could improve addiction recovery efforts. The ravaged faces of methamphetamine addicts tell a terrible tale - abusing the drug dramatically accelerates aging. Now scientists from UC Irvine and the Italian Institute of Technology have discovered how this occurs at the cellular level and identified methods to limit the process. (medicalnewstoday.com 14.2.2015).)

- Tre giftige gasser møtes i mitokondriene.

(Anm: Three toxic gases meet in the mitochondria. Front. Physiol. 2015 (20 August 2015).)

(Anm: Toxic formaldehyde is produced inside our own cells, scientists discover. New research has revealed that some of the toxin formaldehyde in our bodies does not come from our environment -- it is a by-product of an essential reaction inside our own cells. This could provide new targets for developing cancer therapies, according to research led by scientists from the Medical Research Council (MRC) Laboratory of Molecular Biology. (sciencedaily.com 16.8.2017).)

(Anm: Mammals divert endogenous genotoxic formaldehyde into one-carbon metabolism. Nature 2017 (Published online 16 August 2017).)

(Anm: Toxic formaldehyde is produced inside our own cells, scientists discover. (…) The research, published in Nature, has uncovered that formaldehyde is a by-product of a key process called the 'one carbon cycle'. This cycle uses a vitamin - folate - to create DNA and essential amino acids, which cells need to function and multiply. (medicalnewstoday.com 17.8.2017).)

- Eksperimentelle bevis støtter en intrikat forbindelse mellom betennelse og mitokondriell dysfunksjon som hovedbidragsyter ved nevrologiske sykdommer. Inflammatoriske mediatorer produsert av aktiverte mikroglia og infiltrerte immunceller utløser intracellulære signaleringskaskader som kan forandre cellulær mitokondriell metabolisme.

(Anm: Inflammation and mitochondrial dysfunction: a vicious circle in neurodegenerative disorders? Abstract Experimental evidence supports an intricate association between inflammation and mitochondrial dysfunction as main contributors of neurological diseases. Inflammatory mediators produced by activated microglia and infiltrated immune cells trigger intracellular signaling cascades that can alter cellular mitochondrial metabolism. Cytokines, particularly tumor necrosis factor-alpha, impede mitochondrial oxidative phosphorylation and associated ATP production and instigate mitochondrial reactive oxygen species production. This culminates in mitochondrial membrane permeabilization, altered mitochondrial dynamics and might ultimately result in cell death. When severely injured mitochondria are not appropriately removed by mitophagy they can release their contents into the cytosol and extracellular environment and thereby amplify the inflammatory process. Here we provide a comprehensive overview on how inflammatory mediators impair mitochondrial metabolism and discuss how defective mitochondria can elicit and potentiate an inflammatory response.Neurosci Lett. 2017 Jun 28. pii: S0304-3940(17)30542-6 [Epub ahead of print].)

(Anm: Bacterial tail anchors can target to the mitochondrial outer membrane. Biol Direct. 2017 Jul 24;12(1):16.)

- Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt.

(Anm: Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt. (The role of mitochondrial dysfunction in sepsis-induced multi-organ failure). (Virulence. 2013 Nov 1;5(1).)

- Diagnostisering av sepsis. Sepsis, også kjent som blodforgiftning, er kroppens hyperaktive respons på en infeksjon som kan føre til betennelse, vevskader, organsvikt etc.

(Anm: Diagnosing Sepsis. Sepsis, also known as blood poisoning, is the body’s hyperactive response to an infection that can lead to inflammation, tissue damage, organ failure etc. It is a very dangerous state in which the immune system stops fighting with the invading agents  and turns to itself. Around one-third of patients who are affected with sepsis die every year. (news-medical.net 7.9.2017).)

- Reparere mitokondriell dysfunksjon ved sykdom.

(Anm: Repairing Mitochondrial Dysfunction in Disease. Abstract Mitochondria are essential organelles for many aspects of cellular homeostasis, including energy harvesting through oxidative phosphorylation. Alterations of mitochondrial function not only impact on cellular metabolism but also critically influence whole-body metabolism, health, and life span. Diseases defined by mitochondrial dysfunction have also expanded from rare monogenic disorders in a strict sense to now also include many common polygenic diseases, including metabolic, cardiovascular, neurodegenerative, and neuromuscular diseases. This has led to an intensive search for new therapeutic and preventive strategies aimed at invigorating mitochondrial function by exploiting key components of mitochondrial biogenesis, redox metabolism, dynamics, mitophagy, and the mitochondrial unfolded protein response. As such, new findings linking mitochondrial function to the progression or outcome of this ever-increasing list of diseases has stimulated the discovery and development of the first true mitochondrial drugs, which are now entering the clinic and are discussed in this review. Expected final online publication date for the Annual Review of Pharmacology and Toxicology Volume 58 is January 6, 2018. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates. Annu Rev Pharmacol Toxicol. 2017 Sep 27.)

(Anm: Myopathy, Drugs, and Mitochondria. J Korean Med Sci. 2017 Nov;32(11):1732-1733.)

- Effekter av antiepileptiske legemidler (antiepileptika) på mitokondrielle funksjoner, morfologi, kinetikk, biogenese og overlevelse.

(Anm: Effects of antiepileptic drugs on mitochondrial functions, morphology, kinetics, biogenesis, and survival. Abstract OBJECTIVES: Antiepileptic drugs (AEDs) exhibit adverse and beneficial effects on mitochondria, which have a strong impact on the treatment of patients with a mitochondrial disorder (MID) with epilepsy (mitochondrial epilepsy). This review aims at summarizing and discussing recent findings concerning the effect of AEDs on mitochondrial functions and the clinical consequences with regard to therapy of mitochondrial epilepsy and of MIDs in general. (…) CONCLUSIONS: Mitochondrial epilepsy might be initially treated with AEDs with low mitochondrial toxic potential. Only in case mitochondrial epilepsy is refractory to these AEDs, AEDs with higher mitochondrial toxic potential might be tried. In patients carrying POLG1 mutations AEDs with high mitochondrial toxic potential are contraindicated. Epilepsy Res. 2017 Jul 13;136:5-11.)

(Anm: Epilepsi og legemidler (mintankesmie.no).)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Antidepressiva ökar risken för benbrott hos äldre. (…) Den förhöjda risken för höftfraktur gällde alla de vanliga antidepressiva läkemedlen, SSRI-preparat, mirtazapin och SNRI-preparat (selektiva serotonin- och noradrenalinåterupptagshämmare. Sambandet gällde även då det kontrollerats för andra faktorer som ålder, annan medicinering som ökar fallrisken, benskörhet, socioekonomisk status, kroniska sjukdomar och psykiatriska diagnoser.) (lakemedelsvarlden.se 12.1.2017).)

- Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon.

(Anm: Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon. Recognizing Sepsis as a Global Health Priority — A WHO Resolution. “Some very important clinical issues, some of them affecting life and death, stay largely in a backwater which is inhabited by academics and professionals and enthusiasts, dealt with very well at the clinical and scientific level but not visible to the public, political leaders, leaders of healthcare systems... The public and political space is the space in which [sepsis] needs to be in order for things to change.” NEJM (June 28, 2017).)

(Anm: Sepsis – den dödliga sjukdomen som glöms bort. Trots att infektionssjukdomen sepsis förekommer oftare än de vanligaste formerna av cancer och att upp emot hälften som drabbas av den allvarligaste formen dör, så har många knappt hört talas om sjukdomen. Sepsis som är den medicinska termen på blodförgiftning, drabbar omkring 40 000 svenskar varje år. (netdoktor.se 7.6.2017).)

- Hurtigtest finner tegn på sepsis i en enkelt dråpe blod.

(Anm: Hurtigtest finner tegn på sepsis i en enkelt dråpe blod. (- Sepsis, en potensielt livstruende komplikasjon av en infeksjon, har den høyeste byrde mht. død og medisinske utgifter på sykehus over hele verden.) (- Quick test finds signs of sepsis in a single drop of blood. (…) Sepsis, a potentially life-threatening complication of an infection, has the highest burden of death and medical expenses in hospitals worldwide. (medicalnewstoday.com 5.7.2017).)

(Anm: Mechanisms of Neurotoxic Symptoms as a Result of Breast Cancer and Its Treatment: Considerations on the Contribution of Stress, Inflammation, and Cellular Bioenergetics. (…) SUMMARY: We propose reduced cellular energy (mitochondrial dysfunction) induced by inflammation, oxygen radical production, and stress as a result of cancer and/or cancer treatment as a final mechanism underlying neurotoxic symptoms. Curr Breast Cancer Rep. 2017;9(2):70-81.)

- Mitokondrier er immunitetens kraftverk

Mitochondria are the powerhouses of immunity
Nat Immunol. 2017 Apr 18;18(5):488-498. doi: 10.1038/ni.3704.
Nylige bevis indikerer at mitokondrier ligger i hjertet av immunitet. Mitokondriell DNA virker som et fareassosiert molekylært mønster (DAMP), og det mitokondrielle ytre membran er en plattform for signalering av molekyler som MAVS i RIG-I-signalering, og for NLRP3- inflammasome. Mitokondriell biogenese, fusjon og fisjon har roller i aspekter ved immun-celle-aktivering. Viktigste Krebs syklus mellomprodukter som succinat, fumarat og citrat involverer prosesser relatert til immunitet og betennelse, i både medfødte og adaptive immunceller. Disse funnene avslører mitokondrielle mål som potensielt kunne utnyttes for terapeutisk gevinst ed betennelse og kreft. (Recent evidence indicates that mitochondria lie at the heart of immunity. Mitochondrial DNA acts as a danger-associated molecular pattern (DAMP), and the mitochondrial outer membrane is a platform for signaling molecules such as MAVS in RIG-I signaling, and for the NLRP3 inflammasome. Mitochondrial biogenesis, fusion and fission have roles in aspects of immune-cell activation. Most important, Krebs cycle intermediates such as succinate, fumarate and citrate engage in processes related to immunity and inflammation, in both innate and adaptive immune cells. These discoveries are revealing mitochondrial targets that could potentially be exploited for therapeutic gain in inflammation and cancer.)

(Anm: Krebs Cycle Overview. The Krebs cycle is named after its discoverer, Hans Krebs. It is also known as the citric acid cycle or the tricarboxylic acid cycle. It is a series of chemical reactions required for cellular respiration; it involves  redox, dehydration, hydration, and decarboxylation reactions that produce ATP (adenosine triphosphate), a coenzyme energy carrier for cells.  The waste product, in the form of carbon dioxide, is also produced as well as further sets of reactants used to regenerate the original reaction. (news-medical.net 6.9.2017).)

- Mitokondrier er kroppens livsviktige energifabrikker. Siden mitokondrier finnes i stort sett alle celler i alle vev, kan mitokondriesykdommer ramme hvor som helst. Vi kan ikke leve uten mitokondrier. Når de svikter, kan vi bli alvorlig syke.

(Anm: Mitokondrier er kroppens livsviktige energifabrikker. Siden mitokondrier finnes i stort sett alle celler i alle vev, kan mitokondriesykdommer ramme hvor som helst. Vi kan ikke leve uten mitokondrier. Når de svikter, kan vi bli alvorlig syke. Laurence Bindoff, overlege og leder av NeuroAge, Universitetet i Bergen. (…) Inntil nylig kunne man ikke påvise linken mellom avleiring i hjernen og mitokondrieavvik. Det gjorde vi i fjor. (aftenposten.no 22.2.2017).)

(Anm: Powering the Cell: Mitochondria (ed.ted.com).)

(Anm: Cellular Respiration and the Mighty Mitochondria (ed.ted.com).)

(Anm: Dr. Terry Wahls - Minding Your Mitochondria - TED - Documentary, Lecture, Talk NUTRITION (youtube.com 16.4.2017).)

- Mitokondriell kontroll av immunitet: utover ATP. (- I denne gjennomgangen diskuterer vi hvordan mitokondriell metabolisme varierer over ulike immuncelle-undergrupper, hvordan metabolsk signalering dikterer cellens skjebne og hvordan denne signaleringen potensielt kan målrettes terapeutisk.)

(Anm: Mitochondrial control of immunity: beyond ATP. Abstract Mitochondria are important signalling organelles, and they dictate immunological fate. From T cells to macrophages, mitochondria form the nexus of the various metabolic pathways that define each immune cell subset. In this central position, mitochondria help to control the various metabolic decision points that determine immune cell function. In this Review, we discuss how mitochondrial metabolism varies across different immune cell subsets, how metabolic signalling dictates cell fate and how this signalling could potentially be targeted therapeutically. Nat Rev Immunol. 2017 Jul 3. [Epub ahead of print].)

- Mitokondriell dysfunksjons rolle i kreftprogresjon. (- Vi antyder derfor at mitokondriell dysfunksjon spiller en kritisk rolle i kreftprogresjon, og at målrettet mitokondrieller endringer og mitokondriell retrogradsignalering kan være en lovende strategi for utvikling av selektiv kreftbehandling.)

Role of mitochondrial dysfunction in cancer progression.
Exp Biol Med (Maywood). 2016 Jun;241(12):1281-95. Epub 2016 Mar 27.
Abstract Deregulated cellular energetics was one of the cancer hallmarks. Several underlying mechanisms of deregulated cellular energetics are associated with mitochondrial dysfunction caused by mitochondrial DNA mutations, mitochondrial enzyme defects, or altered oncogenes/tumor suppressors. In this review, we summarize the current understanding about the role of mitochondrial dysfunction in cancer progression. Point mutations and copy number changes are the two most common mitochondrial DNA alterations in cancers, and mitochondrial dysfunction induced by chemical depletion of mitochondrial DNA or impairment of mitochondrial respiratory chain in cancer cells promotes cancer progression to a chemoresistance or invasive phenotype. Moreover, defects in mitochondrial enzymes, such as succinate dehydrogenase, fumarate hydratase, and isocitrate dehydrogenase, are associated with both familial and sporadic forms of cancer. Deregulated mitochondrial deacetylase sirtuin 3 might modulate cancer progression by regulating cellular metabolism and oxidative stress. These mitochondrial defects during oncogenesis and tumor progression activate cytosolic signaling pathways that ultimately alter nuclear gene expression, a process called retrograde signaling. Changes in the intracellular level of reactive oxygen species, Ca(2+), or oncometabolites are important in the mitochondrial retrograde signaling for neoplastic transformation and cancer progression. In addition, altered oncogenes/tumor suppressors including hypoxia-inducible factor 1 and tumor suppressor p53 regulate mitochondrial respiration and cellular metabolism by modulating the expression of their target genes. We thus suggest that mitochondrial dysfunction plays a critical role in cancer progression and that targeting mitochondrial alterations and mitochondrial retrograde signaling might be a promising strategy for the development of selective anticancer therapy. (…)

(Anm: Kreft (mintankesmie.no).)

(Anm: Common cancers hijack powerhouses of cells (medicalnewstoday.com 9.4.2015).)

(Anm: Mitochondria in chronic obstructive pulmonary disease and lung cancer: where are we now? Biomark Med. 2017 Jun 9. [Epub ahead of print].)

(Anm: Signaler fra tarmens mikrobiotika til fjerntliggende organer mht. fysiologi og sykdom. Signals from the gut microbiota to distant organs in physiology and disease. (Nat Med. 2016 Oct 6;22(10):1079-1089.)

- Mitokondriell dysfunksjon som trigger av medfødt immunrespons og betennelse.

(Anm: Mitochondrial Dysfunction as a Trigger of Innate Immune Responses and Inflammation. Abstract A growing literature indicates that mitochondria are key participants in innate immune pathways, functioning as both signaling platforms and contributing to effector responses. In addition to regulating antiviral signaling and antibacterial immunity, mitochondria also are important drivers of inflammation caused by sterile injury. Much research on mitochondrial control of immunity now centers on understanding how mitochondrial constituents released during cellular damage simulate the innate immune system. When mitochondrial integrity is compromised, mitochondrial damage-associated molecular patterns engage pattern recognition receptors, trigger inflammation, and promote pathology in an expanding list of diseases. Here, I review the emerging knowledge of mitochondrial dysfunction in innate immune responses and discuss how environmental exposures may induce mitochondrial damage to potentiate inflammation and human disease. Toxicology. 2017 Jul 29. pii: S0300-483X(17)30215-9.)

- Effekt av antipsykotika på mitokondriell bioenergetikk på rotters ovarie (eggstokk)-teca-celler.

Effect of antipsychotics on mitochondrial bioenergetics of rat ovarian theca cells.
Toxicol Lett. 2017 Apr 15;272:94-100. Epub 2017 Mar 18.
Abstract BACKGROUND: Antipsychotics (APs) are widely prescribed drugs, which are well known to cause reproductive adverse effects through mechanisms yet to be determined. The purpose of this study was to investigate the effect of antipsychotics on mitochondrial bioenergetics of rat ovarian theca cells as a possible mechanism of reproductive toxicity.

METHODS: Isolated rat theca interstitial cells (TICs) were treated with two typical (chlorpromazine [CPZ] and haloperidol [HAL]) and two atypical APs (risperidone [RIS] and clozapine [CLZ]). The effects of these APs on TICs bioenergetics (ATP content, mitochondrial complexes I and III activities, oxygen consumption rates (OCRs), mitochondrial membrane potential (MPP) and lactate production) and on steroidogenesis (androstenedione and progesterone synthesis) were investigated.

RESULTS: All APs resulted in a concentration-dependent decrease in the ATP content of TICs. All APs at their estimated IC50s (6μM, 21μM, 35μM and 37μM for CPZ, HAL, CLZ and RIS respectively) significantly decreased TICs OCRs (p<0.0001), MPP (p<0.0001) and significantly (p=0.0003) inhibited mitochondrial complex I activity. Only typical APs inhibited complex III (p=0.005). Also, APs at IC50s increased TICs lactate production to varying degrees. All APs used at their IC50s significantly inhibited progesterone (p=0.0022) and androstenedione (p=0.0027) production. Only CPZ was found to inhibit these hormones at the low concentration (1μM).

KONKLUSJON: Alle fire antipsykotika ser ut til å hemme mitokondriell bioenergetikk og steroidogenese i rotters ovarieceller. Disse funnene støtter hypotesen om at AP-indusert reproduktiv toksisitet kan være gjennom mekanismer som involverer mitokondrielle skader. Videre forskning er nødvendig for å etablere sammenhengen mellom APs-indusert mitokondriell dysfunksjon og forstyrret steroidogenese. (CONCLUSION: All four antipsychotics seem to inhibit mitochondrial bioenergetics and steroidogenesis in rat's ovarian theca cells. These findings support the hypothesis that APs-induced reproductive toxicity may be through mechanisms involving mitochondrial insult. Further research is required to establish the link between APs-induced mitochondrial dysfunction and disordered steroidogenesis.)

(Anm: Antipsykotika (psykofarmaka etc.) (mintankesmie.no).)

(Anm: Lægemiddelstyrelsen opfordrer læger til at være opmærksomme på disse alvorlige bivirkninger hos børn og unge i behandling med aripiprazol (Abilify) (…) Gennemgangen viser også, at børn med ASD (autisme) der behandles med aripiprazol, kan udvikle alvorlige psykiatriske bivirkninger såsom svære kroniske søvnproblemer, aggressiv adfærd og hallucinationer. (…) Hårtab, depression og psykose, Vægtøgning, Hypercholesterolemi, Hypercholesterolemi. (LÆGEMIDDELSTYRELSEN - NYT OM BIVIRKNINGER 2016;7(9).)

(Anm: Variations in ancient mitochondrial DNA may play key role in predisposition to ASD. Wallace and colleagues, including Dimitra Chalkia, Larry Singh and others, published their findings today in JAMA Psychiatry. (news-medical.net 23.8.2017).)

- Studie antyder at kortisol formidler kommunikasjon mellom tarmbakterier og hjernemetabolitter.

(Anm: Cortisol mediates communication between gut bacteria and brain metabolites, study suggests. Gut microbes have been in the news a lot lately. Recent studies show they can influence human health, behavior, and certain neurological disorders, such as autism. But just how do they communicate with the brain? Results from a new University of Illinois study suggest a pathway of communication between certain gut bacteria and brain metabolites, by way of a compound in the blood known as cortisol. And unexpectedly, the finding provides a potential mechanism to explain the characteristics of autism. (news-medical.net 21.8.2017).)

(Anm: «Psykiatrien i Norge har hatt for svak ledelse. På alle nivåer. I alle år». KRONIKK: Helseminister Bent Høie (H). BENT HØIE, Helseminister. (vg.no 23.11.2016).)

(Anm: Antipsykotika øger diabetes-risiko hos børn. En række forskellige antipsykotika har vist sig at medføre op til tre gange så stor en risiko for at udvikle diabetes, hvis børn og unge behandles med dem. Et studie offentliggjort i tidsskriftet JAMA Psychiatry viser ifølge Dagens Medicin, at børn og unge i behandling med antipsykotiske lægemidler har tre gange så stor en risiko for at udvikle diabetes i forhold til lignende personer, der tager andre psykoaktive præparater. (…) Den forøgede risiko indtraf allerede efter blot et års forbrug, og risikoen var fortsat tilstede i mindst et år, efter deltagerne var stoppet med at tage lægemidlerne. (medwatch.dk 9.9.2013).)

- Mitokondriell dysfunksjon (MDF) har blitt identifisert som en viktig faktor i ulike sykdommer som spenner fra nevrologiske lidelser, sykdommer i kardiovaskulærsystemet og metabolske syndromer.

(Anm: Mitochondrial dysfunction and potential anticancer therapy. Abstract Mitochondrial dysfunction (MDF) has been identified as an important factor in various diseases ranging from neurological disorders, to diseases of the cardiovascular system and metabolic syndromes. MDF was also found in cancer as well as in cancer predisposition syndromes with defective DNA damage response (DDR) machinery. Moreover, a recent highlight arises from the detection of MDF in eukaryotic cells upon treatment with antibiotics. In this review, we focus on recent studies of MDF in pathological conditions with a particular emphasis on the effects of various classes of antibiotics on mitochondria. Special attention is given to the role of autophagy/mitophagy in MDF and repurposing antibiotics as anticancer drugs. Med Res Rev. 2017 Jul 6. [Epub ahead of print].)

- Akselerert aldring grunnet legemidlers negative påvirkninger av mitokondrier etc.

(Anm: Editor-in-Chief Henry A. Nasrallah, MD, discusses the possible causes of accelerated aging and premature mortality in younger persons with schizophrenia. Video. Accelerated aging in schizophrenia. Editor-in-Chief Henry A. Nasrallah, MD, discusses the possible causes of accelerated aging and premature mortality in younger persons with schizophrenia. Current Psychiatry. 2017 July;16(7).)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Behandling av barn og ungdom med antipsykotika er et tveegget sverd. (…) To tilleggsfunn fra Pagsberg og kollegers studie er verdt å understreke. For det første erfarte bare 22 (23 %) av pasientene behandlingsrespons. (…)  For det andre erfarte 111 (98 %) av pasientene uheldige reaksjoner. (For det andre erfarte 111 (98 %) av pasientene uheldige reaksjoner.) Blant de 55 pasienter som tok quetiapine, rapporterte 47 (92 %) økt søvnlengde og 46 (87 %) rapporterte vektøkning. Blant de 58 pasienter som tok aripiprazol, rapporterte 52 (91 %) tremor og 44 (77 %) rapporterte sviktende hukommelse. (Blant de 58 pasienter som tok aripiprazol, rapporterte 52 (91 %) tremor og 44 (77 %) rapporterte sviktende hukommelse.) The Lancet Psychiatry 2017;4(8):576–577 (Published: August, 2017).)

(Anm: Antipsykotika øger diabetes-risiko hos børn. En række forskellige antipsykotika har vist sig at medføre op til tre gange så stor en risiko for at udvikle diabetes, hvis børn og unge behandles med dem. Et studie offentliggjort i tidsskriftet JAMA Psychiatry viser ifølge Dagens Medicin, at børn og unge i behandling med antipsykotiske lægemidler har tre gange så stor en risiko for at udvikle diabetes i forhold til lignende personer, der tager andre psykoaktive præparater. (…) Den forøgede risiko indtraf allerede efter blot et års forbrug, og risikoen var fortsat tilstede i mindst et år, efter deltagerne var stoppet med at tage lægemidlerne. (medwatch.dk 9.9.2013).)

(Anm: Antidepressiva og antipsykotika gir økt risiko for diabetes hos barn og voksne (50 til 700 %) (mintankesmie.no).)

(Anm: Diabetes: Risiko for hjerteinfarkt på grunn av tap av små blodårene rundt hjertet. (Diabetes: Heart attack risk due to loss of small blood vessels around the heart.) (medicalnewstoday.com 24.3.2017).)

(Anm: Antidepressiva (øyesykdommer). (mintankesmie.no).)

(Anm: Bruk av antidepressiva ble assosiert med et betydelig eldre utseende og forskere fant også ut at vekten spilte en viktig faktor. I de sett med tvillinger som var yngre enn 40 år ble tyngre tvillinger oppfattet som eldre. (…) I tillegg mistenker forskerne at den vedvarende avslapping av ansiktsmuskler som antidepressiva forårsaker kan forklare årsaken til at ansiktet faller sammen (henger). (mintankesmie.no).)

(Anm: Role of mitochondria and energy metabolism in schizophrenia and psychotic disorders. Abstract. Mitochondria are cell organelles that initially had an independent existence as α-proteobacteria. A symbiotic arrangement with either a proto-eukaryote or an archaeon enabled the newly formed organism to generate levels of cellular energy that could sustain metabolic processes of previously impossible complexity (Gray, 2012). In this singular incident, the course of evolution was profoundly changed. Without mitochondria, multicellular organism might not be possible, and there is no doubt that human life depends on them. Schizophr Res. 2017 Jul 10. pii: S0920-9964(17)30408-5. [Epub ahead of print].)

(Anm: From the Editor. Accelerated aging in schizophrenia: Shortened telomeres, mitochondrial dysfunction, inflammation, and oxidative stress. Several lines of evidence are coalescing into a critical scientific insight: Persons with schizophrenia show evidence of accelerated aging.1 This implies early senescence, segmental aging, and, in young adult patients, premature onset of multi-system medical illnesses associated with aging, including cardiovascular disease, cancer, brain atrophy, and cognitive decline. This might be the real reason why persons with schizophrenia die 25 to 30 years too early, not only because of an unhealthy lifestyle and iatrogenic cardio-metabolic adverse effects. Current Psychiatry. 2016 November;15(11):21-23.)

(Anm: Bias [baies] -en, - skjevhet i vitenskapelig undersøkelse el. resultat pga. mangelfull systematikk i innsamlingen av data. Etym.: eng., fr. biais helning, tendens. Kilde: ordnett.no.)

(Anm: Bias; (...) valg og vurderinger som på systematisk måte avviker fra det som er faktisk korrekt. Kilde: Store norske leksikon.)

(Anm: Pasienter behandlet med antipsykotika (nevroleptika) har signifikant senket platelet complex I aktivitet i mitokondrier i likhet med det som er observert ved idiopatisk Parkinsons sykdom. (...) Antipsykotika (nevroleptika) hemmer kompleks I i elektrontransportkjeden. (Neuroleptic medications inhibit complex I of the electron transport chain. (...) Neuroleptic treated patients have significant depression of platelet complex I activity similar to that seen in idiopathic Parkinson’s disease. Complex I inhibition may be associated with the extrapyramidal side effects of these drugs.) Ann Neurol. 1993;33:512-7).)

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: A mitochondrial proteomics view of complex I deficiency in Candida. albicans. (…) We hypothesize that the loss of energy production in mutants is compensated by increases in protein levels of glycolysis, gluconeogenesis, and anti-ROS scavengers that at least extend mutant survival. Mitochondrion. 2017 Aug 8. pii: S1567-7249(17)30149-6.)

 - Mitokondrier, bioenergi og eksitotoksisitet: Nye terapeutiske mål i perinatal hjerneskade. Mitokondriene er sterkt Impliserte etter iskemisk skade på grunn av sine roller som drivkraft og hovedenergigeneratorer i cellen, såvel som celledødsprosesser.

(Anm: Mitochondria, Bioenergetics and Excitotoxicity: New Therapeutic Targets in Perinatal Brain Injury. Mitochondria are highly implicated following ischemic injury due to their roles as the powerhouse and main energy generators of the cell, as well as cell death processes. (…) Mitochondria are the powerhouses of the cell, primarily responsible for the production of adenosine triphosphate (ATP) as well as playing regulatory roles in cell death, including autophagy and apoptosis (Nunnari and Suomalainen, 2012). Advances in genomic and proteomic sequencing have provided irrefutable evidence that these vestiges of bacterial ancestry also perform more diverse roles, particularly in disease (Hagberg et al., 2014). These range from early work showing that mutations in mitochondrial DNA (mtDNA) are implicated in diseases such as Parkinson’s disease (Swerdlow et al., 1996), to research on the epigenetic modulation of mtDNA, including methylation by DNA methyltransferases, which add yet another layer in which mitochondria can influence and contribute to disease (van der Wijst and Rots, 2015). There is thus a growing appreciation that identifying and targeting mitochondrial pathways thought to be responsible for the manifestation of initial injury post asphyxia as well as long-term neurodevelopment holds great promise in the field of perinatal medicine. Front. Cell. Neurosci., 12 July 2017.)

- Enkelte legemidler (substanser) og fysisk attraktivitet.

(Anm: Antipsykotika og fysisk attraktivitet (Antipsychotics and physical attractiveness) (...) Antipsykotika, som gruppe, fører til vektøkning og kan føre til munntørrhet og dårlig ånde, grå stær, hirsutisme (uvanleg sterk eller altfor utbreidd hårvekst (helst hos kvinner)), akne og stemmeendringer; de kan forstyrre symmetri av gangart og øke risikoen for tics og spasmer og inkontinens, og potensielt undergrave en persons attraktivitet. Clin Schizophr Relat Psychoses. 2011 Oct;5(3):142-146.)

(Anm: Medikamentutløst dystoni. (…) Videoen illustrerer ekstrapyramidale bivirkninger med dystoni i tunge og kjeveområdet. Tidsskr Nor Legeforen 2016; 136:1730-1730 (8.11.2016).)

(Anm: Bruk av antidepressiva ble assosiert med et betydelig eldre utseende og forskere fant også ut at vekten spilte en viktig faktor. I de sett med tvillinger som var yngre enn 40 år ble tyngre tvillinger oppfattet som eldre. (…) I tillegg mistenker forskerne at den vedvarende avslapping av ansiktsmuskler som antidepressiva forårsaker kan forklare årsaken til at ansiktet faller sammen (henger). (mintankesmie.no).)

(Anm: Antipsykotika forårsaker ansiktsgrimasering og andre typer mulige varige hjerneskader (mintankesmie.no).)

(Anm: Skrekkbildene som viser hva røyking gjør med kroppen din (dagbladet.no 19.10.2013).)

(Anm: Dödsdrogens sanna ansikte - Detta är bilderna som säger allt. Om livet före och efter. Med drogen crystal meth. (expressen.se 3.3.2006).)

- Søk etter mitokondrielle mekanismer: linking av kjente syndromer til mitokondriell funksjon.

(Anm: Mining for mitochondrial mechanisms: linking known syndromes to mitochondrial function. Abstract Mitochondrial disorders (MDs) are caused by defects in one or multiple complexes of the oxidative phosphorylation (OXPHOS) machinery. MDs are associated with a broad range of clinical signs and symptoms, and have considerable clinical overlap with other neuromuscular syndromes. This overlap might be due to involvement of mitochondrial pathways in some of these non-mitochondrial syndromes. Here, we give an overview of around 25 non-mitochondrial syndromes, diagnosed in patients who were initially suspected to have a MD on the basis of clinical and biochemical parameters. In addition, we highlight the mitochondrial connections of six of these non-mitochondrial syndromes (e.g. Rett syndrome and Dravet syndrome) diagnosed in multiple patients. Further research to unravel the interplay between these genes and mitochondria may help to increase knowledge on these syndromes. Conversely, it may open new avenues for research on pathways interacting with mitochondrial function in order to find new targets for therapeutics to treat MDs. The data presented in this review underline the importance of careful assessment of clinical, genetic, and biochemical data in all patients suspected of a neuromuscular syndrome, and highlights the importance of the role of clinical geneticists, physicians, and clinical biochemists in recognizing the possible mitochondrial connection of non-mitochondrial syndromes. Clin Genet. 2017 Jul 7. [Epub ahead of print].)

- Rollen til mitokondriell dysfunksjon ved utviklingen av Alzheimers sykdom.

(Anm: Rollen til mitokondriell dysfunksjon ved utviklingen av Alzheimers sykdom. The role of mitochondrial dysfunction in the progression of Alzheimer's disease. Curr Med Chem. 2017 Jun 16. [Epub ahead of print] Abstract The current molecular understanding of Alzheimer's disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain. Curr Med Chem. 2017 Jun 16.)

(Anm: Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt. (The role of mitochondrial dysfunction in sepsis-induced multi-organ failure). (Virulence. 2013 Nov 1;5(1).)

- Diagnostisering av sepsis. Sepsis, også kjent som blodforgiftning, er kroppens hyperaktive respons på en infeksjon som kan føre til betennelse, vevskader, organsvikt etc.

(Anm: Diagnosing Sepsis. Sepsis, also known as blood poisoning, is the body’s hyperactive response to an infection that can lead to inflammation, tissue damage, organ failure etc. It is a very dangerous state in which the immune system stops fighting with the invading agents  and turns to itself. Around one-third of patients who are affected with sepsis die every year. (news-medical.net 7.9.2017).)

- Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon.

(Anm: Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon. Recognizing Sepsis as a Global Health Priority — A WHO Resolution. “Some very important clinical issues, some of them affecting life and death, stay largely in a backwater which is inhabited by academics and professionals and enthusiasts, dealt with very well at the clinical and scientific level but not visible to the public, political leaders, leaders of healthcare systems... The public and political space is the space in which [sepsis] needs to be in order for things to change.” NEJM (June 28, 2017).)

(Anm: Antidepressiva er ifølge ny studie knyttet til mislykkede tannimplantater. (Antidepressants linked to tooth implant failure, new study finds.) (- Forskning viser at bruk av antidepressiva firedobler risikoen for implantat svikt. For hvert år dobler antidepressiva risikoen for svikt.) (medicalnewstoday.com 10.3.2016).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

- Kronisk oksidativ stress, mitokondriell dysfunksjon, Nrf2 aktivering og inflammasjon i Hippocampus-ledsaget av forhøyet systemisk inflammasjon og oksidativ stress i en dyremodell ved GWI (Golfskrigslidelse; engelsk: Gulf War Syndrome).

(Anm: Chronic Oxidative Stress, Mitochondrial Dysfunction, Nrf2 Activation and Inflammation in the Hippocampus Accompany Heightened Systemic Inflammation and Oxidative Stress in an Animal Model of Gulf War Illness. Memory and mood dysfunction are the key symptoms of Gulf war illness (GWI), a lingering multi-symptom ailment afflicting >200,000 veterans who served in the Persian Gulf War-1. Research probing the source of the disease has demonstrated that concomitant exposures to anti-nerve gas agent pyridostigmine bromide (PB), pesticides, and war-related stress are among the chief causes of GWI. Front. Mol. Neurosci., 14 June 2017.)

(Anm: Animal model of Gulf War illness hints at possible ways to mitigate symptoms. (…) To test the effects of such exposure, the researchers must first create an animal model. "We simulate what happened during the war," Shetty said. (…) Additional studies completed recently in Shetty's laboratory have also shown resveratrol as a promising compound for decreasing systemic and brain inflammation, as well as improving cognitive and memory function in animal models of GWI. (medicalnewstoday.com 20.6.2017).)

(Anm: Modeling Gulf War illness: Knowing the cause of brain dysfunction is key to finding a cure. With hundreds of thousands of veterans experiencing long-term side effects of their service, the hunt for a treatment is on. When hundreds of thousands of American troops deployed to the Persian Gulf in 1990 and 1991 in what is now called the First Gulf War, they were exposed to a variety of chemicals. (…) “Together, these findings raise the possibility that hippocampal dysfunction in GWI is one of the adverse outcomes of persistently elevated oxidative stress and inflammation at the systemic level,” he added. (vitalrecord.tamhsc.edu 14.6.2017).)

(Anm: Linking telomere loss and mitochondrial dysfunction in chronic disease. (…) Drawing a mechanistic connection between telomere function and mitochondria biology will provide a broader perspective for understanding the pathophysiology of diseases and their relation to the aging process, and may provide opportunities for new possible treatments. Front Biosci (Landmark Ed). 2017 Jan 1;22:117-127.)

- Kronisk behandling med prebiotika, probiotika og synbiotika redusert hjertedysfunksjon ved å forbedre hjertemittokondriell dysfunksjon hos mannlige overvektige insulinresistente rotter.

(Anm: Chronic treatment with prebiotics, probiotics and synbiotics attenuated cardiac dysfunction by improving cardiac mitochondrial dysfunction in male obese insulin-resistant rats. Abstract PURPOSE: In metabolic syndrome, the composition of gut microbiota has been disrupted, and is associated with left ventricular (LV) dysfunction. Several types of prebiotics, probiotics, and synbiotics have been shown to exert cardioprotection by restoring gut microbiota from dysbiosis and reducing systemic inflammation. However, the effects of prebiotics such as xylooligosaccharides (XOS); probiotics such as Lactobacillus paracasei STII01 HP4, and synbiotics on metabolic and LV function in obese insulin-resistant rats have not been investigated. In this study, we hypothesized that prebiotics and probiotics improve metabolic parameters, heart rate variability (HRV), blood pressure (BP), and LV function by attenuating cardiac mitochondrial dysfunction, systemic inflammation, and oxidative stress, and that synbiotics provide greater efficacy than a single regimen in obese insulin resistance. (…) CONCLUSION: Prebiotics, probiotics, and synbiotics shared similar efficacy in reducing insulin resistance and LV dysfunction in obese insulin-resistant rats. Eur J Nutr. 2017 Jun 12.)

(Anm: Studie linker gastrointestinale forstyrrelser for GWI (Golfskrigslidelse; engelsk: Gulf War Syndrome) med forandringer i mikrobiota (tarmfloraen). (Study links gastrointestinal disturbances of GWI with changes in intestinal microbiota.) (…) "Mennesker og dyr har spesifikke typer bakterier som bidrar til å hjelpe til med forskjellige fysiologiske prosesser, inkludert fordøyelse, absorpsjon, immunitet og tarmintegritet, og når eksterne faktorer endrer den bakterielle sammensetningen i vårt fordøyelsessystem får vi problemer", sier Chatterjee. "Fedme, metabolsk syndrom, inflammatorisk tarmsyndrom og leversykdom er allerede blitt knyttet til endringer i bakteriesammensetningen i tarmen." (news-medical.net.com 23.3.2017).)

(Anm: Antibiotika associeras med högre risk för tarmcancer. (…) Det här är första studien som visar på sambandet mellan antibiotikaanvändning och utveckling av adenom i tjock- och ändtarmen. Studien publiceras i den vetenskapliga tidskriften Gut. (…) Resultatet visade att långvarig antibiotikaanvändning tidigare i livet, i åldern 20 till 59 år, hade samband med diagnostiserade adenom. (lakemedelsvarlden.se 5.4.2017.)

- Er glaukom en mitokondriell neurodegenerativ sykdom.

(Anm: Er glaukom en mitokondriell neurodegenerativ sykdom. [Is glaucoma a mitochondrial neurodegenerative disease]. Abstract. The retinal ganglion cell, due to peculiar structural and energetic constraints, appears acutely susceptible to mitochondrial dysfunction. Emerging evidence suggests that changes in the mitochondrial DNA(mtDNA)and in nuclear DNA genes that encode mitochondrial proteins may influence mitochondrial structure and function and, therefore, contribute to the pathogenesis of primary open angle glaucoma. As the main glaucoma risk factors are elevated intraocular pressure and older age, we discuss their relationship with mitochondrial dysfunction. If the contribution of mitochondrial dysfunction to glaucoma pathogenesis is further established, emerging therapies aiming to optimize mitochondrial function represent potential clinical treatments. (Chin J Ophthalmol, 2016, 52: 714-717).  Zhonghua Yan Ke Za Zhi. 2016 Sep 11;52(9):714-7.)

(Anm: Antidepressiva (øyesykdommer). (mintankesmie.no).)

(Anm: Antidepressiva (nytteverdi) (mintankesmie.no).)

(Anm: Ny forskning: Lykkepiller gør mere skade end gavn. Folk med depression får intet ud af at tage antidepressivet SSRI, bedre kendt som lykkepiller, viser nyt dansk studie. (jyllands-posten.dk 13.2.2017).)

(Anm: I denne studien oppdaget forskerne at det å ta visse antidepressiva, sedativer, beroligende midler eller antipsykotika økte veteranenes risiko for å utvikle demens sammenlignet med risikoen for veteraner som ikke tok slike legemidler. PTSD and psychoactive drugs linked to increased risk for dementia.) (newmedpagetoday.com 9.5.2017.)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Antidepressiva ökar risken för benbrott hos äldre. (…) Den förhöjda risken för höftfraktur gällde alla de vanliga antidepressiva läkemedlen, SSRI-preparat, mirtazapin och SNRI-preparat (selektiva serotonin- och noradrenalinåterupptagshämmare. Sambandet gällde även då det kontrollerats för andra faktorer som ålder, annan medicinering som ökar fallrisken, benskörhet, socioekonomisk status, kroniska sjukdomar och psykiatriska diagnoser.) (lakemedelsvarlden.se 12.1.2017).)

(Anm: Tannkjøttsykdom er et tidlig tegn på diabetes, og tap av tenner er forbundet med risiko for demens, ifølge studier. Gum disease is an early sign of diabetes, and tooth loss is associated with risk of dementia, studies find. Patients with periodontitis have higher plasma concentrations of glycated haemoglobin (HbA1c) than people with healthy gums, and those with severe periodontitis have a significantly higher risk of developing diabetes, a Dutch study has found. BMJ 2017;356:j1225 (Published 09 March 2017).)

(Anm: Tannleger og tannhelse (munnhulen er kroppens speil). (mintankesmie.no/).)

(Anm: Diabetes (mintankesmie.no).)

(Anm: Dementia, Alzheimer's, and Aging Brains (medicinenet.com 22.7.2016).)

(Anm: - Kalsiumubalanse i hjerneceller kan utløse Alzheimers sykdom. (- Ingen har noen gang sett på dette før bruken av disse modellsystemene. Det er mulig at endringer i mitokondrienes kalsiumutveksling er driveren av sykdomsprosessen. Tidligere forskning har vist at en overdreven produksjon av kalsium kan føre til at nerveceller dør, derfor linkes en kalsiumubalanse med den nevrodegenerative prosessen involvert i Alzheimers sykdom. (Calcium imbalance within brain cells may trigger Alzheimer's disease.) (medicalnewstoday.com 15.2.2017).)

(Anm: Mitochondrial Dysfunction Triggers Synaptic Deficits via Activation of p38 MAP Kinase Signaling in Differentiated Alzheimer's Disease Trans-Mitochondrial Cybrid Cells. J Alzheimers Dis. 2017 Jun 6. [Epub ahead of print].)

(Anm: Kurerer eller skaper antidepressiva unormale tilstander i hjernen? (mintankesmie.no).)

- Vi konkluderer med at metadon forårsaker svikt i intracellulær Ca (2+) homeostase, og at denne effekten er forbundet med morfologiske og funksjonelle forandringer av mitokondrier. Sannsynligvis bidrar denne mekanismen til degenerative bivirkninger forbundet med metadonbehandling.

(Anm: Vi konkluderer med at metadon forårsaker svikt i intracellulær Ca (2+) homeostase, og at denne effekten er forbundet med morfologiske og funksjonelle forandringer av mitokondrier. Sannsynligvis bidrar denne mekanismen til degenerative bivirkninger forbundet med metadonbehandling. («We conclude that methadone causes failure of intracellular Ca(2+) homeostasis, and this effect is associated with morphological and functional changes of mitochondria. Likely, this mechanism contributes to degenerative side effects associated with methadone treatment.») Int J Cell Biol. 2012;2012:642482. dEpub 2012 Jun 17).

(Anm: 24 år gammel var hun blitt hektet på illegalt metadon. Behandlingen Melissa fikk, var mer metadon. (…) Hun foreller at det ikke er vanskelig å skaffe seg preparater som er skrevet ut til LAR-pasienter. – Det er nok av tilbud på metadon på gaten. Det er et stort marked, og jeg kunne lett solgt dagdosene mine for 200 kroner stykket. Da ville jeg sittet igjen med penger nok til å kjøpe meg en friskmelding, forteller hun og sikter til en dose heroin. (aftenposten.no 31.10.2016).)

- Samspillet mellom betennelse, oksidativt stress, DNA-skade, DNA-reparasjon og mitokondriell dysfunksjon ved depresjon.

(Anm: The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression. Abstract A growing body of evidence suggests that inflammation, mitochondrial dysfunction and oxidant-antioxidant imbalance may play a significant role in the development and progression of depression. Elevated levels of reactive oxygen and nitrogen species - a result of oxidant-antioxidant imbalance - may lead to increased damage of biomolecules, including DNA. This was confirmed in depressed patients in a research study conducted by our team and other scientists. 8-oxoguanine - a marker of oxidative DNA damage - was found in the patients' lymphocytes, urine and serum. These results were confirmed using a comet assay on lymphocytes. Furthermore, it was shown that the patients' cells repaired peroxide-induced DNA damage less efficiently than controls' cells and that some single nucleotide polymorphisms (SNP) of the genes involved in oxidative DNA damage repair may modulate the risk of depression. Lastly, less efficient DNA damage repair observed in the patients can be, at least partly, attributed to the presence of specific SNP variants, as it was revealed through a genotype-phenotype analysis. In conclusion, the available literature shows that both oxidative stress and less efficient DNA damage repair may lead to increased DNA damage in depressed patients. A similar mechanism may result in mitochondrial dysfunction, which is observed in depression. Prog Neuropsychopharmacol Biol Psychiatry. 2017 Jun 29. pii: S0278-5846(16)30298-6. [Epub ahead of print].)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

- Artrose: Forhindring av mangel på nøkkelmolekyl kan forsinke behov for leddproteser. (- Mitokondrier forsyner cellen med energi i form av kjemiske enheter kalt adenosin trifosfat (ATP), adenosin og ATP er et biprodukt av metabolisme.)

Osteoarthritis: Preventing key molecule deficiency may delay need for joint replacements
medicalnewstoday.com 11.5.2017
New research carried out on rodents reveals, for the first time, that preventing the loss of a molecule that is important for cartilage maintenance could delay the onset of osteoarthritis, a disease of the joints that causes disability and affects millions of people in the United States.

Osteoarthritis (OA) - also referred to as degenerative joint disease - is the most common form of arthritis, a general term used to describe a range of conditions that cause pain or disease in the joints.

The new study, led by the NYU Langone Medical Center in New York and published in the journal Nature Communications, shows that injecting the vital cell molecule adenosine into the joints can prevent OA in rat models of the disease.

OA most commonly affects the hips, hands, and knees, and it results from the gradual wear and tear of the cartilage that cushions the ends of the bones in the joint and stops them rubbing against each other. (…)

Adenosine helps healthy chondrocytes maintain cartilage
The researchers investigated the role that adenosine plays in maintaining a healthy supply of chondrocytes.

They note in their study paper that adenosine levels inside and outside cells are "tightly controlled" by cellular stress, oxygen consumption, and the workings of mitochondria - the pockets inside cells that produce the energy for the cell.

Mitochondria supply the cell with energy in the form of chemical units called adenosine triphosphate (ATP), and adenosine is a byproduct of ATP metabolism.

It was already known that aging and inflammation reduces ATP production in chondrocytes, which in turn reduces levels of adenosine. However, until this study, it was not clear how that might relate to OA.

One of the main discoveries of the study is that reduction in chondrocytes, and therefore greater risk for OA, is driven not only by lower levels of adenosine surrounding the cells, but also by loss of signal-receiving proteins called adenosine A2A receptors on the surface of the cells. (…)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

(Anm: Senescence, apoptosis or autophagy? When a damaged cell must decide its path--a mini-review. Many features of aging result from the incapacity of cells to adapt to stress conditions. When damage accumulates irreversibly, mitotic cells from renewable tissues rely on either of two mechanisms to avoid replication. They can permanently arrest the cell cycle (cellular senescence) or trigger cell death programs. Apoptosis (self-killing) is the best-described form of programmed cell death, but autophagy (self-eating), which is a lysosomal degradation pathway essential for homeostasis, reportedly contributes to cell death as well. Unlike mitotic cells, postmitotic cells like neurons or cardiomyocytes cannot become senescent since they are already terminally differentiated. The fate of these cells entirely depends on their ability to cope with stress. Autophagy then operates as a major homeostatic mechanism to eliminate damaged organelles, long-lived or aberrant proteins and superfluous portions of the cytoplasm. In this mini-review, we briefly summarize the molecular networks that allow damaged cells either to adapt to stress or to engage in programmed-cell-death pathways. Gerontology. 2008;54(2):92-9. Epub 2008 May 2.)

(Anm: ER-Mitochondria signaling regulates autophagy.Autophagy. Abstract. The endoplasmic reticulum (ER) and mitochondria form tight functional contacts that regulate a number of key cellular processes. Finally, our studies revealed that the modulatory effects of ER-mitochondria contacts on autophagy involve their role in mediating ITPR (inositol 1,4,5-trisphosphate receptor) delivery of Ca2+ from ER stores to mitochondria. Autophagy. 2017 May 26:0. [Epub ahead of print].)

(Anm: Control of cell death and mitochondrial fission by ERK1/2 MAP Kinase signalling FEBS J. 2017 May 26. doi: 10.1111/febs.14122. [Epub ahead of print].)

(Anm: Mitochondrial Dysfunction Meets Senescence. Trends Biochem Sci. 2016 Feb 10. pii: S0968-0004(16)00020-7. [Epub ahead of print].)

(Anm: Short Overview. Abstract Mitochondrial autophagy (mitophagy) is a mitochondrial quality control mechanism that selectively removes damaged mitochondria via autophagic degradation. Autophagic adaptor/receptor proteins contribute to the selective degradation of damaged mitochondria by autophagy. A part of them containing both ubiquitin binding domains and Atg8 interacting motif (AIM)/LC3 interacting region (LIR) motifs, which bind to the autophagy-related protein 8 (Atg8) family (LC3 and GABARAP family), lead ubiquitylated (damaged) mitochondria to selective removal. On the other hand, some specific outer mitochondrial membrane-anchored proteins containing AIM/LIR motif function as another type of autophagy adaptor/receptor proteins. Here I briefly summarize mechanisms of mitophagy and its related proteins.) Methods Mol Biol. 2017 May 12. [Epub ahead of print].)

(Anm: Senescence (/sɪˈnɛsəns/) (from Latin: senescere, meaning "to grow old", from senex) or biological aging (also spelled biological ageing) is the gradual deterioration of function characteristic of most complex lifeforms, arguably found in all biological kingdoms, that on the level of the organism increases mortality after maturation. The word senescence can refer either to cellular senescence or to senescence of the whole organism. It is commonly believed that cellular senescence underlies organismal senescence. The science of biological aging is biogerontology. (en.wikipedia.org).)

(Anm: Evig ung. 2. Hvordan bremse det kroppslige forfallet? (…) Episodebeskrivelse For å leve lenge, må vi vedlikeholde kroppen vår. Hjelper det egentlig å trene? Når kroppen blir slitt trenger vi nye deler, forskere mener de nå kan dyrke menneskeorganer inni griser (nrk.no 2.4.2017).)

- Syntetisk stoff som leser mitokondrie-DNA kan føre til behandlinger for nerve, muskel sykdommer. For første gang kan en syntetisk fremstilt forbindelse som kan binde seg til DNA i cellenes kraftstasjoner (mitokondrier), undertrykke et gen med tilknytning til nerve og muskelsykdommer.

(Anm: Synthetic compound that reads mitochondrial DNA could lead to treatments for nerve, muscle diseases. For the first time, a synthetic compound has been made that can bind to DNA in the cells' energy powerhouses, suppressing a gene associated with nerve and muscle disease. Pyrrole-imidazole polyamides (PIPs) are compounds that can read specific DNA sequences inside living cells and silence disease-causing genes. They prevent proteins, called transcription factors, from binding to specific parts of the DNA strand, thus suppressing the transcription of DNA into RNA. Most DNA is found in the nucleus. But mitochondria, the cell's powerhouses, also host a small amount of DNA. PIPs are capable of crossing the nuclear membrane to bind to nuclear DNA, but are incapable of crossing the mitochondrial membrane. (news-medical.net 11.7.2017).)

(Anm: Chronic kidney disease induces autophagy leading to dysfunction of mitochondria in skeletal muscle. Am J Physiol Renal Physiol. 2017 Apr 5:ajprenal.00600.2016.)

(Anm: Disrupted mitochondrial function in the Opa3L122P mouse model for Costeff Syndrome impairs skeletal integrity. Thus, mitochondrial function is important for the development and maintenance of skeletal integrity, impaired bone growth and strength, particularly in limb bones, representing a significant new feature of the Costeff syndrome phenotype. Hum Mol Genet. 2016 Jun 15;25(12):2404-2416. Epub 2016 Apr 22.)

(Anm: Linking mitochondrial dysfunction to neurodegeneration in lysosomal storage diseases. (…) Abstract Lysosomal storage diseases (LSD) are inborn errors of metabolism resulting in multisystem disease. Central nervous system involvement, often with progressive neurodegeneration, accounts for a large portion of the morbidity and mortality seen in many LSD. Available treatments fail to prevent or correct neurologic symptoms and decline. J Inherit Metab Dis. 2017 May 5. [Epub ahead of print].)

(Anm: Oxygen’s surprisingly complex journey through your body - Enda Butler. Oxygen forms about 21% of the air around us. In your body, oxygen forms a vital role in the production of energy in most cells. But if gases can only efficiently diffuse across tiny distances, how does oxygen reach the cells deep inside your body? Enda Butler tracks the surprisingly complex journey of oxygen through your body. (ed.ted.com.)

(Anm: From dysfunctional endoplasmic reticulum-mitochondria coupling to neurodegeneration. Neurochem Int. 2017 Apr 4. pii: S0197-0186(17)30081-5.)

(Anm: Chikusetsu (CHI) triggers mitochondria-regulated apoptosis in human prostate cancer via reactive oxygen species (ROS) production. (…) Moreover, in vivo study showed that prostate tumor was inhibited by CHI administration through apoptosis induction. Thus, the results illustrated that CHI might be an effective therapeutic strategy for prostate cancer treatment in future.Biomed Pharmacother. 2017 Apr 5;90:446-454.)

- Laktat kan være nøkkelen til kreftutvikling. (- Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet.)

Lactate may be key for cancer development (Laktat kan være nøkkelen til kreftutvikling.)
medicalnewstoday.com 19.3.2017
Researchers are working hard to understand the mechanism responsible for oncogenesis, the process through which normal cells become cancerous ones. A new study focuses on lactate - a molecule produced during intense exercise - and explains its role in cancer cell formation.

New research, published in the journal Carcinogenesis, analyzes the role of lactate in oncogenesis.

Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis - the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.)

At the beginning of the 20th century, German scientist Otto Warburg noticed that cancer cells consume a lot more glucose than normal cells. The so-called Warburg effect refers to the fact that cancer cells undergo more glycolysis and produce more lactate compared with normal cells.

The new research - led by Inigo San Millan, director of the Sports Performance Department and physiology laboratory at the University of Colorado-Boulder's Sports Medicine and Performance Center - set out to understand why the Warburg effect happens. Since Warburg's time, the focus in cancer research has shifted from cell metabolism to genetics, but the new paper hopes to put lactate back at the center of cancer research. (…)

(Anm: High serum lactate level may predict death within 24 hours. (…) CONCLUSIONS: The significant independent variable that predicted death within 24 hours of admission was arterial blood lactate level on admission. Older age was also an independent variable; low pH affected only males, but was a less dominant variable. We suggest use of arterial blood lactate level on admission as a bio-marker in patients with suspected sepsis admitted to the hospital for risk assessment and prediction of death within 24 hours of admission. Open Med (Wars). 2015 Jun 11;10(1):318-322. eCollection 2015.)

(Anm: The mobility of mitochondria: intercellular trafficking in health and disease. (…) The ability of mitochondria to move between cells appears to be an evolutionarily-conserved phenomenon, relevant to diseases with compromised mitochondrial function including neurodegenerative, neuromuscular and cardiovascular diseases as well as cancer and ageing. Clin Exp Pharmacol Physiol. 2017 Apr 13.)

- Raskt glukoseopptak gir økt risiko for kreft. Menn med raskt glukoseopptak fra blodbanen har betydelig forhøyet risiko for kreft, viser en fersk, norsk studie fra Oslo Universitetssykehus.

(Anm: Raskt glukoseopptak gir økt risiko for kreft. Menn med raskt glukoseopptak fra blodbanen har betydelig forhøyet risiko for kreft, viser en fersk, norsk studie fra Oslo Universitetssykehus. Dersom det sprøytes glukose, også kjent som druesukker, inn i blodbanen, settes det i gang mekanismer som gjør at overskudd av sukker transporteres inn i kroppens celler. En ny studie av norske menn som har blitt fulgt over mange år, viser at raskt opptak av glukose fra blodbanen er forbundet med økt risiko for kreft senere i livet. Studien er nylig publisert i det vitenskapelige tidsskriftet eBioMedicine. (dagensmedisin.no 12.7.2017).)

- The multidrug resistance-1 (MDR1) gene encodes an ATP-dependent efflux transporter that is highly expressed in the colon.

MDR1 deficiency impairs mitochondrial homeostasis and promotes intestinal inflammation.
Mucosal Immunol. 2017 Apr 12.
Abstract The multidrug resistance-1 (MDR1) gene encodes an ATP-dependent efflux transporter that is highly expressed in the colon. In mice, loss of MDR1 function results in colitis with similarities to human inflammatory bowel diseases (IBD). Here, we show that MDR1 has an unexpected protective role for the mitochondria where MDR1 deficiency results in mitochondrial dysfunction with increased mitochondrial reactive oxygen species (mROS) driving the development of colitis. Exogenous induction of mROS accelerates, while inhibition attenuates colitis in vivo; these effects are amplified in MDR1 deficiency. In human IBD, MDR1 is negatively correlated to SOD2 gene expression required for mROS detoxification. To provide direct evidential support, we deleted intestinal SOD2 gene in mice and showed an increased susceptibility to colitis. We exploited the genome-wide association data sets and found many (∼5%) of IBD susceptibility genes with direct roles in regulating mitochondria homeostasis. As MDR1 primarily protects against xenotoxins via its efflux function, our findings implicate a distinct mitochondrial toxin+genetic susceptibility interaction leading to mitochondrial dysfunction, a novel pathogenic mechanism that could offer many new therapeutic opportunities for IBD. Mucosal Immunology advance online publication, 12 April 2017; doi:10.1038/mi.2017.31. (…)

(Anm: Problem Drugs. Many different drugs and drug classes have been reported to cause problems in dogs with the MDR1 mutation. The VCPL continues to work to identify drugs that may be dangerous to dogs with the MDR1 mutation and to determine alternative drugs and doses for these dogs. (vcpl.vetmed.wsu.edu (13.4.2017)).)

- Her er den bedste træning til at modvirke, at kroppens celler ældes. (- De yngre testdeltagere havde en forbedret ydelse i cellestrukturernes (mitokondriernes) kapacitet på 49 procent og de ældre på hele 69 procent. Det er meget signifikante tal i forhold til at udsætte cellernes aldring.)

Her er den bedste træning til at modvirke, at kroppens celler ældes
jyllands-posten.dk 8.3.2017
Både unge og ældre opnår overraskende gode resultater på kort tid, viser undersøgelse. (…)

Forskere ved Mayo Clinic i Minnesota i USA lod 72 unge og ældre mennesker udføre forskellige typer fysiske øvelser ved forskellige intensiteter for at måle, hvilke der havde de største fordele i forhold til at udsætte kroppens aldringsproces. Og konklusionen var klar, skriver Daily Mail og New Scientist. (...)

Det handlede ikke om den konkrete, fysiske øvelse. I stedet gælder det om at træne maksimalt i fire minutter ad gangen efterfulgt af tre minutters aktivitet ved lidt lavere niveau 12 gange om ugen. Dette program skal suppleres af i alt 90 minutters gang i en stepmaskine eller en tilsvarende gåtur. Øvelserne kan for eksempel fordeles over 3-4 træningspas i løbet af syv dage.

Og resultatet var overbevisende. Ved at tage biopsier af deltagernes muskler kunne forskerne se, at de yngre testdeltagere havde en forbedret ydelse i cellestrukturernes (mitokondriernes) kapacitet på 49 procent og de ældre på hele 69 procent. Det er meget signifikante tal i forhold til at udsætte cellernes aldring.

Den eneste reelle svaghed ved den kortvarige træningsindsats var en begrænset evne til at opbygge musklerne. Her er styrketræning stadig et godt supplement til intervaltræning. (...)

Motionsstudiet er også beskrevet i magasinet Cell Metabolism. (…)

(Anm: Fysisk trening (aktivitet / løping / jogging). (mintankesmie.no).)

(Anm: Linking telomere loss and mitochondrial dysfunction in chronic disease. (…) Drawing a mechanistic connection between telomere function and mitochondria biology will provide a broader perspective for understanding the pathophysiology of diseases and their relation to the aging process, and may provide opportunities for new possible treatments. Front Biosci (Landmark Ed). 2017 Jan 1;22:117-127.)

(Anm: Extreme short and long telomeres linked to increased cancer risk (news-medical.net 5.4.2017).)

(Anm: Mitochondrial dysfunction-a link between antibiotic use and increased risk of severe mental disorders? Acta Psychiatr Scand. 2017 Mar 23.)

(Anm: Mitokondriell dysfunksjon ved luftveissykdom.  Mitochondrial Dysfunction in Airway Disease. Abstract. There is increasing appreciation that mitochondria serve cellular functions beyond oxygen sensing and energy production. Accordingly, it has become important to explore non-canonical roles of mitochondria in normal and pathophysiological processes that influence airway structure and function in the context of diseases such as asthma and COPD. Mitochondria can sense upstream processes such as inflammation, infection, tobacco smoke and environmental insults important in these diseases, and in turn can respond to such stimuli via altered mitochondrial protein expression, structure, and resultant dysfunction. Chest. 2017 Mar 21. pii: S0012-3692(17)30398-7.)

(Anm: Scientists discover master regulator of cellular aging. (…) "Telomeres represent the clock of a cell," said TSRI Associate Professor Eros Lazzerini Denchi, corresponding author of the new study, published online in the journal Science. "You are born with telomeres of a certain length, and every time a cell divides, it loses a little bit of the telomere. Once the telomere is too short, the cell cannot divide anymore." (medicalnewstoday.com 13.1.2017).)

(Anm: Telomere length and depression: prospective cohort study and Mendelian randomisation study in 67 306 individuals. Background. Depression has been cross-sectionally associated with short telomeres as a measure of biological age. However, the direction and nature of the association is currently unclear. (…) Further, purchase of antidepressant medication was not associated with short telomere length cross-sectionally or prospectively. (…) Conclusions. Short telomeres were not associated with depression in prospective or in causal, genetic analyses. The British Journal of Psychiatry Jan 2017, 210 (1) 31-38.)

(Anm: Harvard Scientists Claim to Reverse Aging in Mice. (…) Mitochondria: Aging in a car takes place mainly in the engine. Similarly, aging in the cell takes place in its "engine," the mitochondria. (bigthink.com 3.1.2011).)

(Anm: Gray matter abnormality predicts neurodevelopmental problems in smaller premature babies (medicalnewstoday.com 8.4.2016).)

(Anm: Gray Matter Abnormalities in the Inhibitory Circuitry of Young Binge Drinkers: A Voxel-Based Morphometry Study. (…) Binge drinking (BD) is defined as a pattern of high alcohol intake in a short time followed by periods of abstinence. Front. Psychol., 13 September 2017.)

(Anm: Antipsykotika kan krympe hjernevolumet (Antipsychotics May Shrink Brain Volume) (medpagetoday.com 8.2.2011).)

(Anm: Mitochondrial DNA: Impacting Central and Peripheral Nervous Systems..Neuron. 2014 Dec 17;84(6):1126-1142.)

(Anm: Synthetic sugar against autoimmune diseases. Researchers are working on an innovative approach to treat a rare autoimmune disease of the peripheral nervous system, using a kind of molecular sponge made of sugar to remove pathogenic antibodies from the bloodstream. Developed to treat anti-MAG neuropathy, the approach also has potential applications in the treatment of other autoimmune diseases. Scientists from the University of Basel and University Hospital Basel have reported their findings in the scientific journal PNAS. (medicalnewstoday.com 18.4.2017).)  

(Anm: Forskere kan have fundet nøgle til sklerosebehandling. Fejl i kommunikationen mellem nerveceller og immunsystemet kan være årsag til sygdommen sklerose. (…) Når personer bliver ramt af sklerose, skyldes det, at immuncellerne i stedet for at beskytte mod sygdomme og vira angriber kroppens egne celler og skaber det, der kaldes en autoimmun sygdom. (jyllands-posten.dk 24.4.2017).)

(Anm: Is Coenzyme Q10 Effective in Statin Myopathy? Atherosclerosis 2015 Feb. - During 8 weeks of treatment, CoQ10 had no effect on muscle symptoms. (NEJM 2017 (January 27, 2015).)

(Anm: Curcumin Protects Mitochondria and Cardiomyocytes from Oxidative Damage and Apoptosis Induced by Hemiscorpius Lepturus Venom. (…) Our findings suggest H. lepturus venom cusses a disruptive effect on mitochondrial respiratory chain, especially on complex II, and IV that predispose cardiomyocytes to ATP depletion and death signaling that could be protected with administration of curcumin. Drug Res (Stuttg). 2017 Oct 10.)

(Anm: Coenzyme Q10 protects against statin-induced myotoxicity in zebrafish larvae (Danio rerio). Environ Toxicol Pharmacol. 2017 Apr 1;52:150-160.)

(Anm: Is Coenzyme Q10 Effective in Statin Myopathy? Atherosclerosis 2015 Feb. - During 8 weeks of treatment, CoQ10 had no effect on muscle symptoms. (NEJM 2017 (January 27, 2015).)

(Anm: Coenzyme Q10 protects against statin-induced myotoxicity in zebrafish larvae (Danio rerio). Environ Toxicol Pharmacol. 2017 Apr 1;52:150-160.)

(Anm: Neurobiology: Mitochondria make nerves grow. After an injury, some young neurons can regrow their long signalling arms known as axons, but mature cells cannot. Zu-Hang Sheng of the National Institutes of Health in Bethesda, Maryland, and his colleagues… Nature. 2016 Jun 22;534(7608):439.)

(Anm: ATP: The crucial component of secretory vesicles. Abstract. (…) To our knowledge, our data provide the first demonstration that ATP, in addition to serving as an energy source and purinergic transmitter, is an essential element in the concentration of catecholamines in secretory vesicles. In this way, cells can use ATP to accumulate neurotransmitters and other secreted substances at high concentrations, supporting quantal transmission. PNAS (Proceedings of the National Academy of Sciences) 2016 (May 20, 2016).)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

(Anm: Proteinstrukturen til ATP-syntase kartlagt. Den komplette strukturen til ATP-syntasen viser det molekylære grunnlaget for mitokondrienes morfologi. ATP-syntasene er lokalisert i mitokondriens indre membran. Disse små molekylære maskinene produserer ATP i cellen og er viktige i utviklingen av nevrodegenerative sykdommer. Kjennskap til proteinets tredimensjonale struktur kan gi informasjon om proteinets mekanismer. (…) En slik modell gir verdifull informasjon om funksjon, molekylær virkningsmekanisme, interaksjon og samspill med andre cellulære komponenter, og ikke minst hvordan enkelte kritiske mutasjoner og defekter i proteiner kan gi patologiske fenotyper. Slike modeller kan være viktige verktøy i design av legemidler, sier Dalhus. Tidsskr Nor Legeforen 2016 (20. desember 2016.)

(Anm: Adenosintrifosfat (ATP). Adenosin-5'-trifosfat (ATP, etter det engelske navnet Adenosine triphosphate) er et multifunksjonelt nukleotid som brukes i celler som et koenzym. ATP blir ofte kalt «molekylær valutaenhet» for intracellulær energioverføring.[1] ATP frakter kjemisk energi i cellene for metabolismen. ATP dannes under fotofosforylering og cellulær respirasjon, og brukes av enzymer og strukturelle proteiner i mange cellulære prosesser, herunder biosyntetiske reaksjoner, motilitet og celledeling.[2] Ett ATP-molekyl inneholder tre fosfatgrupper, og det blir produsert fra uorganisk fosfat og adenosindifosfat (ADP) eller adenosinmonofosfat (AMP) ved hjelp av enzymet ATP-syntase. (no.wikipedia.org).)

(Anm: A high-fat diet may alleviate mitochondrial disease. Salk scientists find that dietary fat, coupled with a natural hormone, can relieve metabolic dysfunction associated with mitochondrial disease in mice (salk.edu 30.6.2015).)

- Kalsiumtransport og signalering i mitokondriene. Calcium Transport and Signaling in Mitochondria. (- Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies. Moreover, altered mitochondrial Ca2+ homeostasis has been linked to metabolic diseases like cancer, obesity, and pulmonary hypertension.)

Calcium Transport and Signaling in Mitochondria. (Kalsiumtransport og signalering i mitokondriene.)
Compr Physiol. 2017 Mar 16;7(2):623-634.
Abstract Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies. Moreover, altered mitochondrial Ca2+ homeostasis has been linked to metabolic diseases like cancer, obesity, and pulmonary hypertension. In this review article, we summarize the mechanisms that coordinate mitochondrial and Ca2+ responses and how they affect human health. © 2017 American Physiological Society. Compr Physiol 7:623-634, 2017. (…)

(Anm: Mitochondrial Dysfunction and Neurodegeneration in Lysosomal Storage Disorders. Trends. Abstract Lysosomal storage disorders (LSDs) are rare inherited debilitating and often fatal disorders. Caused by mutations affecting lysosomal proteins, LSDs are characterized by the accumulation of undegraded material in lysosomes and by lysosomal dysfunction. Although LSDs are multisystemic diseases, the majority display neurologic symptoms and neurodegeneration. Only recently has a role emerged for mitochondrial dysfunction in the pathophysiology of LSDs, suggesting an impact of lysosomal dysfunction on mitochondria. Moreover, mitochondrial damage may also cause lysosomal dysfunction, further supporting the activity of common signaling pathways and crosstalk between the two organelles. In this review we explore the mechanisms linking lysosomal and mitochondrial dysfunction to assess whether specific mitochondrial pathways represent a new therapeutic frontier in the management of LSDs. Mol Med. 2017 Jan 19. pii: S1471-4914(16)30188-5. [Epub ahead of print].)

(Anm: Mitochondrial Dysfunction in Lysosomal Storage Disorders. (…) Mitochondrial dysfunction has been reported to occur in numerous cellular and mouse models of GD. The aim of this manuscript is to review the current knowledge and implications of mitochondrial dysfunction in LSDs. Diseases. 2016 Oct 11;4(4). pii: E31.)

(Anm: ER-Mitochondria signaling regulates autophagy. Autophagy. Abstract. The endoplasmic reticulum (ER) and mitochondria form tight functional contacts that regulate a number of key cellular processes. Finally, our studies revealed that the modulatory effects of ER-mitochondria contacts on autophagy involve their role in mediating ITPR (inositol 1,4,5-trisphosphate receptor) delivery of Ca2+ from ER stores to mitochondria. Autophagy. 2017 May 26:0. [Epub ahead of print].)

(Anm: Control of cell death and mitochondrial fission by ERK1/2 MAP Kinase signalling FEBS J. 2017 May 26. doi: 10.1111/febs.14122. [Epub ahead of print].)

(Anm: Anti-aging effects of melatonin on the myocardial mitochondria of rats and associated mechanisms. Mol Med Rep. 2016 Dec 7. doi: 10.3892/mmr.2016.6002. [Epub ahead of print].)

(Anm: Melatonin and alcohol: Are they safe to mix? Though many people assume natural sleep supplements, such as melatonin, are always safe, it is essential for anyone who starts taking a supplement to learn about its use, effectiveness, and how to take it safely. (medicalnewstoday.com 28.9.2017).)

Pathogenic mechanisms of acute pancreatitis (Patogene mekanismer ved akutt pankreatitt)
Curr Opin Gastroenterol. 2012 Sep;28(5):507-15
RECENT FINDINGS: Pathologic intra-acinar trypsinogen activation had been hypothesized to be the central mechanism of pancreatitis for over a century. This hypothesis could be explored for the first time with the development of a novel mouse model lacking pathologic intra-acinar trypsinogen activation. It became clear that intra-acinar trypsinogen activation contributes to early acinar injury, but local and systemic inflammation progress independently during pancreatitis. Early intra-acinar nuclear factor kappa B (NFκB) activation, which occurs parallel to but independent of trypsinogen activation, may be crucial in pancreatitis. Although the mechanism of NFκB and trypsinogen activation is not entirely clear, further insights have been made into key pathogenic cellular events such as calcium signaling, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, autophagy and impaired trafficking, and lysosomal and secretory responses. Cellular intrinsic damage-sensing mechanisms that lead to activation of the inflammatory response aimed at repair, but lead to disease when overwhelmed, are beginning to be understood.

SUMMARY: New findings necessitate a paradigm shift in our understanding of acute pancreatitis. Intra-acinar trypsinogen activation leads to early pancreatic injury, but the inflammatory response of acute pancreatitis develops independently, driven by early activation of inflammatory pathways. (...)

(Anm: Impact of Aging on Calcium Signaling and Membrane Potential in Endothelium of Resistance Arteries: A Role for Mitochondria. (…) We conclude that the ability of resistance artery endothelium to release Ca2+ from intracellular stores (ie, ER and mitochondria) and hyperpolarize Vm via SKCa/IKCa activation is augmented as compensation for reduced NO bioavailability during advanced age. J Gerontol A Biol Sci Med Sci. 2017 May 16. [Epub ahead of print].)

- Dine mitokondrier er hva du spiser: en høyfettdiett eller høysukkerdiett eliminerer metabolsk fleksibilitet i isolerte mitokondrier fra rotteskjelettmuskulatur. (- However, it is not known if these diets alter normal interactions of pyruvate and fatty acid oxidation at the level of the mitochondria.)

Your mitochondria are what you eat: a high-fat or a high-sucrose diet eliminates metabolic flexibility in isolated mitochondria from rat skeletal muscle. (Dine mitokondrier er hva du spiser: en høyfettdiett eller høysukkerdiett eliminerer metabolsk fleksibilitet i isolerte mitokondrier fra rotteskjelettmuskulatur.)
Physiol Rep. 2017 Mar;5(6). pii: e13207.
Abstract Extreme diets consisting of either high fat (HF) or high sucrose (HS) may lead to insulin resistance in skeletal muscle, often associated with mitochondrial dysfunction. However, it is not known if these diets alter normal interactions of pyruvate and fatty acid oxidation at the level of the mitochondria. Here, we report that rat muscle mitochondria does show the normal Randle-type fat-carbohydrate interaction seen in vivo. The mechanism behind this metabolic flexibility at the level of the isolated mitochondria is a regulation of the flux-ratio: pyruvate dehydrogenase (PDH)/β-oxidation to suit the actual substrate availability, with the PDH flux as the major point of regulation. We further report that this regulatory mechanism of carbohydrate-fat metabolic interaction surprisingly is lost in mitochondria obtained from animals exposed for 12 weeks to a HF- or a HS diet as compared to rats given a normal chow diet. The mechanism seems to be a loss of the PDH flux decrease seen in controls, when fatty acid is supplied as substrate in addition to pyruvate, and vice versa for the supply of pyruvate as substrate to mitochondria oxidizing fatty acid. Finally, we report that the calculated TCA flux in the isolated mitochondria under these circumstances shows a significant reduction (~50%) after the HF diet and an even larger reduction (~75%) after the HS diet, compared with the chow group. Thus, it appears that obesogenic diets as those applied here have major influence on key metabolic performance of skeletal muscle mitochondria. (…)

(Anm: False alarm from the body may be responsible for acute pancreatitis (medicalnewstoday.com 9.9.2015).)

(Anm: Pancreatic cancer risk linked to changes in mouth bacteria. The presence of certain bacteria in the mouth may indicate a raised risk for pancreatic cancer - a disease that often begins with no symptoms and for which there is no routine screening test. (…) The researchers suggest the finding may lead to earlier, more precise treatments for pancreatic cancer, a disease with a pitifully low survival rate as it often escapes early diagnosis. (medicalnewstoday.com 20.4.2016).)

(Anm: Pancreatitis often caused by gallstones - also statins increase risk. Idiopathic pancreatitis is often caused by small gallstones that are difficult to observe prior to surgery, shows a study from the University of Eastern Finland. Small gallstones were found in surgery from two out of three idiopathic pancreatitis patients. The study also showed that acute pancreatitis was more common in statin users than non-users. (medicalnewstoday.com 7.12.2015).)

- Hemmet enzymaktivitet ved kronisk utmattelsessyndrom? (- Nivåene av de 20 aminosyrene ble undersøkt med massespektometri, der man fant en spesifikk nedgang av aminosyrer hos kvinner. Disse aminosyrene tilhører en gruppe som brytes ned uavhengig av enzymet pyruvatdehydrogenase (PDH).)

Hemmet enzymaktivitet ved kronisk utmattelsessyndrom?
Tidsskr Nor Legeforen 2017; 137:443 (21.3.2017)
Pasienter med kronisk utmattelsessyndrom har svekket enzymfunksjon relatert til energiomsetningen, ifølge en studie ved Haukeland universitetssykehus.

Tidligere studier har vist at pasienter med kronisk utmattelsessyndrom, ofte kalt ME/CSF, har senket nivå av enkelte aminosyrer i serum. Forskningsmiljøer ved Haukeland universitetssykehus har nylig publisert en studie der serum fra 200 pasienter og 100 kontrollpersoner ble undersøkt (1). Pasientene ble utredet for kronisk utmattelsessyndrom i henhold til de kanadiske kriteriene for sykdommen. Nivåene av de 20 aminosyrene ble undersøkt med massespektometri, der man fant en spesifikk nedgang av aminosyrer hos kvinner. Disse aminosyrene tilhører en gruppe som brytes ned uavhengig av enzymet pyruvatdehydrogenase (PDH). I de hvite blodcellene ble mRNA-nivået for ulike regulerende faktorer for dette enzymet undersøkt, og der fant man oppregulert uttrykk av faktorer som virker hemmende på enzymfunksjonen. Disse endringene var til stede i begge kjønn.

– Funksjonell pyruvatdehydrogenase er en av de viktigste faktorene for velfungerende mitokondrier, sier Zhenhe Suo, førsteamanuensis ved Avdeling for patologi ved Universitetet i Oslo.

– Velfungerende mitokondrier vil sørge for normal funksjon av celler og organer. Funnet av unormal energiomsetning ved kronisk utmattelsessyndrom kan forklare flere av de kliniske metabolske manifestasjonene ved sykdommen, sier Suo.

Funnene støttes også av in vitro-studier der pyruvatdehydrogenase er inaktivert med såkalt knockoutgenteknologi (2). – Når pyruvatdehydrogenase blir inaktivert, blir cellene tvunget til aerob glykoslyse, slik at de produserer mindre energi, men gir overskudd av laktat. Disse studiene har nye funn som fremhever den funksjonen pyruvatdehydrogenase har i sykdomsutviklingen ved kronisk utmattelsessyndrom, sier Suo. (…)

- Mitokondriell kvalitetskontroll ved hjertesykdommer. (- Mitokondrier er viktige organeller for vedlikehold av homeostase ved hjerteinfarkt. De spiller en avgjørende rolle i bioenergi, redoksbalanse, ion homeostase, og celledød.)

Mitochondrial Quality Control in Cardiac Diseases.
Front. Physiol., 21 October 2016
Disruption of mitochondrial homeostasis is a hallmark of cardiac diseases. Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for cardiomyocyte survival. In this review, we discuss the most recent findings on the central role of mitochondrial quality control processes including regulation of mitochondrial redox balance, aldehyde metabolism, proteostasis, dynamics, and clearance in cardiac diseases, highlighting their potential as therapeutic targets. (…)

Summary and Perspectives
Mitochondria are essential organelles for the maintenance of myocardial homeostasis. They play critical role in bioenergetics, redox balance, ion homeostasis, and cell death. The importance of functional mitochondrial to the heart has been highlighted by the fact that situations that lead to mitochondrial dysfunction are often associated with cardiac diseases. Many of these diseases manifest later in life, where mitochondria seems to be less functional. Therefore, different levels of mechanisms of surveillance and quality control capable of detecting and fixing defects that affect mitochondrial performance are critical for the maintenance of long-lived cells with high energy demand such as cardiomyocytes. The central role of mitochondrial quality control in the health of myocardium has been recently reported. As described above, the machinery regulating mitochondrial quality control including mitochondrial redox balance, aldehyde metabolism, proteostasis, dynamics, and clearance are potential novel therapeutic targets for cardiac diseases. However, future research focusing on the critical molecular events involved in mitochondrial quality control is needed to develop better pharmacological interventions. (…)

(Anm: Homeostase, organismens opprettholdelse av konstante og stabile fysikalsk-kjemiske forhold i det væskemiljøet som omgir de enkelte celler, det såkalte «indre miljø». Både surhetsgrad, temperatur, kjemisk sammensetning med mer i det indre miljø er nøye regulert og varierer meget lite over tid, noe cellene er avhengige av for å funksjonere normalt. En rekke organer som for eksempel hjerte, lunger og nyrer bidrar gjennom kontrollerte justeringer av sin virksomhet til homeostasen. Kilde: Store norske leksikon.)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose, til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis- the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.) (medicalnewstoday.com 19.3.2017).)

(Anm: - Kalsiumubalanse i hjerneceller kan utløse Alzheimers sykdom. (- Ingen har noen gang sett på dette før bruken av disse modellsystemene. Det er mulig at endringer i mitokondrienes kalsiumutveksling er driveren av sykdomsprosessen. Tidligere forskning har vist at en overdreven produksjon av kalsium kan føre til at nerveceller dør, derfor linkes en kalsiumubalanse med den nevrodegenerative prosessen involvert i Alzheimers sykdom. (Calcium imbalance within brain cells may trigger Alzheimer's disease.) (medicalnewstoday.com 15.2.2017).)

- Parkinsons er delvis en autoimmun sykdom, ifølge studie. (- Parkinson’s disease-related proteins PINK1 and Parkin repress mitochondrial antigen presentation.)

(Anm: Parkinson’s Is Partly An Autoimmune Disease, Study Finds. First direct evidence that abnormal protein in Parkinson’s disease triggers immune response. New York, NY (June 21, 2017)—Researchers have found the first direct evidence that autoimmunity—in which the immune system attacks the body’s own tissues—plays a role in Parkinson’s disease, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response. The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published today in Nature. “The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology, and pharmacology) at CUMC. “But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson’s, can activate the T cells involved in autoimmune attacks. (cumc.columbia.edu 21.6.2017).)

(Anm: T cells from patients with Parkinson’s disease recognize α-synuclein peptides. Nature 546, 656–661 (29 June 2017).)

(Anm: Parkinson’s disease-related proteins PINK1 and Parkin repress mitochondrial antigen presentation. Cell 166, 314–327 (2016).)

(Anm: Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? Are Mitochondria the Key to Cracking Parkinson’s Disease? European Medical Journal 2017 (Februar 20, 2017).)

- Oppdagelse kan påvirke forståelse, behandling av autoimmune og inflammatoriske sykdommer.

(Anm: Discovery could impact understanding, treatment of autoimmune and inflammatory diseases. Scientists from the Research Institute of the McGill University Health Centre (RI-MUHC) may have cracked the code to understanding the function of special cells called regulatory T Cells. Treg cells, as they are often known, control and regulate our immune system to prevent excessive reactions. The findings, published in Science Immunology, could have a major impact in our understanding and treatment of all autoimmune diseases and most chronic inflammatory diseases such as arthritis, Crohn's disease as well as broader conditions such as asthma, allergies and cancer. Researchers made this discovery by investigating a rare human mutation in a gene called FOXP3. Although the importance of the FOXP3 gene in the proper function of Treg cells has been well documented, its mechanisms were still not fully understood by scientists. (news-medical.net 5.7.2017).)

(Anm: Surprising finding provides more support for Alzheimer's being an autoimmune disease. Brain levels of the lipid ceramide are high in Alzheimer's disease, and now scientists have found increased levels of an antibody to the lipid in their disease model. (medicalnewstoday.com 10.3.2015).)

(Anm: Relationships Between Mitochondria and Neuroinflammation: Implications for Alzheimer's Disease. Curr Top Med Chem. 2015 Aug 26. [Epub ahead of print].)

(Anm: Problems finding your way around may be earliest sign of Alzheimer's disease (medicalnewstoday.com 22.4.2016).)

(Anm: T cell type that promotes damaging immune response discovered. For the first time, researchers have identified a type of T cell that plays a key role in promoting the damaging autoimmune response that inflames and attacks the joints in rheumatoid arthritis. The discovery - made with technologies that help to analyze just a "handful of cells" - offers vital new clues to the biology of the disease and could lead to more powerful, targeted treatments. The study - led by Brigham and Women's Hospital (BWH), a teaching affiliate of Harvard Medical School in Boston, MA - is published in the journal Nature. (medicalnewstoday.com 2.2.2017).)

- Preklinisk studie antyder at Parkinson sykdom kan starte i tarm-endokrine celler. (- Ifølge funnene som er publisert i tidsskriftet JCI Insight hevder forskere og samarbeidspartnere fra University of California, San Francisco, at et stoff i tarmen kan forstyrre alfa-synuclein i endokrine celler i tarmen, og deformere proteinet. Det deformerte eller misfoldede proteinet kan da spre seg via nervesystemet til hjernen som et prion eller infeksjonsprotein, på samme måte som kugalskap.)

(Anm: Pre-clinical study suggests Parkinson's could start in gut endocrine cells. Recent research on Parkinson's disease has focused on the gut-brain connection, examining patients' gut bacteria, and even how severing the vagus nerve connecting the stomach and brain might protect some people from the debilitating disease. But scientists understand little about what's happening in the gut - the ingestion of environmental toxins or germs, perhaps - that leads to brain damage and the hallmarks of Parkinson's such as tremors, stiffness and trouble walking. According to findings published in the journal JCI Insight, Duke researchers and collaborators from the University of California, San Francisco, hypothesize that an agent in the gut might interfere with alpha-synuclein in gut endocrine cells, deforming the protein. The deformed or misfolded protein might then spread via the nervous system to the brain as a prion, or infectious protein, in similar fashion to mad cow disease. (medicalnewstoday.com 19.6.2017).)

(Anm: Two new studies expand understanding of link between PD and gastrointestinal dysfunction. (news-medical.ne 31.7.2017).)

(Anm: Bacterial community in the gut of Parkinson's patients differs from that of healthy people. Parkinson's disease is an insidious disease: by the time it manifests as the typical motor dysfunctions such as tremors or muscle rigidity, portions of the brain have already been irreversibly destroyed. (news-medical.net 29.8.2017).)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Promise and Pitfalls of Mitochondrial Replacement for Prevention and Cure of Heritable Neurodegenerative Diseases Caused by Deleterious Mutations in Mitochondrial DNA. Front. Cell. Neurosci., 23 September 2016.)

(Anm: Mitophagy is the selective degradation of mitochondria by autophagy. (en.wikipedia.org).)

- Brukere av metamfetamin er tre ganger mer utsatt for å få Parkinsons sykdom enn folk som ikke bruker illegale rusmidler

Meth users 'three times more likely' to develop Parkinson's
medicalnewstoday.com 17.12.2014
Users of methamphetamine are at three times more risk for getting Parkinson's disease than people who do not use illegal drugs, according to new research from the University of Utah and Intermountain Healthcare

A previous study that examined nearly 250,000 California hospital discharge records found that meth users had an increased risk for Parkinson's. The new study - published in the journal Drug and Alcohol Dependence - includes both inpatient and outpatient clinic records, and so draws data from a wider sample of the population. (…)

(Anm: Metamfetamin er et syntetisk sentralstimulerende narkotikum. Det har mye av de samme virkningene og ligner kjemisk på amfetamin. (no.wikipedia.org).)

- Metamfetaminbruk knyttet til økt risiko for hjerneslag hos de unge.

(Anm: Methamphetamine use linked to heightened stroke risk in the young. The stimulant methamphetamine, also popularly known as 'speed,' 'ice' and 'meth,' is linked to a heightened risk of stroke among young people, reveals a review of the available evidence, published online in the Journal of Neurology Neurosurgery & Psychiatry. (medicalnewstoday.com 25.8.2017).)

(Anm: Stroke and methamphetamine use in young adults: a review. Neurology Neurosurgery & Psychiatry 2017 published online 23 August 2017.)

(Anm: International study finds meth messes up brains of youths far more than those of adults (medicalnewstoday.com 16.2.2015).)

- Mitokondriell energimangel fører til hyperproliferasjon av skjelettmuskel-mitokondrier og økt insulinfølsomhet. (...) Vi fremlegger bevis på at mitokondrier bidrar til etiologien (sykdomsårsaken) til metabolsk sykdom. (- Diabetes er assosiert med svekket glukosemetabolisme i nærvær av overskudd av insulin.)

Mitochondrial energy deficiency leads to hyperproliferation of skeletal muscle mitochondria and enhanced insulin sensitivity. (Mitokondriell energimangel fører til hyperproliferasjon av skjelettmuskel-mitokondrier og økt insulinfølsomhet.)
Proceedings of the National Academy of Sciences) 2017;114(10):2705–2710
Significance

Mitochondrial dysfunction is associated with type II diabetes and metabolic syndrome, but whether it is cause or consequence is debated. By showing that increased mitochondrial respiration can impart glucose tolerance, insulin sensitivity, and resistance to high fat diet (HFD) toxicity, we provide evidence that mitochondria contributes to the etiology of metabolic disease. Inactivation of adenine nucleotide translocator isoform 1 (ANT1) results in proliferation of partially uncoupled muscle mitochondrial respiration, creating a sink for excess calories. Although ANT1-deficient muscle induces expression of Fgf21, FGF21 level is not elevated in blood, and FGF21 and UCP1 mRNAs are not increased in liver or brown adipose tissue (BAT). If increased mitochondrial respiration prevents HFD toxicity, then decreased mitochondrial respiration may contribute to metabolic disease.

Abstract
Diabetes is associated with impaired glucose metabolism in the presence of excess insulin. Glucose and fatty acids provide reducing equivalents to mitochondria to generate energy, and studies have reported mitochondrial dysfunction in type II diabetes patients. If mitochondrial dysfunction can cause diabetes, then we hypothesized that increased mitochondrial metabolism should render animals resistant to diabetes. This was confirmed in mice in which the heart–muscle–brain adenine nucleotide translocator isoform 1 (ANT1) was inactivated. ANT1-deficient animals are insulin-hypersensitive, glucose-tolerant, and resistant to high fat diet (HFD)-induced toxicity. In ANT1-deficient skeletal muscle, mitochondrial gene expression is induced in association with the hyperproliferation of mitochondria. The ANT1-deficient muscle mitochondria produce excess reactive oxygen species (ROS) and are partially uncoupled. Hence, the muscle respiration under nonphosphorylating conditions is increased. Muscle transcriptome analysis revealed the induction of mitochondrial biogenesis, down-regulation of diabetes-related genes, and increased expression of the genes encoding the myokines FGF21 and GDF15. However, FGF21 was not elevated in serum, and FGF21 and UCP1 mRNAs were not induced in liver or brown adipose tissue (BAT). Hence, increased oxidation of dietary-reducing equivalents by elevated muscle mitochondrial respiration appears to be the mechanism by which ANT1-deficient mice prevent diabetes, demonstrating that the rate of mitochondrial oxidation of calories is important in the etiology of metabolic disease. (…)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

(Anm: Antipsykotika øger diabetes-risiko hos børn. En række forskellige antipsykotika har vist sig at medføre op til tre gange så stor en risiko for at udvikle diabetes, hvis børn og unge behandles med dem. Et studie offentliggjort i tidsskriftet JAMA Psychiatry viser ifølge Dagens Medicin, at børn og unge i behandling med antipsykotiske lægemidler har tre gange så stor en risiko for at udvikle diabetes i forhold til lignende personer, der tager andre psykoaktive præparater. (…) Den forøgede risiko indtraf allerede efter blot et års forbrug, og risikoen var fortsat tilstede i mindst et år, efter deltagerne var stoppet med at tage lægemidlerne. (medwatch.dk 9.9.2013).)

(Anm: Antidepressiva og antipsykotika gir økt risiko for diabetes hos barn og voksne (50 til 700 %) (mintankesmie.no).)

(Anm: Diabetes: Risiko for hjerteinfarkt på grunn av tap av små blodårene rundt hjertet. (Diabetes: Heart attack risk due to loss of small blood vessels around the heart.) (medicalnewstoday.com 24.3.2017).)

(Anm: Orale steroider (glukokortikoider) linket til 10 ganger økt risiko for diabetes. (Oral steriods linked with ten-fold increased risk of diabetes. (pulsetoday.co.uk 5.5.2016).)

(Anm: Bivirkninger (legemiddelinduserte organskader og sykdommer) (mintankesmie.no).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Antidepressiva (SSRI-er) kan utløse sentral fatigue (sentral utmattelse) (mintankesmie.no).)

(Anm: Konklusjoner. Bruk av SSRI var assosiert med vektøkning og forekomst av usunn atferd, inkludert vestlig diett, "sedentarisme" (blir stillesittende/inaktiv) og røyking. (Conclusions SSRIs use was associated with weight gain in the presence of unhealthy behaviours including Western diet, sedentarism and smoking. BMJ Open 2017;7:e016224.)

- Effekter av MPTP på serotonerge nevronale systemer og mitokondrie Complex I aktiviteten i den levende hjernen: En PET-studie på bevisste rhesusaper.

Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys.)
J Nucl Med. 2017 Mar 9. pii: jnumed.116.189159. [Epub ahead of print]
Abstract The objective of the present positron emission tomography (PET) study was to assess the effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on serotonergic neuronal systems and mitochondrial complex-I (MC-I) activity and compare them with those of dopamine in living brains of rhesus monkeys (Macaca mulatta). Methods: A Parkinson's disease (PD) monkey model was prepared by the repeated administration of MPTP. In PET measurements under conscious conditions, 11C-3-amino-4-(2-dimethylaminomethylphenylsulfanyl)-benzonitrile (11C-DASB) for serotonin transporter (SERT), 4-(2'-methoxyphenyl)-1-[2'-(N-2''-pyridinyl)-p-18F-fluorobenzamido]ethylpiperazine (18F-MPPF) for serotonin 1A receptor (5-HT1AR), 11C-N-(3-iodoprop-2E-enyl)-2β-carbomethoxy-3β-(4-methyl-phenyl) nortropane (11C-PE2I) for dopamine transporter (DAT), 6-11C-methyl-m-tyrosin (11C-6MemTyr) for dopamine synthesis, 11C-raclopride for dopamine D2 receptor (D2R), or 2-tert-butyl-4-chrolo-5-{6-[2-(2-18F-fluoroethoxy)-ethoxy]-pyridin-3-ylmethoxy}-2H-pyridazin-3-one (18F-BCPP-EF) for MC-I was intravenously injected into normal and MPTP-treated monkeys. Serotonin and dopamine parameters were calculated using time activity curves in the cerebellum as input functions. The total distribution volume (VT) of 18F-BCPP-EF was assessed using a Logan plot graphical analysis with the metabolite-corrected plasma input function. Results: MPTP-induced diffuse reductions in MC-I activity was observed throughout the brain, except the cerebellum. Significant reductions in presynaptic dopamine parameters, DAT and synthesis, were detected in the striatum and substantia nigra pars compacta (SNc) of MPTP-treated monkeys, whereas no significant differences were observed in postsynaptic D2R binding. SERT binding was reduced by MPTP not only in the striatal regions, but also in the extra-striatal regions. In contrast, 5-HT1AR binding throughout the brain was not affected by MPTP. The degree of reductions in SERT binding correlated with those in MC-I in the cortex. Conclusion: The results obtained by multiparametric PET measurements demonstrated that chronic MPTP treatments induced reductions not only in the dopaminergic system in the nigrostriatal pathway, but also in SERT in the cortical and sub-cortical regions of PD monkey model. These results suggest that the neurotoxicity of MPTP is not exclusive to the nigrostriatal pathway, as predicted from MC-I damage in the extra-striatal regions of the brain. (…)

(Anm: Pasienter behandlet med antipsykotika (nevroleptika) har signifikant senket platelet complex I aktivitet i mitokondrier i likhet med det som er observert ved idiopatisk Parkinsons sykdom. (...) Antipsykotika (nevroleptika) hemmer kompleks I i elektrontransportkjeden. (Neuroleptic medications inhibit complex I of the electron transport chain. (...) Neuroleptic treated patients have significant depression of platelet complex I activity similar to that seen in idiopathic Parkinson’s disease. Complex I inhibition may be associated with the extrapyramidal side effects of these drugs.) Ann Neurol. 1993;33:512-7).)

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: Effekter av MPTP på serotonerge nevronale systemer og mitokondrie Complex I aktiviteten i den levende hjernen: En PET-studie på bevisste rhesusaper. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys.) J Nucl Med. 2017 Mar 9. pii: jnumed.116.189159.)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

(Anm: Mitochondrial damage elicits a TCDD-inducible poly(ADP-ribose) polymerase-mediated antiviral response. PNAS (Proceedings of the National Academy of Sciences) 2017;114(8) (January 6, 2017).)

(Anm: Bruk av annengenerasjons antipsykotiske legemidler øker parametre for metabolsk syndrom. (dgnews.docguide.com 17.3.2016).)

- Studien viser sammenhengen mellom metabolsk syndrom og risiko for kognitive sykdommer.

(Anm: Study shows link between metabolic syndrome and risk of cognitive disorders. A study presented at the European Academy of Neurology Congress in Amsterdam has shown that obesity alone is not a risk factor for cognitive disorders, but commonly associated co-morbidities such as diabetes, high blood pressure, and metabolic disorders are. Dementia diseases in patients who suffer from diabetes are often treated inadequately, a new research paper reveals. It has long been supposed that patients with metabolic syndrome are more likely to suffer from cognitive impairment - and to a greater extent. Reasons are thought to include chronic inflammatory processes which can induce neuroinflammatory and neurodegenerative changes. Whether obese individuals without risk factors such as diabetes mellitus, metabolic disorders and the presence of albumin in the urine have an increased risk of cognitive impairment is still little researched. (news-medical.net 27.6.2017).)

(Anm: Metabolic Syndrome Components Are Associated With Symptomatic Polyneuropathy Independent of Glycemic Status. Diabetes Care 2016 (Published online before print March 10, 2016).)

(Anm: Patients With Polyneuropathy Receive Long-Term Opioid Therapy, No Clear Benefit. CHICAGO -- May 23, 2017 -- Polyneuropathy is associated with an increased likelihood of long-term opioid therapy, but therapy does not appear to improve functional status, according to a study published online by JAMA Neurology. Polyneuropathy is a common painful condition, especially among older patients, which can result in functional impairment. (dgnews.docguide.com 23.5.2017).)

(Anm: Prepsychosis links with elevated metabolic syndrome. MADRID – Untreated people at high risk for developing psychosis also showed an increased prevalence of certain components of metabolic syndrome in data collected from 163 German study participants, a finding that gives new insight into the well-documented but poorly delineated link between schizophrenia and metabolic syndrome. (...) He also suggested prescribing antipsychotic medications that pose the lowest risk for causing further metabolic derangements in patients. (clinicalpsychiatrynews.com.com 2.4.2016).)

(Anm: Joachim Raese, MD. Metabolic syndrome is defined by the aggregation of hypertriglyceridemia, low high-density lipoprotein (HDL) levels, elevated fasting glucose, hypertension, and increased waist circumference. Metabolic syndrome confers an increased risk of developing diabetes and of dying from coronary artery disease. Cardiovascular disease is the leading cause of death among patients with schizophrenia, who have a life expectancy about 20 years shorter than the general population. (…) For a more detailed discussion, I suggest watching a YouTube video that we have prepared. (cmeinstitute.com 27.4.2016).)

(Anm: Video Lecture 8: Metabolic Syndrome Lectures 1 (By Dr. Joachim Raese) (youtube.com).)

- Ny norsk forskning kan gi Parkinson-svar. (- Nå viser ny forskning fra Universitetet i Bergen at Parkinson kan være forårsaket av at mitokondriene – som er cellenes energifabrikker, ikke klarer å tilpasse segaldringsforandringer i hjernen hos dem som utvikler sykdommen.)

Ny norsk forskning kan gi Parkinson-svar
vg.no 25.11.2016
Mer enn ti millioner personer er på verdensbasis rammet av den hyppig forekommende hjernesykdommen, hvorav cirka 6000 av disse er nordmenn.

Nå viser ny forskning fra Universitetet i Bergen at Parkinson kan være forårsaket av at mitokondriene – som er cellenes energifabrikker, ikke klarer å tilpasse seg aldringsforandringer i hjernen hos dem som utvikler sykdommen.

Den ferske studien ble tirsdag publisert i tidsskriftet Nature Communications, og kaster nytt lys over hva som kan være årsaken til at noen personer er mer utsatt til å utvikle Parkinson sykdom enn andre:

De som rammes av Parkinson sykdom har en sviktende biologisk mekanisme i hjernen, som gjør at de ikke blir beskyttet mot aldringsrelaterte skader på mitokondrienes arvestoff. (…)

(Anm: Yoshinori Ohsumi – a deserving winner of the Nobel Prize for physiology or medicine. am delighted that Yoshinori Ohsumi won this year’s Nobel Prize in physiology or medicine. His pioneering work in yeast led to the discovery of genes and biological processes that are needed for autophagy. Autophagy (from the Greek for “self-eating”) is the mechanism by which cells break down and recycle cellular content. Without this vital housekeeping role we’d be more prone to cancer, Parkinson’s and other age-related disorders. (theconversation.com 3.10.2016).)

(Anm: Autophagy (or autophagocytosis) (from the Greek auto-, "self" and phagein, "to eat"), is the natural, destructive mechanism that disassembles, through a regulated process, unnecessary or dysfunctional cellular components.[1] (en.wikipedia.org).)

(Anm: Communications between Mitochondria, the Nucleus, Vacuoles, Peroxisomes, the Endoplasmic Reticulum, the Plasma Membrane, Lipid Droplets, and the Cytosol during Yeast Chronological Aging. Front. Genet., 27 September 2016.)

(Anm: Cancer cell metabolism and mitochondria: nutrient plasticity for TCA cycle fueling. Abstract Warburg's hypothesis that cancer cells take up a lot of glucose in the presence of ambient oxygen but convert pyruvate into lactate due to impaired mitochondrial function led to the misconception that cancer cells rely on glycolysis as their major source of energy. Most recent 13C-based metabolomic studies, including in cancer patients, indicate that cancer cells may also fully oxidize glucose. In addition to glucose-derived pyruvate, lactate, fatty acids and amino acids supply substrates to the TCA cycle to sustain mitochondrial metabolism. Here, we discuss how the metabolic flexibility afforded by these multiple mitochondrial inputs allows cancer cells to adapt according to the availability of the different fuels and the microenvironmental conditions such as hypoxia and acidosis. In particular, we focused on the role of the TCA cycle in interconnecting numerous metabolic routes in order to highlight metabolic vulnerabilities that represent attractive targets for a new generation of anticancer drugs. Biochim Biophys Acta. 2017 Jan 18. pii: S0304-419X(16)30094-4.)

- Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? (- Are Mitochondria the Key to Cracking Parkinson’s Disease?)

- Are Mitochondria the Key to Cracking Parkinson’s Disease? (Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom?)
European Medical Journal 2017 (Februar 20, 2017)
Mitokondriene av dopaminproduserende celler har vært knyttet til Parkinsons sykdom, med forskere som finner at berørte enkeltpersoner har dopaminceller som i hjernen er mindre i stand til å beskytte sitt mitokondrie-DNA mot aldersrelatert skade, sammenlignet med celler i friske individer. Parkinsons sykdom antas å være en kombinasjon av både genetiske og miljømessige faktorer, den nøyaktige kombinasjon av disse varierer sterkt mellom enkeltpersoner. (THE MITOCHONDRIA of dopamine-producing cells have been linked to Parkinson’s disease, with researchers finding that affected individuals have dopamine cells in their brains less able to protect their mitochondrial DNA against age-related damage, compared with cells in healthy individuals. Parkinson’s disease is believed to be a combination of both genetic and environmental factors, the exact combination of which can vary greatly between individuals.)

Som et hjerne- ødeleggende, progressiv sykdom, påvirker Parkinsons hovedsakelig dopaminproduserende neuroner eller nerveceller i en hjernenstruktur som er kjent som substantia nigra; dette fører til at disse cellene svikter og dør og nivåer av dopamin blir dermed utarmet, noe som resulterer i symptomer som begrenset bevegelse, talefeil, og nedsatt balanse. Studieleder Dr Charalampos Tzoulis, Nevrologisk avdeling, Haukeland universitetssykehus og Institutt for klinisk medisin, Universitetet i Bergen, Bergen, Norge, uttalte at disse problemene blir mer fremtredende med alderen, og uttalte at: "Det er kjent at DNA av mitokondriene er skades under aldring, og forårsaker svikt i kraftgeneratorer, mangel på energi, og sykdom." (Dr Tzoulis and his researchers investigated mitochondrial DNA, comparing the brains of patients with Parkinson’s disease and healthy, older individuals. Their findings suggested that the mitochondrial DNA of healthy dopamine-producing cells in the brain was efficiently protected against aging-induced damage. By contrast, the dopamine-producing cells of individuals with Parkinson’s disease could not replenish their DNA as successfully, which led to a gradual loss of healthy DNA within their mitochondria.)

Disse resultatene antyder eksistensen av en viktig mekanisme som normalt ville forsvare hjernen mot aldringsindusert skade. Men personer som lider av Parkinsons sykdom synes å ha feil, en svakere mekanismer, som forårsaker at deres hjerner blir mer sårbare for virkningene av aldring. Dr. Tzoulis mener at denne forskningen har gjort at de selv og andre forskere bedre forstår utviklingen og patogenesen av Parkinsons sykdom. Han konkluderer at: "Det er generelt veldig lite kunnskap om hvilke mekanismer som forårsaker Parkinsons sykdom. Nå er vi et skritt nærmere å forstå disse mekanismene, og vi kan ha et mål for behandlinger." (…) (These results imply the existence of an important mechanism that would normally defend the brain against aging-induced damage. However, individuals that suffer from Parkinson’s disease seem to have malfunctioning, weaker mechanisms, causing their brains to become more vulnerable to the effects of aging. Dr Tzoulis believes that this research has allowed himself and other researchers to better understand the development and pathogenesis of Parkinson’s disease. Concluding, he stated, “There is generally very little knowledge about the mechanisms causing Parkinson’s disease. Now, we are a step closer to understanding these mechanisms and we may have a target to strike at for therapy.”)

(Anm: Defective mitochondrial DNA homeostasis in the substantia nigra in Parkinson disease. Nat Commun. 2016 Nov 22;7:13548.)

- Multippel sklerose – en mitokondriemediert sykdom? (- Mitokondrieskade sekundært til inflammasjon kombinert med økt energikrav sekundært til demyelinisering kan føre til en kronisk energimangel i sentralnervesystemet. Dette kan igjen føre til nevrodegenerasjon.)

Multippel sklerose – en mitokondriemediert sykdom?
Tidsskr Nor Legeforen 2017; 137:284-7(16.2.2017)
BAKGRUNN Mitokondrier spiller en viktig rolle i patogenesen ved ulike nevrodegenerative lidelser, som for eksempel Parkinson sykdom. Nevrodegenerative forandringer forekommer tidlig i forløpet av multippel sklerose (MS). Formålet med denne artikkelen er å presentere kunnskap om mulig sammenheng mellom mitokondriedysfunksjon og multippel sklerose.

KUNNSKAPSGRUNNLAG Artikkelen er basert på original- og oversiktsartikler valgt ut etter et litteratursøk i PubMed, begrenset til engelskspråklige artikler og avsluttet i mai 2016. Litteratursøket resulterte i totalt 2 276 artikler. Etter en skjønnsmessig vurdering ble 71 artikler lest i sin helhet. Av disse ble 19 brukt som referanser. I tillegg plukket vi ut 15 artikler fra referanselistene og syv fra eget litteraturarkiv.

RESULTATER Mitokondrieforandringer er påvist i affiserte hjerneområder hos pasienter med multippel sklerose. Mens noen av forandringene kan skyldes skade på mitokondrier sekundært til inflammasjon, kan andre være kompensatoriske grunnet økt energikrav i aksoner som er rammet av demyelinisering. Type mitokondrieskade varierer og avhenger av utløsende skade.

FORTOLKNING Mitokondrieskade sekundært til inflammasjon kombinert med økt energikrav sekundært til demyelinisering kan føre til en kronisk energimangel i sentralnervesystemet. Dette kan igjen føre til nevrodegenerasjon. Økt kunnskap om mitokondrienes rolle ved multippel sklerose, både sekundært til inflammasjon og eventuelt som et direkte bidrag til nevrodegenerasjon, kan gi bedre forståelse for patogenesen ved sykdommen og kanskje bidra til nye behandlingsmuligheter. (…)

(Anm: Powering the Cell: Mitochondria (ed.ted.com).)

(Anm: Cellular Respiration and the Mighty Mitochondria (ed.ted.com).)

(Anm: Dr. Terry Wahls - Minding Your Mitochondria - TED - Documentary, Lecture, Talk NUTRITION (youtube.com 16.4.2017).)

- Lundbeck i millionsamarbejde med big pharma om hjernesygdomme. (- Med i alliancen er blandt andet danske Lundbeck, der sammen med en række spillere fra big pharma som eksempelvis Novartis, Eli Lilly og AbbVie nu skal forsøge at løse gåden om de komplicerede hjernesygdomme Alzheimers og Parkinsons sygdom. Det skriver Berlingske.) (- Fokus har meget været på at fjerne proteinerne, når de ikke er i cellerne. Her prøver vi at se, om vi kan fjerne dem, når de er inde i cellerne.)

Lundbeck i millionsamarbejde med big pharma om hjernesygdomme.
medwatch 10.4.2017
Danske Lundbeck har indgået en stor international forskningsaftale med en række topuniversiteter og konkurrenter fra big pharma om at løse gåden om Alzheimers og Parkinsons sygdom.

Et nyt europæisk hjernesamarbejde har set dagens lys. Med i alliancen er blandt andet danske Lundbeck, der sammen med en række spillere fra big pharma som eksempelvis Novartis, Eli Lilly og AbbVie nu skal forsøge at løse gåden om de komplicerede hjernesygdomme Alzheimers og Parkinsons sygdom. Det skriver Berlingske.

Også de to eliteuniversiteter Cambridge og Oxford samt danske Aarhus Universitet er ed i samarbejdet. Formålet med samarbejdet er at finde en metode til at stoppe spredningen af de proteiner - såkaldte toksiske proteiner - der ødelægger hjernecellerne.

"Fokus har meget været på at fjerne proteinerne, når de ikke er i cellerne. Her prøver vi at se, om vi kan fjerne dem, når de er inde i cellerne. Det handler om at få styrket de mekanismer, som nedbryder de toksiske proteiner, så de ikke spreder sig til hele cellen, som dermed dør," siger Jan Egebjerg, underdirektør i Lundbecks afdeling for forskning i neurodegeneration, til Berlingske.

De enkelte virksomheder kan efter projektets afslutning gå videre med udvikling af en egentlig lægemiddelkandidat, hvis der skulle være dukket lovende forskning op undervejs.

Forskningsprojektet er sat til at løbe i fire år med et budget på godt 80 mio. kr. Samarbejdet er støttet af EU med 35 mio. kr. (...)

- Kalsiumubalanse i hjerneceller kan utløse Alzheimers sykdom. (- Ingen har noen gang sett på dette før bruken av disse modellsystemene. Det er mulig at endringer i mitokondrienes kalsiumutveksling er driveren av sykdomsprosessen.)

Calcium imbalance within brain cells may trigger Alzheimer's disease (Kalsium ubalanse i hjerneceller kan utløse Alzheimers sykdom)
medicalnewstoday.com 15.2.2017
Mitokondrier - noen ganger referert til som "cellenes kraftverk" - er små strukturer som omdanner energien fra mat til celledrivstoff. (Mitochondria - sometimes referred to as the "powerhouse of the cell" - are small structures that transform energy from food into cell "fuel.")

I mitokondriene hos en hjernecelle kontrollerer kalsiumioner hvor mye energi som produseres av hjernen for å få hjernen til å fungere. Tidligere forskning har vist at en overdreven produksjon av kalsium kan føre til at nerveceller dør, derfor linkes en kalsiumubalanse med den nevrodegenerative prosessen involvert i Alzheimers sykdom. (In the mitochondria of a brain cell, calcium ions control how much energy is produced for the brain to function. Previous research has shown that an excessive production of calcium can cause neurons to die, therefore linking a calcium imbalance with the neurodegenerative process involved in Alzheimer's disease.)

Until now, however, the exact mechanism that links Alzheimer's-related neurodegeneration and mitochondrial calcium imbalance was unknown. The new research - led by Pooja Jadiya, a postdoctoral fellow at Temple University in Philadelphia, PA - sheds light on this association.

The study was carried out by researchers from the Center for Translational Medicine at Temple University, and the findings were presented at the 61st Meeting of the Biophysical Society in New Orleans, LA. (…)

"Ingen har noen gang sett på dette før bruken av disse modellsystemene. Det er mulig at endringer i mitokondrienes kalsiumutveksling er driveren av sykdomsprosessen." (...) ("No one has ever looked at this before using these model systems. It is possible that alterations in mitochondrial calcium exchange may be driving the disease process.")

"Our hope is that if we can change either the expression level or the activity of this exchanger, it could be a viable therapy to use early on to perhaps impede Alzheimer's disease development - that is the home run," Elrod says. "We are not even close to that, but that would be the idea."

Learn how scientists can stop and reverse Alzheimer's-related brain damage in mice. (…)

(Anm: Study unravels mystery of how nerve cells are damaged in neurodegenerative diseases. A new study has uncovered a molecular mechanism in the prion protein, a protein responsible for neurodegenerative diseases, which may explain why nerve cells degenerate in these disorders. The findings, which appear in the journal eLife, may one day lead to better therapies and treatments for these diseases. (…) Prion diseases are part of larger group of human neurodegenerative disorders, including Alzheimer's, Parkinson's and Huntington's diseases, which are all due to the abnormal accumulation of protein aggregates in the brain. (…) The researchers hope their study will lead to better therapies for neurodegenerative disorders, as well as help clinicians avoid the possible dangerous side-effects of using anti-prion protein antibodies for therapeutic purposes. (news-medical.net 25.5.2017).)

(Anm: Study unravels mystery of how nerve cells are damaged in neurodegenerative diseases. A new study has uncovered a molecular mechanism in the prion protein, a protein responsible for neurodegenerative diseases, which may explain why nerve cells degenerate in these disorders. The findings, which appear in the journal eLife, may one day lead to better therapies and treatments for these diseases. (…) Prion diseases are part of larger group of human neurodegenerative disorders, including Alzheimer's, Parkinson's and Huntington's diseases, which are all due to the abnormal accumulation of protein aggregates in the brain. (…) The researchers hope their study will lead to better therapies for neurodegenerative disorders, as well as help clinicians avoid the possible dangerous side-effects of using anti-prion protein antibodies for therapeutic purposes. (news-medical.net 25.5.2017).)

- Miljøets betydning ved multippel sklerose

Miljøets betydning ved multippel sklerose
Tidsskr Nor Legeforen 2015; 135:856-60 (16.2.2017)
BAKGRUNN Epidemiologiske studier tyder på at miljøfaktorer spiller en betydelig rolle for utviklingen av multippel sklerose. Vi gir her en oppdatering om miljøets betydning for sykdomsrisiko og sykdomsforløp.

KUNNSKAPSGRUNNLAG Vi har gjort litteratursøk i PubMed med søkeordet «multiple sclerosis» kombinert med «environment» samt aktuelle miljøfaktorer.

RESULTATER Det er overveiende sannsynlig at et samspill mellom genetiske og miljømessige faktorer avgjør hvem som utvikler multippel sklerose. Epstein-Barr-virusinfeksjon, røyking og lave nivåer av vitamin D er de miljøfaktorene som har vist sterkest og mest konsistent assosiasjon med utvikling av sykdommen. Lavt vitamin D-nivå er også forbundet med høy sykdomsaktivitet. Andre aktuelle risikofaktorer er overvekt og høyt saltinntak.

FORTOLKNING Selv om man i epidemiologiske studier har identifisert en rekke potensielle etiologiske miljøfaktorer og betydningen av disse støttes av eksperimentelle studier, er det fortsatt ikke tilstrekkelige holdepunkter for å fastslå at de spiller en kausal rolle.

Forekomsten av multippel sklerose er økende, og det er beregnet at om lag 10 000 mennesker i Norge har sykdommen (1). Multippel sklerose reduserer livslengden med 5 – 10 år og er en hyppig årsak til nevrologisk invaliditet. Til tross for bedret behandling er det derfor fortsatt behov for kunnskap som kan bidra til å forebygge sykdommen.

Forskning innen epidemiologi, genetikk og immunologi har gitt økt innsikt i hvilke faktorer som kan forårsake multippel sklerose. Målet med denne artikkelen er å drøfte miljøets betydning for sykdomsrisiko og sykdomsprogrediering. (…)

(Anm: Miljø og helse (mintankesmie.no).)

(Anm: Powering the Cell: Mitochondria (ed.ted.com).)

(Anm: Cellular Respiration and the Mighty Mitochondria (ed.ted.com).)

(Anm: Dr. Terry Wahls - Minding Your Mitochondria - TED - Documentary, Lecture, Talk NUTRITION (youtube.com 16.4.2017).)

- Mitokondriell dysfunksjon bidrar til "Hypertensive Target Organ Damage»: Lærdom fra en dyremodell for sykdom hos mennesker.

Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease.
Oxid Med Cell Longev. 2016;2016:1067801. Epub 2016 Aug 9.
Abstract Mechanisms underlying hypertensive target organ damage (TOD) are not completely understood. The pathophysiological role of mitochondrial oxidative stress, resulting from mitochondrial dysfunction, in development of TOD is unclear. The stroke-prone spontaneously hypertensive rat (SHRSP) is a suitable model of human hypertension and of its vascular consequences. Pathogenesis of TOD in SHRSP is multifactorial, being determined by high blood pressure levels, high salt/low potassium diet, and genetic factors. Accumulating evidence points to a key role of mitochondrial dysfunction in increased susceptibility to TOD development of SHRSP. Mitochondrial abnormalities were described in both heart and brain of SHRSP. Pharmacological compounds able to protect mitochondrial function exerted a significant protective effect on TOD development, independently of blood pressure levels. Through our research efforts, we discovered that two genes encoding mitochondrial proteins, one (Ndufc2) involved in OXPHOS complex I assembly and activity and the second one (UCP2) involved in clearance of mitochondrial ROS, are responsible, when dysregulated, for vascular damage in SHRSP. The suitability of SHRSP as a model of human disease represents a promising background for future translation of the experimental findings to human hypertension. Novel therapeutic strategies toward mitochondrial molecular targets may become a valuable tool for prevention and treatment of TOD in human hypertension. (…)

(Anm: Powering the Cell: Mitochondria (ed.ted.com).)

(Anm: Cellular Respiration and the Mighty Mitochondria (ed.ted.com).)

(Anm: Dr. Terry Wahls - Minding Your Mitochondria - TED - Documentary, Lecture, Talk NUTRITION (youtube.com 16.4.2017).)

- Antibiotika kan utløse mitokondriell dysfunksjon som induserer psykiatriske lidelser.

Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders.
Med Sci Monit. 2017 Jan 7;23:101-106.
Abstract Clinical usage of several classes of antibiotics is associated with moderate to severe side effects due to the promotion of mitochondrial dysfunction. We contend that this may be due to perturbation of unique evolutionary relationships that link selective biochemical and molecular aspects of mitochondrial biology to conserved enzymatic processes derived from bacterial progenitors. Operationally, stereo-selective conformational matching between mitochondrial respiratory complexes, cytosolic and nuclear signaling complexes appears to support the conservation of a critically important set of chemical messengers required for existential regulation of homeostatic cellular processes. Accordingly, perturbation of normative mitochondrial function by select classes of antibiotics is certainly reflective of the high degree of evolutionary pressure designed to maintain ongoing bidirectional signaling processes between cellular compartments. These issues are of critical importance in evaluating potentially severe side effects of antibiotics on complex behavioral functions mediated by CNS neuronal groups. The CNS is extremely dependent on delivery of molecular oxygen for maintaining a required level of metabolic activity, as reflected by the high concentration of neuronal mitochondria. Thus, it is not surprising to find several distinct behavioral abnormalities conforming to established psychiatric criteria that are associated with antibiotic usage in humans. The manifestation of acute and/or chronic psychiatric conditions following antibiotic usage may provide unique insights into key etiological factors of major psychiatric syndromes that involve rundown of cellular bioenergetics via mitochondrial dysfunction. Thus, a potential window of opportunity exists for development of novel therapeutic agents targeting diminished mitochondrial function as a factor in severe behavioral disorders. (…)

(Anm: Mitochondrial dysfunction-a link between antibiotic use and increased risk of severe mental disorders? Acta Psychiatr Scand. 2017 Mar 23.)

- Ny studie knytter autisme mutasjoner i mitokondrie-DNA

New study links autism to mutations in mitochondrial DNA
medicalnewstoday.com 31.10.2016
Autism is a developmental disorder affecting over 3.5 million Americans. While there is no known cure for it, there are options for treating some of its associated symptoms. A new study by a team of researchers at Cornell University has found a connection between autism and mutations in mitochondrial DNA. This could eventually lead to developing new and more effective types of treatment. (…)

(Anm: A cannabinoid link between mitochondria and memory. Cellular activity in the brain depends on the high energetic support provided by mitochondria, the cell organelles which use energy sources to generate ATP. Acute cannabinoid intoxication induces amnesia in humans and animals, and the activation of type-1 cannabinoid receptors present at brain mitochondria membranes (mtCB1) can directly alter mitochondrial energetic activity. (…) By directly linking mitochondrial activity to memory formation, these data reveal that bioenergetic processes are primary acute regulators of cognitive functions. Nature. 2016 Nov 9. [Epub ahead of print].)

(Anm: Fakta: Nobelprismodtagere har reddet millioner af liv. Japansk cellebiolog modtager årets nobelpris i medicin. Tidligere modtagere står bag livreddende forskning. (jyllands-posten.dk 3.10.2016).)

(Anm: Mitochondrial Changes in Cancer. (…) This chapter summarizes various changes in mitochondria in relevance to cancer, behavior of mitochondria during tumorigenesis, and the progress on using mitochondria as a therapeutic target for cancer. Handb Exp Pharmacol. 2016 Oct 8. [Epub ahead of print].)

(Anm: Researchers discover a new regulator of mitochondria in invasive cancer growth. Cancer cells' ability to invade and spread is what makes them deadly. In a recent study published in the journal Current Biology, Texas A&M College of Medicine researchers demonstrate that mitochondria, the so-called powerhouses of the cell, play a crucial role in a tumor's ability to grow. With a better understanding of how this process is regulated, new targets for cancer treatments could be identified. (medicalnewstoday.com 28.11.2016).)

(Anm: Kan barneautisme komme av stoffskiftefeil? Det interessante er hvordan Raugland arbeidet for å hjelpe Tim. Forfatteren forteller om de utradisjonelle analysene hun har benyttet seg av: antistoffprøver mot enkelte matvarer, fettsyrebalanse, inflammasjonspanel for eventuell immunologisk dysfunksjon, cøliakiutredning, gentest for eventuelle enzymfeil i stoffskiftet, forhøyede peptider i urin, avføringsanalyse, håranalyse og ortomolekylær utredning. Sentralt er metyleringsreaksjonene. Hans genfeil i stoffskiftet ble omgått ved «genetisk bypass» ved kosttilskudd. Dette behandlingsopplegget kaller hun «Tim-modellen». Forfatteren presiserer at diett og kosttilskudd er individuelt. Tidsskr Nor Legeforen 2017; 137:557 (30.4.2017).)

(Anm: On mitochondrial metabolism in tumor biology. (…) Therapeutic targeting of cancer cell mitochondria remains experimental but promising, and more predictive markers will be needed for metabolism-based treatments and personalized medicine.Curr Opin Oncol. 2016 Oct 26. [Epub ahead of print].)

(Anm: Regulators of mitochondrial dynamics in cancer. (…) This review focuses on key regulators of mitochondrial dynamics and their role in cancer. Curr Opin Cell Biol. 2016 Apr;39:43-52.)

(Anm: Signaler fra tarmens mikrobiotika til fjerntliggende organer mht. fysiologi og sykdom. Signals from the gut microbiota to distant organs in physiology and disease. (Nat Med. 2016 Oct 6;22(10):1079-1089.)

(Anm: Mitochondrial Neurogastrointestinal Encephalomyopathy Caused by Thymidine Phosphorylase Enzyme Deficiency: From Pathogenesis to Emerging Therapeutic Options. Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a progressive metabolic disorder caused by thymidine phosphorylase (TP) enzyme deficiency. The lack of TP results in systemic accumulation of deoxyribonucleosides thymidine (dThd) and deoxyuridine (dUrd). In these patients, clinical features include mental regression, ophthalmoplegia, and fatal gastrointestinal complications. Front. Cell. Neurosci., 15 February 2017.)

- Endrede mitokondrier assosiert med økt autisme risiko. Mitokondrier, de små strukturer i cellene våre som genererer energi, kan spille en nøkkelrolle i autisme spektrumforstyrrelser (ASD).

(Anm: Altered mitochondria associated with increased autism risk. Mitochondria, the tiny structures inside our cells that generate energy, may play a key role in autism spectrum disorders (ASD). A provocative new study by Children's Hospital of Philadelphia (CHOP)'s pioneering mitochondrial medicine team suggests that variations in mitochondrial DNA (mtDNA) originating during ancient human migrations may play an important role in predisposition to ASDs. "Our findings show that differences in mitochondrial function are important in ASD," said study leader Douglas C. Wallace, PhD, director of the Center for Mitochondrial and Epigenomic Medicine at CHOP. "Our team demonstrates that a person's vulnerability to ASD varies according to their ancient mitochondrial lineage." Wallace and colleagues, including Dimitra Chalkia, Larry Singh and others, published their findings in JAMA Psychiatry. (…) Mitochondria contain their own DNA, distinct from the more familiar nuclear DNA (nDNA) inside the cell nucleus. The mtDNA codes for essential genes governing cellular energy production, and those genes exchange biological signals with nDNA to affect our physiology and overall health. (medicalnewstoday.com 14.2.2015).)
(Anm: Association Between Mitochondrial DNA Haplogroup Variation and Autism Spectrum Disorders. JAMA Psychiatry 2017 (published online 23 August 2017.).)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

- Forandrede mitokondrier assosiert med økt autismerisiko.

(Anm: Altered Mitochondria Associated with Increased Autism Risk. CHOP Scientist: Ancient Mitochondrial DNA Genetic Patterns May Play Role in this Neurodevelopmental Condition. PHILADELPHIA, Aug. 23, 2017 /PRNewswire-USNewswire/ -- Mitochondria, the tiny structures inside our cells that generate energy, may play a key role in autism spectrum disorders (ASDs). A provocative new study by Children's Hospital of Philadelphia (CHOP)'s pioneering mitochondrial medicine team suggests that variations in mitochondrial DNA (mtDNA) originating during ancient human migrations may play an important role in predisposition to ASDs. (prnewswire.com 30.8.2017).)

- Mitokondrielle funksjoner modulerer nevroendokrine, metabolske, inflammatoriske og transkripsjonelle responser på akutt psykologisk stress.

(Anm: Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress. Abstract The experience of psychological stress triggers neuroendocrine, inflammatory, metabolic, and transcriptional perturbations that ultimately predispose to disease. However, the subcellular determinants of this integrated, multisystemic stress response have not been defined. Central to stress adaptation is cellular energetics, involving mitochondrial energy production and oxidative stress. We therefore hypothesized that abnormal mitochondrial functions would differentially modulate the organism's multisystemic response to psychological stress. By mutating or deleting mitochondrial genes encoded in the mtDNA [NADH dehydrogenase 6 (ND6) and cytochrome c oxidase subunit I (COI)] or nuclear DNA [adenine nucleotide translocator 1 (ANT1) and nicotinamide nucleotide transhydrogenase (NNT)], we selectively impaired mitochondrial respiratory chain function, energy exchange, and mitochondrial redox balance in mice. The resulting impact on physiological reactivity and recovery from restraint stress were then characterized. We show that mitochondrial dysfunctions altered the hypothalamic-pituitary-adrenal axis, sympathetic adrenal-medullary activation and catecholamine levels, the inflammatory cytokine IL-6, circulating metabolites, and hippocampal gene expression responses to stress. Each mitochondrial defect generated a distinct whole-body stress-response signature. These results demonstrate the role of mitochondrial energetics and redox balance as modulators of key pathophysiological perturbations previously linked to disease. This work establishes mitochondria as stress-response modulators, with implications for understanding the mechanisms of stress pathophysiology and mitochondrial diseases. Proc Natl Acad Sci U S A. 2015 Dec 1;112(48):E6614-23.)

(Anm: Hjernen (mintankesmie.no).)

- Tarmbakterier og hjernen: Er vi styrt av mikrober?

(Anm: Tarmbakterier og hjernen: Er vi styrt av mikrober? (Gut bacteria and the brain: Are we controlled by microbes? Although the interaction between our brain and gut has been studied for years, its complexities run deeper than initially thought. It seems that our minds are, in some part, controlled by the bacteria in our bowels. (…) On the other side of the fence, recent research infers that dysregulation of gut bacteria might be an important factor in inflammatory and autoimmune conditions. The microbiome's role in health and disease is only slowly giving up its secrets. The latest and perhaps most remarkable finding is the ability that gut bacteria have to moderate our brain and behavior.) (medicalnewstoday.com 7.9.2016).)

- Har Mitokondrier et immunsystem?

(Anm: Do Mitochondria Have an Immune System? Abstract The question if mitochondria have some kind of immune system is not trivial. The basis for raising this question is the fact that bacteria, which are progenitors of mitochondria, do have an immune system. The CRISPR system in bacteria based on the principle of RNA interference serves as an organized mechanism for destroying alien nucleic acids, primarily those of viral origin. We have shown that mitochondria are also a target for viral attacks, probably due to a related organization of genomes in these organelles and bacteria. Bioinformatic analysis performed in this study has not given a clear answer if there is a CRISPR-like immune system in mitochondria. However, this does not preclude the possibility of mitochondrial immunity that can be difficult to decipher or that is based on some principles other than those of CRISPR. Biochemistry (Mosc). 2016 Oct;81(10):1229-1236.)

(Anm: Signaler fra tarmens mikrobiotika til fjerntliggende organer mht. fysiologi og sykdom. Signals from the gut microbiota to distant organs in physiology and disease. (Nat Med. 2016 Oct 6;22(10):1079-1089.)

- Rebalansering av mikrobiom i tarmer forlenger overlevelsen i ALS-musemodell. (- Mekanismen for virkningen til butyrat er relatert til fremming av energiforbruk og induksjon av mitokondriefunksjon.)

Rebalancing gut microbiome lengthens survival in mouse model of ALS
medicalnewstoday.com 31.2.2017
sclerosis, or ALS - a progressive, neurodegenerative disease.

Researchers at the University of Illinois at Chicago College of Medicine report that in a mouse model of ALS, the compound butyrate helped correct a gut microbiome imbalance and reduced gut leakiness - both symptoms of ALS. The treated mice lived also longer compared to mice that weren't given butyrate.

The finding is reported in Clinical Therapeutics.

ALS, also known as Lou Gehrig's disease, slowly destroys the motor neurons that control movement. Patients gradually lose the ability to walk, speak and swallow - and eventually, to breathe. Conventional treatments include physical therapy and medications, but researchers have recently started looking to the gut as a new target for intervention.

"The brain and the gut are linked, so it's not too surprising that the health of the gut can impact the functioning of neurons," says Jun Sun, associate professor of gastroenterology and hepatology at UIC and corresponding author of the paper. In March, she and her coworkers were the first to identify a gut component to ALS progression.

The gut microbiome - the myriad bacteria, viruses and other microbes that make the gut their home - when in balance, helps maintain health, starting with the gut lining. Leaky gut in ALS may lead to increased inflammation. Reducing this gut-associated inflammation has been a goal of clinicians and researchers, and rebalancing the gut microbiome has shown promise in small-animal studies.

Sun and her colleagues studied transgenic mice that were engineered to carry human genes known to contribute to certain forms of ALS. The mice were found to have an abnormal microbiome, along with damaged junctions between the cells of the intestinal lining. Poorly functioning junctions can cause the tissue to become leaky, and have been found to be associated with the onset of ALS in humans. (…)

Mekanismen for virkningen til butyrat er relatert til fremming av energiforbruk og induksjon av mitokondriefunksjon. (...) (The mechanism of butyrate action is related to promotion of energy expenditure and induction of mitochondrial function.)

(Anm: Butyrate (also known as butanoate) is the traditional name for the conjugate base of butyric acid (also known as butanoic acid). The formula of the butyrate ion is C4H7O2−. The name is used as part of the name of esters and salts of butyric acid, a short chain fatty acid. (en.wikipedia.org).)

(Anm: Potential beneficial effects of butyrate in intestinal and extraintestinal diseases. Abstract The multiple beneficial effects on human health of the short-chain fatty acid butyrate, synthesized from non-absorbed carbohydrate by colonic microbiota, are well documented. At the intestinal level, butyrate plays a regulatory role on the transepithelial fluid transport, ameliorates mucosal inflammation and oxidative status, reinforces the epithelial defense barrier, and modulates visceral sensitivity and intestinal motility. In addition, a growing number of studies have stressed the role of butyrate in the prevention and inhibition of colorectal cancer. (…) These data suggest a wide spectrum of positive effects exerted by butyrate, with a high potential for a therapeutic use in human medicine. World J Gastroenterol. 2011 Mar 28; 17(12): 1519–1528.)

- Mitochondrial Respiratory Chain Dysfunction in Muscle From Patients With Amyotrophic Lateral Sclerosis (ALS) (- In 7 patients, the oxidative defect was severe enough to support the hypothesis that mitochondrial dysfunction must play a role in the pathogenesis of the disease.)

Mitochondrial Respiratory Chain Dysfunction in Muscle From Patients With Amyotrophic Lateral Sclerosis
Arch Neurol. 2010;67(7):849-854 (July)
Background Amyotrophic lateral sclerosis (ALS) is a major cause of neurological disability and its pathogenesis remains elusive despite a multitude of studies. Although defects of the mitochondrial respiratory chain have been described in several ALS patients, their pathogenic significance is unclear.

Objective To review systematically the muscle biopsy specimens from patients with typical sporadic ALS to search for possible mitochondrial oxidative impairment. (...)

Conclusions Our data confirm that the histochemical finding of COX-negative fibers is common in skeletal muscle from patients with sporadic ALS. We did not find a correlation between severity of the oxidative defect and age of the patients or duration of the disease. However, the only patient who underwent a second muscle biopsy did show a correlation between severity of symptoms and worsening of the respiratory chain defect. In 7 patients, the oxidative defect was severe enough to support the hypothesis that mitochondrial dysfunction must play a role in the pathogenesis of the disease. (...)

(Anm: Mitochondrial dysfunction in blood cells from amyotrophic lateral sclerosis patients. J Neurol. 2015 Apr 18. [Epub ahead of print].)

- Mitokondrierens rolle i ALS (amyotrofisk lateral sklerose).

(Anm: The Role of Mitochondria in Amyotrophic Lateral Sclerosis. Mitochondria are unique organelles that are essential for a variety of cellular processes including energy metabolism, calcium homeostasis, lipid biosynthesis, and apoptosis. Mitochondrial dysfunction is a prevalent feature of many neurodegenerative diseases including motor neuron disorders such as amyotrophic lateral sclerosis (ALS). Disruption of mitochondrial structure, dynamics, bioenergetics and calcium buffering has been extensively reported in ALS patients and model systems and has been suggested to be directly involved in disease pathogenesis. Here we review the alterations in mitochondrial parameters in ALS and examine the common pathways to dysfunction. Neurosci Lett. 2017 Jun 29. pii: S0304-3940(17)30544-X. [Epub ahead of print].)

- Aspirin øker mitokondriell fettsyreoksidasjon. (- These studies provide insight into the pathophysiology of Reye Syndrome, which is known to be triggered by aspirin ingestion in patients with fatty acid oxidation disorders.)

Aspirin increases mitochondrial fatty acid oxidation.
Biochem Biophys Res Commun. 2016 Nov 14. pii: S0006-291X(16)31922-2. [Epub ahead of print]
Abstract The metabolic effects of salicylates are poorly understood. This study investigated the effects of aspirin on fatty acid oxidation. Aspirin increased mitochondrial long-chain fatty acid oxidation, but inhibited peroxisomal fatty acid oxidation, in two different cell lines. Aspirin increased mitochondrial protein acetylation and was found to be a stronger acetylating agent in vitro than acetyl-CoA. However, aspirin-induced acetylation did not alter the activity of fatty acid oxidation proteins, and knocking out the mitochondrial deacetylase SIRT3 did not affect the induction of long-chain fatty acid oxidation by aspirin. Aspirin did not change oxidation of medium-chain fatty acids, which can freely traverse the mitochondrial membrane. Together, these data indicate that aspirin does not directly alter mitochondrial matrix fatty acid oxidation enzymes, but most likely exerts its effects at the level of long-chain fatty acid transport into mitochondria. The drive on mitochondrial fatty acid oxidation may be a compensatory response to altered mitochondrial morphology and inhibited electron transport chain function, both of which were observed after 24 h incubation of cells with aspirin. These studies provide insight into the pathophysiology of Reye Syndrome, which is known to be triggered by aspirin ingestion in patients with fatty acid oxidation disorders. (…)

(Anm: Hva er Reyes syndrom? Reyes syndrom er en svært sjelden men alvorlig tilstand, som man mener kan utløses når et barn med virusinfeksjon og feber behandles med acetylsalisylsyre (albyl/globoid). Det typiske forløpet er at man kort tid etter at virusinfeksjonen er over på ny blir syk med forandret bevissthet, etter hvert kramper, bevisstløshet og i mange tilfeller død. Magesmerter og oppkast er også vanlig. Symptomene skyldes alvorlig betennelse i hjerne og lever. Dette er også årsaken til at helsemyndigheter advarer mot bruk av acetylsalisylsyre ved feber hos barn. (nhi.no 28.1.2014).)

- Bupropion (Zyban) er et mye foreskrevet antidepressiva / røykesluttpille. Imidlertid er hepatotoksisitet (levertoksisitet) en av dets bivirkninger som er rapportert hos enkelte brukere.

Mechanistic Approach for Toxic Effects of Bupropion in Primary Rat Hepatocytes.
Drug Res (Stuttg). 2017 Jan 24. doi: 10.1055/s-0042-123034. [Epub ahead of print]
Abstract Bupropion is a widely prescribed antidepressant/smoke cessation drug. However, hepatotoxicity is one of its side effects reported in some recipients. The mechanisms by which bupropion induces hepatotoxicity is not clear yet. This experiment was intended to assess the cytotoxic mechanisms of bupropion toward primary rat hepatocytes. Additionally, the effect of α-tocopherol succinate (ALPHA-TOS) and N-acetyl cysteine (NAC) and mitochondrial permeability transition (MPT) pore sealing agent cyclosporine A (Cs A) on this toxicity was investigated. Cell death, LDH leakage, reactive oxygen species (ROS) generation, lipid peroxidation (LPO), and mitochondrial depolarization were examined as toxicity indicators. Results revealed that bupropion led to a surge in ROS formation, depletion of intracellular glutathione, elevation of LPO, and mitochondrial collapse. ALPHA-TOS, NAC and Cs A administration diminished the intensity of cellular damage caused by bupropion. This experiment suggests the protective role of ALPHA-TOS, NAC and Cs A against bupropion-mediated cytotoxicity possibly through their reactive radical scavenging properties and their impacts on mitochondria. Furthermore, mitochondria might be contributed to the oxidative stress response and subsequent toxicological results observed by bupropion. (…)

(Anm: Cytotoksisk, om et stoff eller påvirkning som skader en celle, eventuelt så alvorlig at cellen dør (i noen tilfeller ved at cellen løses opp; cytolyse). Kilde: Store norske leksikon.)

(Anm: Cytotoxicity is the quality of being toxic to cells. Examples of toxic agents are an immune cell or some types of venom, e.g. from the puff adder (Bitis arietans) or brown recluse spider (Loxosceles reclusa). (en.wikipedia.org).)

- En hurtig mitokondriell toksisitetsanalyse ved anvendelse av skiftende celleenergimetabolisme.

A rapid mitochondrial toxicity assay utilizing rapidly changing cell energy metabolism.
J Toxicol Sci. 2017;42(3):349-358. doi: 10.2131/jts.42.349.
Abstract Drug-induced liver injury is a major cause of safety-related drug-marketing withdrawals. Several drugs have been reported to disrupt mitochondrial function, resulting in hepatotoxicity. The development of a simple and effective in vitro assay to identify the potential for mitochondrial toxicity is thus desired to minimize the risk of causing hepatotoxicity and subsequent drug withdrawal. An in vitro test method called the "glucose-galactose" assay is often used in drug development but requires prior-culture of cells over several passages for mitochondrial adaptation, thereby restricting use of the assay. Here, we report a rapid version of this method with the same predictability as the original method. We found that replacing the glucose in the medium with galactose resulted in HepG2 cells immediately shifting their energy metabolism from glycolysis to oxidative phosphorylation due to drastic energy starvation; in addition, the intracellular concentration of ATP was reduced by mitotoxicants when glucose in the medium was replaced with galactose. Using our proposed rapid method, mitochondrial dysfunction in HepG2 cells can be evaluated by drug exposure for one hour without a pre-culture step. This rapid assay for mitochondrial toxicity may be more suitable for high-throughput screening than the original method at an early stage of drug development. (…)

(Anm: Statlig legemiddelkontroll (Statens legemiddelverk etc.) (mintankesmie.no).)

(Anm: Statlig hvitvasking av legemiddelinformasjon (Tidsskr Nor Legeforen 2010; 130:368 (25.2.2010).)

- Venlafaksin-indusert cytotoksisitet mot isolerte hepatocytter fra rotter innebærer oksidativt stress og mitokondrie/lysosomal dysfunksjon. (- Venlafaxine-Induced Cytotoxicity Towards Isolated Rat Hepatocytes Involves Oxidative Stress and Mitochondrial/Lysosomal Dysfunction.)

Venlafaxine-Induced Cytotoxicity Towards Isolated Rat Hepatocytes Involves Oxidative Stress and Mitochondrial/Lysosomal Dysfunction.
Adv Pharm Bull. 2016 Dec;6(4):521-530. Epub 2016 Dec 22.
Abstract Purpose: Depression is a public disorder worldwide. Despite the widespread use of venlafaxine in the treatment of depression, it has been associated with the incidence of toxicities. Hence, the goal of the current investigation was to evaluate the mechanisms of venlafaxine-induced cell death in the model of the freshly isolated rat hepatocytes. Methods: Collagenase-perfused rat hepatocytes were treated with venlafaxine and other agents. Cell damage, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial membrane potential decline, lysosomal damage, glutathione (GSH) level were analyzed. Moreover, rat liver mitochondria were isolated through differential centrifugation to assess respiratory chain functionality. Results: Our results demonstrated that venlafaxine could induce ROS formation followed by lipid peroxidation, cellular GSH content depletion, elevated GSSG level, loss of lysosmal membrane integrity, MMP collapse and finally cell death in a concentration-dependent manner. N-acetyl cysteine, taurine and quercetine significantly decreased the aforementioned venlafaxine-induced cellular events. Also, radical scavenger (butylatedhydroxytoluene and α-tocopherol), CYP2E1 inhibitor (4-methylpyrazole), lysosomotropic agents (methylamine and chloroquine), ATP generators (L-gluthamine and fructose) and mitochondrial pore sealing agents (trifluoperazine and L-carnitine) considerably reduced cytotoxicity, ROS generation and lysosomal leakage following venlafaxine treatment. Mitochondrion dysfunction was concomitant with the blockade of the electron transfer complexes II and IV of the mitochondrial respiratory system. Conclusion: Therefore, our data indicate that venlafaxine induces oxidative stress towards hepatocytes and our findings provide evidence to propose that mitochondria and lysosomes are of the primary targets in venlafaxine-mediated cell damage. (…)

(Anm: Cytotoksisk, om et stoff eller påvirkning som skader en celle, eventuelt så alvorlig at cellen dør (i noen tilfeller ved at cellen løses opp; cytolyse). Kilde: Store norske leksikon.)

(Anm: Cytotoxicity is the quality of being toxic to cells. Examples of toxic agents are an immune cell or some types of venom, e.g. from the puff adder (Bitis arietans) or brown recluse spider (Loxosceles reclusa). (en.wikipedia.org).)

- Vi har funnet at paroxetine (paroksetin; Seroxat; Paxil etc.) har cytotoksisk aktivitet mot tumorceller, både av murine eller human opprinnelse i det mikromolarer konsentrasjonsområdet.. (- We found that paroxetine has cytotoxic activity against tumor cells, both of murine or human origin in the micromolar concentration range.)

(Anm: Ulike selektive serotonin reopptakshemmeres (SSRI-er) cytotoksisitet mot kreftceller. (Cytotoxicity of different selective serotonin reuptake inhibitors (SSRIs) against cancer cells.) (…) Vi har funnet at paroxetine (paroksetin; Seroxat; Paxil etc.) har cytotoksisk aktivitet mot tumorceller, både av murine eller human opprinnelse i det mikromolarer konsentrasjonsområdet.. (- We found that paroxetine has cytotoxic activity against tumor cells, both of murine or human origin in the micromolar concentration range.) J Exp Ther Oncol. 2006;6(1):23-9.)

(Anm: Cytotoksisk, om et stoff eller påvirkning som skader en celle, eventuelt så alvorlig at cellen dør (i noen tilfeller ved at cellen løses opp; cytolyse). Kilde: Store norske leksikon.)

(Anm: Cytotoxicity is the quality of being toxic to cells. Examples of toxic agents are an immune cell or some types of venom, e.g. from the puff adder (Bitis arietans) or brown recluse spider (Loxosceles reclusa). (en.wikipedia.org).)

(Anm: Efexor / Effexor (venlafaxine) - Pristiq (desvenlafaxine) (mintankesmie.no).)

(Anm: paroksetin (paroxetine); markesføres i Norge under handelsnavn som bl.a. Seroxat; Paxil i USA.)

(Anm: Akutt toksisitet for 8 antidepressiva: hva er deres virkningsmekanismer? (Acute toxicity of 8 antidepressants: what are their modes of action? Currently, the hazard posed by pharmaceutical residues is a major concern of ecotoxicology. Most of the antidepressants belong to a family named the Cationic Amphipathic Drugs known to have specific interactions with cell membranes. The present study assessed the impact of eight antidepressants belonging to selective serotonin reuptake inhibitors or serotonin norepinephrine reuptake inhibitors.) Chemosphere. 2014 Aug;108:314-9. Epub 2014 Feb 14. (PDF).)

(Anm: Cell membranes are way more complicated than you think - Nazzy Pakpour (ed.ted.com).)

(Anm: Cytotoxic immune cell in sick and healthy skin a key to understanding vitiligo. With the aid of thousands of skin biopsies and over a hundred kilograms of skin, researchers at Karolinska Institutet have observed how two subgroups of immune cell behave in healthy skin. This functional dichotomy is preserved in the inflammatory diseases psoriasis and vitiligo. The study, which is published in the journal Immunity, opens the way for more targeted local treatments for patchy inflammatory skin disorders. (medicalnewstoday.com 22.2.2017).)

- Ulike selektive serotonin reopptakshemmeres (SSRI-er) cytotoksisitet mot kreftceller. (- We found that paroxetine has cytotoxic activity against tumor cells, both of murine or human origin in the micromolar concentration range, whereas venlafaxine has not.)

Cytotoxicity of different selective serotonin reuptake inhibitors (SSRIs) against cancer cells.
J Exp Ther Oncol. 2006;6(1):23-9.
Abstract Cell membrane ion transporters expression and activity are altered in cancer cells and these phenotypic alterations offer potential targets for cancer therapies. Among the therapeutic agents affecting cell membrane transporters, serotonin reuptake inhibitors (SSRIs) have been shown to have anticancer potential. In this work, we have compared two SSRIs, one very specific for serotonin reuptake transporters (paroxetine) and another which also inhibit norepinephrine and dopamine transporters (venlafaxine), for their ability to counteract growth of various murine and human cancer cell lines. We found that paroxetine has cytotoxic activity against tumor cells, both of murine or human origin in the micromolar concentration range, whereas venlafaxine has not. A neurotransmitter receptor mediated mechanism of action appears thus unlikely for SSRIs cytotoxicity on cancer cells. With ranges of SSRIs cytotoxicity on cancer cells defined, limits in their possible applicability in cancer therapy is discussed. (…)

(Anm: Cytotoksisk, om et stoff eller påvirkning som skader en celle, eventuelt så alvorlig at cellen dør (i noen tilfeller ved at cellen løses opp; cytolyse). Kilde: Store norske leksikon.)

(Anm: Cytotoxicity is the quality of being toxic to cells. Examples of toxic agents are an immune cell or some types of venom, e.g. from the puff adder (Bitis arietans) or brown recluse spider (Loxosceles reclusa). (en.wikipedia.org).)

- Doserelaterte parestesier med venlafaxin (Venlafaksin; Efexor; Effexor etc.)

Dose-related paresthesias with venlafaxine
J Pharm Pract. 2013 Oct;26(5):514-7. Epub 2013 Jun 13.
INTRODUCTION: Venlafaxine is a serotonin norepinephrine reuptake inhibitor that is used for mood, anxiety, and pain disorders. We report a case of dose-related paresthesias in association with venlafaxine use in a patient with major depressive disorder.

CASE REPORT: A young male patient with major depression started treatment with venlafaxine XR at 37.5 mg/d, and the dose was titrated to 75 mg/d with no significant adverse effects. Upon increasing the dose to 150 mg/d, the patient reported tingling, numbness, and itching in his upper extremities. The dose was reduced to 75 mg/d, at which time, the symptoms disappeared. Since the patient still had target symptoms of depression, the patient was willing to try increasing the dose back to 150 mg/d. Upon rechallenge, the tingling, numbness, and itching reappeared. The dose of venlafaxine was decreased back to 75 mg/d. Per the Naranjo scale, the probability score for the above adverse drug reaction is 5 (probable). We discuss the published evidence of paresthesias associated with antidepressants and clinical implications for recognizing paresthesias during venlafaxine treatment that may be useful for clinicians.

CONCLUSION: Clinicians need to be aware of the possible emergence of paresthesias with venlafaxine treatment, especially at doses of ≥ 150 mg/day. Patients who receive venlafaxine for pain disorders should be closely monitored for worsening of pain symptoms and may require adjustment of their doses. (...)

(Anm: Antidepressiva (nytteverdi) (mintankesmie.no).)

(Anm: Ny forskning: Lykkepiller gør mere skade end gavn. Folk med depression får intet ud af at tage antidepressivet SSRI, bedre kendt som lykkepiller, viser nyt dansk studie. (jyllands-posten.dk 13.2.2017).)

(Anm: Parestesi, hudfornemmelse som ikke skyldes ytre påvirkning. Disse fornemmelsene kan føles som brenning, stikking og prikking, kløe, nummenhet, maurkryping, varme eller kulde. Parestesier kan skyldes sykdom i nerver eller blodårer, som igjen for eksempel kan være utløst av visse former for anemi, diabetes og forgiftninger (for eksempel ved alkoholisme). Behandlingen retter seg mot eventuell underliggende sykdom. Kilde: Store norske leksikon.)

- Konklusjon: Dekonstruksjon av rettsdokumenter avslørte at protokollspesifikke resultater ikke viste statistisk signifikant forskjell mellom citalopram og placebo. Den publiserte artikkelen konkluderte imidlertid med at citalopram var trygt og betydelig mer effektivt enn placebo for barn og ungdom, med mulige bivirkninger mht. pasientsikkerhet.

(Anm: The citalopram CIT-MD-18 pediatric depression trial: Deconstruction of medical ghostwriting, data mischaracterisation and academic malfeasance. OBJECTIVE: Deconstruction of a ghostwritten report of a randomized, double-blind, placebo-controlled efficacy and safety trial of citalopram in depressed children and adolescents conducted in the United States. (…) CONCLUSION: Deconstruction of court documents revealed that protocol-specified outcome measures showed no statistically significant difference between citalopram and placebo. However, the published article concluded that citalopram was safe and significantly more efficacious than placebo for children and adolescents, with possible adverse effects on patient safety. Int J Risk Saf Med. 2016 Mar 16;28(1):33-43.)

(Anm: Cipralex (Lexapro) (escitalopram) - Cipramil (Celexa) (cipramil) (citalopram) - H. Lundbeck A/S (mintankesmie.no).)

- Betennelser endrer mitokondrier til giftige fabrikker

Inflammation turns mitochondria into toxic factories (Betennelser endrer mitokondrier til giftige fabrikker)
medicalnewstoday.com 25.9.2016
Å lære hvordan å kontrollere betennelser kan ha store implikasjoner for behandlingen av mange sykdommer. Banebrytende forskning oppdager hvordan makrofager endrer mitokondriene til giftige kjemisk-produserende betennelsespromotører. (Learning how to control inflammation could have huge implications for the treatment of many diseases. Breaking research discovers how macrophages turn mitochondria into toxic chemical-producing inflammation-promoters.)

Inflammation plays a significant role in a number of serious medical conditions. Efforts to understand and control it are ongoing.

Inflammation is the body's attempt to protect itself from harmful stimuli. For instance, after a knock to the knee, inflammation helps prevent further damage; it has evolved to become an essential part of our immune system.

However, during disease, the inflammatory response can go awry and cause damage to healthy tissue; it is a powerful mechanism that must be tightly controlled.

For instance, inflammatory bowel disease, arthritis, and septic shock all involve high levels of poorly controlled inflammation.

In fact, inflammation can actually cause diseases and conditions to occur, such as hay fever, periodontitis, and some cancers. (…)

(Anm: Når cellens kraftverk streiker. Mitokondriesykdom gir energisvikt i cellen, og kan forårsake varierte nevrologiske symptomer som lammelser, epilepsi og anstrengelsesintoleranse. Tidsskr Nor Legeforen 2012; 132:1068 (15.5.2012).)

(Anm: Antibiotika (tarmbakterier, probiotika, mikrobiota etc.) (Dysbiose; dysbiosis (also called dysbacteriosis (dysbakteriose)). (mintankesmie.no).)

(Anm: Signaler fra tarmens mikrobiotika til fjerntliggende organer mht. fysiologi og sykdom. (Signals from the gut microbiota to distant organs in physiology and disease.) (Nat Med. 2016 Oct 6;22(10):1079-1089.)

(Anm: Three toxic gases meet in the mitochondria. Front. Physiol. 2015 (20 August 2015).)

(Anm: Blocking transfer of calcium to cell's powerhouse selectively kills cancer cells. Inhibiting the transfer of calcium ions into the cell's powerhouse is specifically toxic to cancer cells, according to an article published this week in Cell Reports by researchers from the Perelman School of Medicine at the University of Pennsylvania. (medicalnewstoday.com 4.3.2016).)

(Anm: Foods That Fight Inflammation. Inflammation, a response that can affect even the healthiest of bodies, is caused by many factors. One major factor that we can control is the food we eat. Try to incorporate these half a dozen foods to help fight inflammation and keep a balanced diet. (time.com 4.1.2017).)

- Sammenlignet med friske kontrollpersoner hadde suicidale pasienter påfallende økte nivåer av mitokondrie DNA i deres cellefrie blodplasma. (Compared to the healthy control subjects, the suicidal patients had strikingly increased levels of mitochondrial DNA in their cell-free blood plasma.)

New biomarker is higher in suicide attempters and associated with stress response
medicalnewstoday.com 11.12.2016
Researchers at Lund and Malmö universities in Sweden have measured a biomarker in cell-free blood
plasma which can be linked to an overactive stress system in suicidal individuals. This biomarker can
hopefully be used in future psychiatric studies.

"We don't expect the marker to be able to predict who will try to commit suicide, but it may serve as a biological marker indicating greater stress exposure in vulnerable people suffering from various
psychiatric conditions such as anxiety and depression. We would like to test the marker in future
psychiatric studies and see how it is affected by, for example, lifestyle interventions, psychotherapy and pharmacological treatment", says Daniel Lindqvist, associate professor of experimental psychiatry at Lund University and psychiatry resident at Psykiatri Skåne.

The researchers compared 37 patients who had been hospitalised at a psychiatric clinic after attempting suicide with an equal number of healthy control subjects. About 70 per cent of both groups were female, and the average age of the patients was approximately 40. (…)

Compared to the healthy control subjects, the suicidal patients had strikingly increased levels of
mitochondrial DNA in their cell-free blood plasma.

The researchers also found that the large amount of mitochondrial DNA in the plasma was linked to
higher levels of cortisol in the blood. Cortisol is an important hormone in the body's stress system and
high levels of cortisol, which have been found in depressed and suicidal patients in previous studies, are a sign of an overactive stress system.

Previous studies have shown that depressed individuals have an increased level of mitochondrial DNA in their immune cells and that this is linked to stressful life events. Furthermore, studies on animals have shown that increased stress and cortisol levels are linked to higher mitochondrial DNA, but this is the first study to be tested on psychiatric patients.

"We believe the increased levels in suicidal patients are due to their exposure to severe stress for longer periods than the healthy subjects we compared them to. An increased level of cortisol can cause the body's cells to malfunction, which in turn contributes to increased levels of cell-free mitochondrial DNA in the blood", says Lars Ohlsson, senior lecturer at Malmö University. (…)

(Anm: Increased plasma levels of circulating cell-free mitochondrial DNA in suicide attempters: associations with HPA-axis hyperactivity. Translational Psychiatry (2016) 6, e971 (Published online 6 December 2016).)

(Anm: Valeant’s Siliq approved but suicidal thoughts warning will weigh heavy. Valeant has gained FDA approval for psoriasis drug Siliq – but side effect warnings about suicidal ideation look set to limit sales. (biopharmadive.com 16.2.2017).)

- Celleprotein gir nytt håp i kampen mot effektene av aldring. (- Forskning ved University of Nottingham har vist at et protein funnet i kraftverket (mitokondrie) til en celle kan være nøkkelen til å holde tilbake tidens tann, har vist.)

Cell protein offers new hope in fighting the effects of aging (Celleprotein gir nytt håp i kampen mot effektene av aldring.)
medicalnewstoday.com 12.10.2016
A protein found within the powerhouse of a cell could be the key to holding back the march of time, research by scientists at The University of Nottingham has shown. (…) (Forskning ved University of Nottingham har vist at et protein funnet i kraftverket (mitokondriene) til en celle kan være nøkkelen til å holde tilbake tidens tann, har vist.)

And their research, published in the academic journal Aging, could have special significance for combatting age-related decline and halting the progression of neurodegenerative conditions such as Alzheimer's and Parkinson's Disease.

The work, led by Dr Lisa Chakrabarti and PhD student Amelia Pollard in the University's School of Veterinary Medicine and Science, has centred on a family of proteins called carbonic anhydrase found within mitochondria - the cells' 'batteries' which convert the oxygen we breathe into the energy (ATP) needed to power our body.

Dr Chakrabarti said: "What's really exciting about this development is that we have been able to surmise that the function of this protein is playing a role in the aging process within the cell. (…)

(Anm: Mitochondrial proteomic profiling reveals increased carbonic anhydrase II in aging and neurodegeneration. AGING 2016 (published online 10 October 2016).)

(Anm: Legemiddelindusert kreft og andre typer celleskader (mintankesmie.no).)

(Anm: Three toxic gases meet in the mitochondria. Front. Physiol. 2015 (20 August 2015).)

(Anm: Fluoksetin (Prozac; SSRI) og mitokondriene: En gjennomgang av de toksikologiske aspekter. (- Fluoksetin induserer også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser. (...) På den annen side har inntak av fluoxetin blitt assosiert med økt risiko for kreft. Likevel forblir data motstridende og ingen konklusjoner er trukket.) (Fluoxetine and the mitochondria: A review of the toxicological aspects. (Fluoksetin og mitokondriene: En gjennomgang av de toksikologiske aspekter. (...) On the other hand, fluoxetine intake has been associated with increased cancer risk.) Toxicol Lett. 2016 Jul 5. pii: S0378-4274(16)32264-0.)

(Anm: Translational Identification of Transcriptional Signatures of Major Depression and Antidepressant Response. (…) Of the 13 identified genes that we tested for biomarker validation in human MDE patients, one of the genes HK1 has been previously linked to mood and psychotic disorders. HK1 encodes hexokinase 1, an initial and rate-limiting enzyme of glycolysis (Regenold et al., 2012). It has been known that genes associated with energy production are altered in postmortem brains as well as in peripheral tissues of MDD patients (Sibille et al., 2004; Klempan et al., 2009; Tobe, 2013; Garbett et al., 2015), and that molecular entities that are part of glycolysis pathway and the mitochondria in general serve as biomarkers and potential therapeutic targets for diagnosis and treatment of depression (Gormanns et al., 2011). Therefore, it was not surprising that the biological processes of the mitochondria are shared by the blood and the brain and are differentially regulated by chronic stress and fluoxetine treatment (Figure 3C). Front. Mol. Neurosci., 08 August 2017.)

(Anm: Bruk av annengenerasjons antipsykotiske legemidler øker parametre for metabolsk syndrom. (dgnews.docguide.com 17.3.2016).)

- Studien viser sammenhengen mellom metabolsk syndrom og risiko for kognitive sykdommer.

(Anm: Study shows link between metabolic syndrome and risk of cognitive disorders. A study presented at the European Academy of Neurology Congress in Amsterdam has shown that obesity alone is not a risk factor for cognitive disorders, but commonly associated co-morbidities such as diabetes, high blood pressure, and metabolic disorders are. Dementia diseases in patients who suffer from diabetes are often treated inadequately, a new research paper reveals. It has long been supposed that patients with metabolic syndrome are more likely to suffer from cognitive impairment - and to a greater extent. Reasons are thought to include chronic inflammatory processes which can induce neuroinflammatory and neurodegenerative changes. Whether obese individuals without risk factors such as diabetes mellitus, metabolic disorders and the presence of albumin in the urine have an increased risk of cognitive impairment is still little researched. (news-medical.net 27.6.2017).)

(Anm: Metabolic Syndrome Components Are Associated With Symptomatic Polyneuropathy Independent of Glycemic Status. Diabetes Care 2016 (Published online before print March 10, 2016).)

(Anm: Patients With Polyneuropathy Receive Long-Term Opioid Therapy, No Clear Benefit. CHICAGO -- May 23, 2017 -- Polyneuropathy is associated with an increased likelihood of long-term opioid therapy, but therapy does not appear to improve functional status, according to a study published online by JAMA Neurology. Polyneuropathy is a common painful condition, especially among older patients, which can result in functional impairment. (dgnews.docguide.com 23.5.2017).)

(Anm: Video Lecture 8: Metabolic Syndrome Lectures 1 (By Dr. Joachim Raese) (youtube.com).)

- Mitokondriell dysfunksjon og mitokondrie-dynamikk-Kreft-linken.

Mitochondrial dysfunction and mitochondrial dynamics-The cancer connection.
Biochim Biophys Acta. 2017 Jan 16. pii: S0005-2728(17)30005-1. [Epub ahead of print]
Abstract Mitochondrial dysfunction is a hallmark of many diseases. The retrograde signaling initiated by dysfunctional mitochondria can bring about global changes in gene expression that alters cell morphology and function. Typically, this is attributed to disruption of important mitochondrial functions, such as ATP production, integration of metabolism, calcium homeostasis and regulation of apoptosis. Recent studies showed that in addition to these factors, mitochondrial dynamics might play an important role in stress signaling. Normal mitochondria are highly dynamic organelles whose size, shape and network are controlled by cell physiology. Defective mitochondrial dynamics play important roles in human diseases. Mitochondrial DNA defects and defective mitochondrial function have been reported in many cancers. Recent studies show that increased mitochondrial fission is a pro-tumorigenic phenotype. In this paper, we have explored the current understanding of the role of mitochondrial dynamics in pathologies. We present new data on mitochondrial dynamics and dysfunction to illustrate a causal link between mitochondrial DNA defects, excessive fission, mitochondrial retrograde signaling and cancer progression. This article is part of a Special Issue entitled Respiratory complex I, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (…)

(Anm: Exercise increases mitochondrial complex I activity and DRP1 expression in the brains of aged mice. Abstract. Exercise is known to have numerous beneficial effects. Recent studies indicate that exercise improves mitochondrial energetics not only in skeletal muscle but also in other tissues. (…) Our results suggest that exercise training in old mice can improve brain mitochondrial function through effects on electron transport chain function and mitochondrial dynamics without increasing mitochondrial biogenesis. Exp Gerontol. 2017 Jan 17. pii: S0531-5565(16)30505-8. [Epub ahead of print].)

(Anm: Exercise prevents cellular aging by boosting mitochondria (medicalnewstoday.com 8.3.2017).)

(Anm: Trening er best for å redusere tilbakefall av brystkreft. Exercise is best for reducing breast cancer recurrence. The research was conducted by Dr. Ellen Warner, of the Sunnybrook Health Sciences Centre in Canada, in collaboration with coauthor Dr. Julia Hamer, and the findings were published in the Canadian Medical Association Journal (CMAJ). (medicalnewstoday.com 22.2.2017).)

(Anm: Hyppigheten av kreft var (...) signifikant høyere i undergruppen antipsykotika (p = 0,05) etter enn før medisinering (J Child Adolesc Psychopharmacol. 2013 Apr;23(3):208-13).)

(Anm: Hva er det forskrivere og pasienter ikke vet om bivirkninger av antidepressiva? (What do prescribers and patients not know about the side effects of antidepressant drugs?) (medicalnewstoday.com 15.9.2016).)

(Anm: Forskere: Alvorlige bivirkninger, når antidepressiver droppes. Angst, depression og selvmordstanker er nogle af de bivirkninger, som tit forekommer, når man holder op med at tage antidepressiv medicin. Bivirkningerne kan i nogle tilfælde være langvarige og kroniske, viser et nyt studie. (videnskab.dk 16.3.2015).)

(Anm: Bruk av visse smertestillende midler (og antidepressiva (+ 31 %)) forbundet med økt risiko for drap (Use of certain painkillers linked with increased risk of homicide) Enkelte legemidler som påvirker sentralnervesystemet - som smertestillende og beroligende benzodiazepiner - er assosiert med økt risiko for å begå et drap, finner en ny studie publisert i tidsskriftet World Psychiatry. (medicalnewstoday.com 1.6.2015).)

(Anm: Psykiatriske patienter ender i private botilbud. Drab og vold har de seneste år fyldt debatten om de danske bosteder for patienter med psykiske problemer. (…) Psykiatriske patienter ender i private botilbud. (…) Mens Folketinget kæmper for en løsning på problemet med vold på offentlige bosteder, vælger flere kommuner at sende tunge patienter til private tilbud. (politiken.dk 18.3.2017.)

(Anm: Aggresjon knyttet til økt risiko for substansmisbruk. Aggression disorder linked to greater risk of substance abuse. (…) In the study, published in the Journal of Clinical Psychiatry, Emil Coccaro, MD, and colleagues analyzed data from more than 9,200 subjects in the National Comorbidity Survey, a national survey of mental health in the United States. They found that as the severity of aggressive behavior increased, so did levels of daily and weekly substance use. The findings suggest that a history of frequent, aggressive behavior is a risk factor for later substance abuse, and effective treatment of aggression could delay or even prevent substance abuse in young people. (medicalnewstoday.com 2.3.2017).)

(Anm: Halvparten av norske drap begått av rusede. (…) I 125 av drapene – eller 54 prosent – er det beskrevet i dommen at gjerningspersonen var påvirket av rusmidler under drapet. (nrk.no 13.12.2016).)

- En pasient på UNN døde av blodforgiftning som følge av et legemiddel mot psykiske lidelser, opplyser Statens helsetilsyn.

(Anm: En pasient på UNN døde av blodforgiftning som følge av et legemiddel mot psykiske lidelser, opplyser Statens helsetilsyn. (- Pasienten døde etter kort tid, og dødsårsaken var nøytropen sepsis (blodforgiftning), heter det i tilsynets rapport. (nrk.no 12.10.2016).)

(Anm: Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body, frequently a response of the immune system to infection. (en.wikipedia.org).)

(Anm: Sepsis. Definisjon: SIRS + påvist/mistenkt infeksjon (f. eks. positiv blodkultur). SIRS- kriteriene er: - Feber > 38 ºC eller hypotermi < 36 ºC - Puls > 90/minutt - Respirasjonsfrekvens > 20/minutt eller hypokapni med pCO2 < 4,3 kPa i blodgass - Leukocytose ≥ 12 × 109/l eller leukopeni < 4 × 109/l eller > 10 % umodne leukocytter. (helsebiblioteket.no - Metodebok for indremedisinere, 2012).)

(Anm: Rollen til mitokondriell dysfunksjon (mitokondriedysfunksjon) ved sepsis (blodforgiftning)-indusert multiorgansvikt. (The role of mitochondrial dysfunction in sepsis-induced multi-organ failure). (Virulence. 2013 Nov 1;5(1).)

- Diagnostisering av sepsis. Sepsis, også kjent som blodforgiftning, er kroppens hyperaktive respons på en infeksjon som kan føre til betennelse, vevskader, organsvikt etc.

(Anm: Diagnosing Sepsis. Sepsis, also known as blood poisoning, is the body’s hyperactive response to an infection that can lead to inflammation, tissue damage, organ failure etc. It is a very dangerous state in which the immune system stops fighting with the invading agents  and turns to itself. Around one-third of patients who are affected with sepsis die every year. (news-medical.net 7.9.2017).)

- Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon.

(Anm: Å anerkjenne sepsis som en global helseprioritet - En WHO- resolusjon. Recognizing Sepsis as a Global Health Priority — A WHO Resolution. “Some very important clinical issues, some of them affecting life and death, stay largely in a backwater which is inhabited by academics and professionals and enthusiasts, dealt with very well at the clinical and scientific level but not visible to the public, political leaders, leaders of healthcare systems... The public and political space is the space in which [sepsis] needs to be in order for things to change.” NEJM (June 28, 2017).)

(Anm: Sepsis – den dödliga sjukdomen som glöms bort. Trots att infektionssjukdomen sepsis förekommer oftare än de vanligaste formerna av cancer och att upp emot hälften som drabbas av den allvarligaste formen dör, så har många knappt hört talas om sjukdomen. Sepsis som är den medicinska termen på blodförgiftning, drabbar omkring 40 000 svenskar varje år. (netdoktor.se 7.6.2017).)

- Hurtigtest finner tegn på sepsis i en enkelt dråpe blod.

(Anm: Hurtigtest finner tegn på sepsis i en enkelt dråpe blod. (- Sepsis, en potensielt livstruende komplikasjon av en infeksjon, har den høyeste byrde mht. død og medisinske utgifter på sykehus over hele verden.) (- Quick test finds signs of sepsis in a single drop of blood. (…) Sepsis, a potentially life-threatening complication of an infection, has the highest burden of death and medical expenses in hospitals worldwide. (medicalnewstoday.com 5.7.2017).)

(Anm: Nye sepsiskriterier kan føre til forsinket behandling. (…) Sepsis er en svært alvorlig tilstand med høy morbiditet og mortalitet (2). Den totale insidensen er ukjent, men man regner med at sepsis er en av de viktigste årsakene til alvorlig, akutt sykdom på verdensbasis (1). (…) Sepsis har inntil nylig vært definert som mistenkt infeksjon med samtidig tilstedeværelse av to eller flere SIRS-kriterier (1). Endringer i hjertefrekvens, kroppstemperatur, respirasjonsfrekvens og leukocytter er kroppens tegn på inflammasjon, og de indikerer ikke nødvendigvis en livstruende, dysregulert vertsrespons på infeksjon. Tidsskr Nor Legeforen 2017; :609-10 (20.4.2017).)

(Anm: LEGENE FORSTO IKKE AT HAN VAR DØDSSYK: Stian (19) døde etter 18 timer på sykehus uten legetilsyn. (…) Helsetilsynet konkluderer med at sykehusets behandling var uforsvarlig. (…) Fikk ikke beskjed. (…) Fastlegen sendte med dem papirer som foreldrene leverte på Akuttmottaket ved Ahus, der sto det; «Diagnose: Obs sepsis».  (tv2.no 29.4.2017).)

(Anm: Svikt i behandlingen av akutt syk ung mann i akuttmottaket – brudd på helselovgivningen. (…) Pasienten ble lagt på observasjonsposten (Akutt 24) ved akuttmottaket frem til neste morgen. I løpet av tiden på observasjonsposten ble han ikke tilsett av lege. På morgenen var han betydelig verre og han fikk tegn på fullt utviklet blodforgiftning. Behandling med antibiotika ble iverksatt, men han døde kort tid etter som følge av meningokokksepsis og hjerneødem. (helsetilsynet.no 2.5.2017).)

(Anm: Sepsis; grunnleggende kliniske observasjoner. Sepsis= En systemisk inflammatorisk respons (SIRS) pga. en infeksjon Tre alvorlighetsgrader: 1) Sepsis (to eller flere symptomer på SIRS som følge av infeksjon) 2) Alvorlig sepsis (sepsis med akutt organdysfunksjon, hypoperfusjon eller hypotensjon) 3) Septisk sjokk (hypotensjon til tross for adekvat væsketerapi, samt forekomst av perfusjonsforstyrrelser og organdysfunksjon) (hnt.no 5.11.2013).)

- Alle bryt lova i behandling av blodforgifting. Pasientar med alvorleg blodforgifting (sepsis) blir undersøkt av lege for seint.

(Anm: Alle bryt lova i behandling av blodforgifting. Pasientar med alvorleg blodforgifting blir undersøkt av lege for seint. Helsetilsynet fann brot ved 24 akuttmottak over heile landet. – Svært alvorleg. – Dette er svært alvorleg, for det dreier seg om ein alvorleg infeksjonssjukdom som i verste fall kan medføra død dersom behandlinga ikkje blir igangsett til riktig tid, seier avdelingsdirektør i Helsetilsynet, Ragnar Hermstad. OVER EIN TIME: Pasientar som kjem inn med teikn på alvorleg infeksjonssjukdom som blodforgifting skal ifølge nasjonale retningslinjer få anitibiotikabehandling innan maks ein time. Alle dei 24 akuttmottaka hadde svikt på dette området. (nrk.no 16.6.2017).)

(Anm: Lege sier improvisert «kur» for sepsis har hatt bemerkelsesverdige resultater. (…) Spesialist i intensivbehandling Paul Marik sier at enkel behandling med infusjon av vitamin C og steroider har bemerkelsesverdig effekt på pasienter med potensielt dødelig tilstand. (independent.co.uk 24.3.2017).)

(Anm: Bivirkninger underrapporteres i videnskabelige tidsskrifter. (...) Mellem 43 og 100 procent af de bivirkninger, der, ifølge det ikke-publicerede materiale, er fundet ved de testede lægemidler, er ikke lagt frem i de videnskabelige artikler, viser Yoon Loke og kollegernes gennemgang. (videnskab.dk 5.10.2016).)

(Anm: Dødsfall på grunn av nøytropen sepsis (blodforgiftning) etter behandling med legemiddelet klozapin – uforsvarlig oppfølging – mangelfull samhandling og informasjon. (…)  Manglende informasjon fra spesialisthelsetjenesten og mangelfull samhandling mellom kommunehelsetjenesten, fastlegen, pasienten og pårørende bidro til hendelsen. Helseforetaket skal gjennomgå hendelsen for å redusere risikoen ved lignende tilfeller. (helsetilsynet.no 12.10.2016).)

(Anm: Examining mitochondrial DNA may help identify unknown ancestry that influences breast cancer risk (medicalnewstoday.com 23.9.2016).)

(Anm: The rise of mitochondria in medicine. Once considered exclusively the cell's powerhouse, mitochondria are now recognized to perform multiple essential cellular functions beyond energy production, impacting most areas of cell biology and medicine. Mitochondrion. 2016 Jul 13. pii: S1567-7249(16)30098-8. [Epub ahead of print].)

- Teknologi fra hydrogenbiler kan forklare hvorfor livet oppstod. (- I cellene til mennesker og dyr blir energien produsert i det som kalles cellenes kraftverk, mitokondriene. De har et membran, som på mange måter tilsvarer membranet i brenselcellen.)

Teknologi fra hydrogenbiler kan forklare hvorfor livet oppstod
nrk.no 21.3.2014
Brenselceller i hydrogenbiler har noe til felles med levende celler. Undersjøiske varme kilder kan ha skapt naturlige brenselceller, forløperen til stoffskiftet i cellene.

Forskere fra USA og Storbritannia har vist hvordan brenselceller kan oppstå naturlig rundt undersjøiske varme kilder.

Disse brenselcellene kan ha skaffet energien som dyttet livet i gang på jorda for over tre milliarder år siden.

Brenselceller ligner levende celler
- Dette er en original måte å angripe problemet om livets opprinnelse på, sier Tom Kristensen fra Universitet i Oslo.

- Jeg har ingen motforestillinger mot at en slik forløper til stoffskiftet kan ha gitt den energien som må til for å bygge opp større molekyler som RNA og arvestoffet DNA i de første levende celler, fortsetter han. (...)

Elektrolyttmembran
Elektrolytten i en moderne brenselcelle virker på liknende måte. Den skiller hydrogengass fra tanken og oksygen fra lufta, oftest med en membran. Membranen lar de elektrisk ladede hydrogenatomene passere, slik at de kan møte oksygenet. (...)

Rotasjonsmotor i cellene
I cellene til mennesker og dyr blir energien produsert i det som kalles cellenes kraftverk, mitokondriene. De har et membran, som på mange måter tilsvarer membranet i brenselcellen

•Les også: Slik oppsto den moderne cellen

- Spenningsforskjellen over mitokondriets membran pumper ladede hydrogenatomer ut av mitokondriene. Så blir det ført inn igjen når det energibærende stoffet ATP produseres, forteller Tom Kristensen.

Han sammenligner denne mekanismen med en ørliten roterende motor. Slik sett er det enda en morsom sammenheng mellom brenselcellene i en bil og cellene i en levende kropp. (...)

(Anm: Three toxic gases meet in the mitochondria. Front. Physiol. 2015 (20 August 2015).)

(Anm: Feeling Worn Out? PGC1α to the Rescue for Dysfunctional Mitochondria in T Cell Exhaustion. Abstract In chronic viral infections and cancer, T cells acquire a functional state characterized by reduced effector functionality, termed exhaustion. In two related studies by Scharping et al. (2016) and Bengsch et al. (2016) in this issue of Immunity, dysfunctional mitochondria are identified as a key correlate of CD8+ T cell exhaustion. Immunity. 2016 Aug 16;45(2):233-235.)

(Anm: T cell type that promotes damaging immune response discovered. For the first time, researchers have identified a type of T cell that plays a key role in promoting the damaging autoimmune response that inflames and attacks the joints in rheumatoid arthritis. The discovery - made with technologies that help to analyze just a "handful of cells" - offers vital new clues to the biology of the disease and could lead to more powerful, targeted treatments. The study - led by Brigham and Women's Hospital (BWH), a teaching affiliate of Harvard Medical School in Boston, MA - is published in the journal Nature. (medicalnewstoday.com 2.2.2017).)

(Anm: Mitochondrial Cardiomyopathies. Mitochondria are found in all nucleated human cells and perform various essential functions, including the generation of cellular energy.  (…) Cardiomyopathies are frequent manifestations of mitochondrial diseases associated with defects in electron transport chain complexes subunits and their assembly factors, mitochondrial transfer RNAs, ribosomal RNAs, ribosomal proteins, translation factors, mtDNA maintenance, and coenzyme Q10 synthesis. Other mitochondrial diseases with cardiomyopathies include Barth syndrome, Sengers syndrome, TMEM70-related mitochondrial complex V deficiency, and Friedreich ataxia. Front Cardiovasc Med. 2016 Jul 25;3:25. eCollection 2016.)

(Anm: Mitochondrial Complex V α Subunit Is Critical for Candida albicans Pathogenicity through Modulating Multiple Virulence Properties. Front. Microbiol., 23 February 2017.)

(Anm: Coenzyme Q10 partially restores pathological alterations in a macrophage model of Gaucher disease. (…) CONCLUSION: These data suggest that targeting mitochondria function and oxidative stress by CoQ can ameliorate the pathological phenotype of Gaucher cells. Chemically-induced Gaucher macrophages provide cellular models that can be used to investigate disease pathogenesis and explore new therapeutics for GD. Orphanet J Rare Dis. 2017 Feb 6;12(1):23.)

(Anm: Study suggests new therapy for Gaucher disease. Scientists propose in Nature blocking a molecule that drives inflammation and organ damage in Gaucher and maybe other lysosomal storage diseases as a possible treatment with fewer risks and lower costs than current therapies. (…) "Current enzyme replacement and substrate reduction therapies are expensive and still associated with inflammation, increased risk of malignancies and Parkinson's disease," says Manoj Pandey, PhD, study first author and a scientist in the Division of Human Genetics at Cincinnati Children's. "We suggest that targeting a molecule called C5aR1 may serve as a viable treatment option for patients with Gaucher disease and possibly other LSDs." (medicalnewstoday.com 24.2.2017).)

(Anm: Magnesium hjelper mot depresjon. (nhi.no 26.7.2017).)

(Anm: High magnesium prevents matrix vesicle-mediated mineralization in human bone marrow-derived mesenchymal stem cells via mitochondrial pathway and autophagy. (…) Our results contribute to the understanding of the role of magnesium homeostasis in osteoporosis and the design of magnesium alloys. Cell Biol Int. 2017 Oct 10.)

(Anm: Magnesium can be key to treat a range of health issues. Magnesium has been hailed as the ‘super supplement’ to give us the boost we need this winter, says experts on BBC Radio Two’s Breakfast Show with Chris Evans. (news-medical.net 23.10.2017).)

(Anm: Role of magnesium supplementation in the treatment of depression: A randomized clinical trial. (…) Conclusions Daily supplementation with 248 mg of elemental magnesium as four 500 mg tablets of magnesium chloride per day leads to a significant decrease in depression and anxiety symptoms regardless of age, gender, baseline severity of depression, or use of antidepressant medications. While the cross over design of this trial is robust in controlling for internal biases, it would be reassuring to see the results replicated in larger clinical trials that test long term efficacy and provide additional data on subgroups. However, this efficacy trial showed magnesium supplements may be a fast, safe, and easily accessible alternative, or adjunct, to starting or increasing the dose of antidepressant medications. PLoS ONE 12(6): e0180067.)

(Anm: Magnesium hjelper mot depresjon. (nhi.no 26.7.2017).)

(Anm: Magnesium can be key to treat a range of health issues. Magnesium has been hailed as the ‘super supplement’ to give us the boost we need this winter, says experts on BBC Radio Two’s Breakfast Show with Chris Evans. (news-medical.net 23.10.2017).)

(Anm: High magnesium prevents matrix vesicle-mediated mineralization in human bone marrow-derived mesenchymal stem cells via mitochondrial pathway and autophagy. (…) Our results contribute to the understanding of the role of magnesium homeostasis in osteoporosis and the design of magnesium alloys. Cell Biol Int. 2017 Oct 10.)

(Anm: Too much or too little magnesium can raise dementia risk. A new study published in the journal Neurology suggests that both very high and very low levels of magnesium may put people at risk of developing dementia. The first author of the study is Dr. Brenda Kieboom, of the Erasmus University Medical Center in Rotterdam, the Netherlands. (…) Low serum magnesium levels were defined as equal to or lower than 0.79 millimoles per liter, and high magnesium levels were defined as equal to or above 0.90 millimoles per liter. Magnesium levels were divided into quintiles, or fifths; the researchers examined the association between dementia and serum magnesium using the third quintile as a reference. (medicalnewstoday.com 21.9.2017).)

(Anm: Magnesium, terapi. Magnesium er et viktig mineral i kroppen. Hos noen personer kan det oppstå situasjoner med magnesiummangel. (…) Magnesium er det fjerde hyppigst forekommende mineralet i kroppen1. Det er fordelt med ca. halvparten i skjelettet og den andre halvparten i muskulatur og annet bløtvev. Mindre enn 1% finnes i blodet. (…) Magnesiums rolle i kroppen. Magnesium deltar i mer enn 300 ulike metabolske reaksjoner i kroppen4-5. Disse prosessene inkluderer proteinsyntese, produksjon og lagring av celleenergi, cellevekst og reproduksjon, DNA og RNA syntese og stabilisering av mitokondrienes membraner6-7. (nhi.no 28.4.2014).)

(Anm: The Emerging Role for Zinc in Depression and Psychosis. (…) Zinc is an essential trace element required by all organisms for various biological processes. Its general actions are well reviewed, as briefly described in this paper and several excellent reviews (Marger et al., 2014; Nowak, 2015; Prakash et al., 2015), but a role for zinc homeostasis with respect to clinical depression and psychosis is not well appreciated by psychiatrists. Front. Pharmacol., 30 June 2017.)

(Anm: Improvement of mitochondrial function by celastrol in palmitate-treated C2C12 myotubes via activation of PI3K-Akt signaling pathway. Biomed Pharmacother. 2017 Jul 13;93:903-912.)

(Anm: Get Enough Vitamin B Today? All Kinds? (webmd.com 20.6.2016).)

(Anm: Magnesium could offer fresh hope to tinnitus sufferers. We showed that tinnitus sets in at a specific sound frequency, after the experience of loud sound exposure. Better yet, we showed that a high magnesium diet can prevent the dorsal cochlear nucleus from turning the dials all the way up and locking this in place as a memory. With that intervention, we were able to prevent the subsequent perception of tinnitus. (theconversation.com 8.3.2017).)

(Anm: Vitamin B-3 successfully prevents glaucoma in mice. (…) The research - led by Jackson Laboratory professor and Howard Hughes medical investigator Simon W.M. John - investigates the effect of vitamin B-3 on mice that had been genetically modified to be prone to developing glaucoma. The findings were published in the journal Science. (…) The condition reportedly affects more than 60 million people worldwide, with 3 million cases of glaucoma suspected in adults in the United States. (medicalnewstoday.com 17.2.2017).)

(Anm: Can I use vitamins for hair growth? (medicalnewstoday.com 20.7.2017).)

(Anm: Seven benefits of kefir (medicalnewstoday.com 13.7.2017).)

(Anm: Vitamin B12 tabletter - et godt alternativ til injeksjoner. Vitamin B12 tabletter, Cyankobalamin 1 mg (Behepan) fikk nylig markedsføringstillatelse og refunderes på blå resept fra 1. juni. Ubehandlet B12 mangel kan gi pernisiøs anemi, beinmargssvikt og alvorlige, irreversible skader på nervesystemet. I Norge har B12-mangel nesten utelukkende vært behandlet med injeksjoner til tross for god dokumentasjon for at tablettbehandling kan være like effektivt (1). (...) Det anbefales ikke alminnelig screening for B12 mangel, men lav terskel for å måle B12 hos pasienter med anemi, såre munnslimhinner, polynevropati, demens, asteni eller uklare nevrologiske eller psykiatriske symptomer. (legemiddelverket.no 31.5.2017).)

(Anm: What Do You Know About Vitamin B12 Deficiency? (webmd.com 28.2.2017).)

(Anm: Led av vitamin B12-mangel – FIKK PERMANENTE SKADER. Hun følte seg nummen i føtter og hender, svimmel og glemsk. Eva Svärd (49) hadde de typiske symptomene, men fikk likevel ingen diagnose. En blodprøve hadde vist at hun led av vitamin B12-mangel. Men det drøyde i tre år før hun fikk hjelp. (vg.no 19.9.2017).)

– Gjennombrudd i svangerskapsforskning: Vitamin kan redusere misdannelser. (…) Hver tredje kvinne har lave B3-nivå. (– De har for første gang funnet gener som er viktige for fosterutviklingen, som er avhengige av vitamin B3 for å utvikle seg normalt, sier Salvesen. Han legger til at funnet er identisk med oppdagelsen av folat eller B9 mangel.)

(Anm: Gjennombrudd i svangerskapsforskning: Vitamin kan redusere misdannelser. (…) Hver tredje kvinne har lave B3-nivå. (…) Mangel på dette vitaminet kan føre til misdannelser og spontanabort mente forskerne. (…) Ett av Australias største medisinske funn. Professor Sally Dunwoodie som ledet studien, sier til Sky News Australia at hun tror ringvirkningene av studien kan bli enorme. (…) – Kjempespennende. – Dette er kjempespennende, sier klinikksjef ved Kvinneklinikken, St. Olavs Hospital, Kjell Åsmund Salvesen. – De har for første gang funnet gener som er viktige for fosterutviklingen, som er avhengige av vitamin B3 for å utvikle seg normalt, sier Salvesen. Han legger til at funnet er identisk med oppdagelsen av folat eller B9 mangel. Etter å ha funnet en sammenheng mellom folatmangel og blant annet ryggmargsbrokk, gikk myndighetene i 1998 ut og anbefalte gravide å ta folattilskudd. Ifølge Salvesen ble forekomsten av nevralrørsdefekter (NTD), som inngår i ryggmargsbrokk, anencefali (manglende hjerne) og hjernebrokk, halvert på ti år. – Salget av folat tok for alvor av i 2006, vi kan anta at nedgangen i tilfeller med NTD skyldes folat-tilskudd, sier Salvesen. Årlig fødes to prosent med alvorlig medfødte utviklingsavvik. Risiko for spontanabort før uke 12 er 15 prosent. (aftenposten.no 11.8.2017).)

(Anm: Aktivisering av syke mitokondrier med vitamin B3: Effektiv behandling for mitokondriesykdom. (Energizing sick mitochondria with vitamin B3: Effective treatment for mitochondrial disease.) (sciencedaily.com 17.8.2014.)

(Anm: Vitamins - Building the Body and Fighting Disease. Get your vitamins. Who has not heard the words "You need your vitamins!" as a child? Vitamins help us grow up healthy and strong, so our parents told us, as they recited the vitamins' own peculiar version of the alphabet, which starts with 'A', and has a letter (sometimes with a number) to represent each of these essential nutrients. The Nobel Prize has acknowledged the importance of vitamins by awarding the seven scientists below. Several Nobel Laureates who have been awarded for other achievements have also performed research on the substances that continue to be as vital to our health today as they were hundreds of years ago. Read about some important breakthroughs in vitamin research (nobelprize.org).)

(Anm: Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice. Abstract Glaucomas are neurodegenerative diseases that cause vision loss, especially in the elderly. The mechanisms initiating glaucoma and driving neuronal vulnerability during normal aging are unknown. Studying glaucoma-prone mice, we show that mitochondrial abnormalities are an early driver of neuronal dysfunction, occurring before detectable degeneration. Retinal levels of nicotinamide adenine dinucleotide (NAD+, a key molecule in energy and redox metabolism) decrease with age and render aging neurons vulnerable to disease-related insults. Oral administration of the NAD+ precursor nicotinamide (vitamin B3), and/or gene therapy (driving expression of Nmnat1, a key NAD+-producing enzyme), was protective both prophylactically and as an intervention. At the highest dose tested, 93% of eyes did not develop glaucoma. This supports therapeutic use of vitamin B3 in glaucoma and potentially other age-related neurodegenerations. Science. 2017 Feb 17;355(6326):756-760.)

(Anm: Probiotic could help alleviate hay fever symptoms. Researchers found that a probiotic consisting of both Lactobacilli and Bifidobacteria helped to alleviate hay fever symptoms and improved quality of life during allergy season. (medicalnewstoday.com 3.3.2017).)

(Anm: Microbiota promotes systemic T-cell survival through suppression of an apoptotic factor. PNAS (Proceedings of the National Academy of Sciences) 2017 (Published ahead of print May 9, 2017).)

(Anm: Link between chronic fatigue syndrome and gut bacteria explored. Chronic fatigue syndrome is a poorly understood condition; its exact causes are still not known. As medical researchers dig deeper, the potential involvement of gut bacteria is coming to the fore, revealing that the microbiome may play a significant role. (…) When the species of bacteria were analyzed, many of them were shown to be significantly associated with CFS. These were: - Faecalibacterium - Roseburia - Dorea - Coprococcus - Clostridium - Ruminococcus - Coprobacillus Their combined relative abundance was found to predict diagnosis. Other species were also seen in different levels, depending on whether or not IBS was present alongside CFS. The top biomarkers for CFS with IBS were increased levels of unclassified Alistipes and decreased levels of Faecalibacterium, while the top biomarkers for CFS without IBS were increased levels of unclassified Bacteroides and decreased Bacteroides vulgatus. (medicalnewstoday.com 26.4.2017).)

(Anm: Discovery of novel mechanism in the gut microbiome has implications for people with IBD. (…) Published last week in Cell, a study by Santamaria and Kathy McCoy, PhD, from the University of Calgary's Cumming School of Medicine (CSM) reveals a new mechanism in the gut microbiome that regulates pro- and anti-inflammatory cells. "We found that a protein expressed by gut bacteria called Bacteroides works to prevent IBD by rapidly recruiting white blood cells to kill a cell of the immune system that is responsible for orchestrating IBD," says McCoy. "We think that this mechanism is likely involved in preventing most people from developing IBD." (news-medical.net 23.10.2017).)

(Anm: Kronisk tretthetssyndrom/Myalgisk encefalopati (CFS/ME). (mintankesmie.no).)

(Anm: Chronic Fatigue Syndrome Causes and Treatment (webmd.com 1.6.2016).)

(Anm: Lutein inhibits the migration of retinal pigment epithelial cells via cytosolic and mitochondrial Akt pathways (lutein inhibits RPE cells migration. Int J Mol Sci. 2014 Aug 8;15(8):13755-67.)

(Anm: Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress. (…) DISCUSSION: Our current results revealed that lutein possessed protection on dopaminergic neurons by enhancing antioxidant defense and diminishing mitochondrial dysfunction and apoptotic death, suggesting the potential benefits of lutein for PD treatment. Nutr Neurosci. 2016 Jul;19(6):237-46. Epub 2015 Mar 2.)

(Anm: Antioxidant vitamin and mineral supplements for preventing age-related macular degeneration. Abstract BACKGROUND: There is inconclusive evidence from observational studies to suggest that people who eat a diet rich in antioxidant vitamins (carotenoids, vitamins C, and E) or minerals (selenium and zinc) may be less likely to develop age-related macular degeneration (AMD). (…) AUTHORS' CONCLUSIONS: Taking vitamin E or beta-carotene supplements will not prevent or delay the onset of AMD. The same probably applies to vitamin C and the multivitamin (Centrum Silver) investigated in the one trial reported to date. There is no evidence with respect to other antioxidant supplements, such as lutein and zeaxanthin. Although generally regarded as safe, vitamin supplements may have harmful effects, and clear evidence of benefit is needed before they can be recommended. People with AMD should see the related Cochrane Review on antioxidant vitamin and mineral supplements for slowing the progression of AMD, written by the same review team. Cochrane Database Syst Rev. 2017 Jul 30;7:CD000253.)

(Anm: Mitochondrial Therapies in Heart Failure. Abstract. The current therapy for patients with stable systolic heart failure is largely limited to treatments that interfere with neurohormonal activation. Critical pathophysiological hallmarks of heart failure are an energetic deficit and oxidative stress, and both may be the result of mitochondrial dysfunction. (…) Here, we discuss the mechanisms and results of these mitochondria-targeted therapies, but also of interventions that were not primarily thought to target mitochondria but may have important impact on mitochondrial biology as well, such as iron and exercise. Future research should be directed at further delineating the details of mitochondrial dysfunction in patients with heart failure to further optimize these treatments. Handb Exp Pharmacol. 2017 Feb 9. [Epub ahead of print].)

(Anm: Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells. BACKGROUND: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. (…) CONCLUSION: These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance. BMC Neurosci. 2017 Jan 19;18(1):15.)

(Anm: Inhibition of the Mitochondrial Glutamate Carrier SLC25A22 in Astrocytes Leads to Intracellular Glutamate Accumulation. Discussion Glutamate homeostasis is crucial for the proper functioning of the central nervous system and its extracellular concentration is maintained low thanks to the astroglial glutamate transporters GLT-1 and GLAST (EAAT 1 and 2; Takahashi et al., 1997; Danbolt, 2001; Robinson and Jackson, 2016). (…) The balance between the extent of oxidative consumption of glutamate (reflecting mitochondrial glutamate catabolism) and synthesis of glutamine by GS is dependent on extracellular glutamate concentration, with relatively more glutamate being oxidized at higher glutamate concentrations (from 15% to 43% as extracellular glutamate concentration increased from 0.1 mM to 0.5 mM in primary culture of cortical astrocytes; McKenna et al., 2000). Front. Cell. Neurosci., 31 May 2017.)

(Anm: Astrocytes play important part in regulation of breathing, study shows. Star-shaped cells called astrocytes are much more than simple support cells in the brain. In a new study on mice, researchers at Karolinska Institutet demonstrate that they also play a key part in the respiratory center of the brainstem and release inflammatory molecules that regulate breathing. The results, which are presented in the scientific journal eLife, can provide important clues as to the causes of respiratory disease and the sudden unexpected postnatal collapse of newborn infants (SUPC). (news-medical.net 10.10.2017).)

(Anm: The Use of Antioxidants in the Treatment of Traumatic Brain Injury. AIMS: To discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. (…) CONCLUSION: The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury. J Adv Nurs. 2017 Jan 19. [Epub ahead of print].)

(Anm: Broccolivitamin gør gamle mus unge igjen. Endnu en grund til at spise broccoli: En særlig "ungdomseliksir", som findes i grøntsager, satte kroppens forfald på pause hos en gruppe forsøgsmus. De amerikanske forskere bag studiet tror på, at resultaterne kan overføres til mennesker. (…) Når forskerne bag det nye studie gav ældre mus den naturligt forekommende 'ungdomseliksir', også kendt som vitaminet nikotinamid mononukleotid (NMN), medførte det en række fordelagtige virkninger for musene: Det fysiske aktivitetsniveau blev forøget. Deres knogletæthed og muskler blev forbedret. Immunsystemet og leveren præsterede bedre. Forbedret syn. Et mindre vægttab. (jyllands-posten.dk 14.2.2017).)

(Anm: How does broccoli help prevent cancer? Study sheds light. Researchers from Oregon State University (OSU) found that sulforaphane reduced the expression of long noncoding RNAs (lncRNAs) in prostate cancer cells, which disrupted the cells' ability to form colonies - a hallmark of metastatic cancer. Previously believed to be "junk DNA" with no significant function, lncRNAs have increasingly emerged as key players in the development of numerous cancers, including prostate, breast, stomach, and lung cancers. (medicalnewstoday.com 18.3.2017).)

(Anm: Insight into cancer cells' abnormal behavior. Scientists at Lancaster University have shed light on the metabolic switch observed in abnormal cells like cancer. The change in cellular energy metabolism is a hallmark of many diseases as cells change from healthy to abnormal metabolic states. (medicalexpress.com 4.8.2016).)

- Tarmbakterier frigjør antialdringseffekt av granatepler. (- Dersom utslitte mitokondrier ikke blir resirkulert, bygger de og deres oppløste komponenter seg opp inne i cellene, og etter hvert forårsaker problemer i mange vev, inkludert muskler, som gradvis blir svakere.)

Gut bacteria unleash anti-aging power of pomegranates (Tarmbakterier frigjør antialdringseffekt av granatepler)
medicalnewstoday.com 11.7.2016
In uncovering a compound's potential anti-aging properties, researchers reveal a fascinating result of the co-evolution of plants, bacteria, and animals over millions of years. They show the compound enables muscle cells in animals to protect themselves against one of the major causes of aging. The compound - called urolithin A - is naturally produced in the gut when a molecule that is present in pomegranates is digested by intestinal bacteria.

Tests of urolithin A's effect in humans are not yet complete, say researchers from the École Polytechnique Fédérale in Lausanne (EPFL), Switzerland, who report promising results from studies using nematodes and rodents in the journal Nature Medicine.

Det har vært mange påstander om de helsemessige fordelene av granatepler - inkludert deres antatte anti-aging egenskaper. Men forfatterne oppmerksom på at mangel på bevis - pluss kontroversiell markedsføring - har ført til mye skepsis. Så bestemte de seg for å ta en nærmere titt. (There have been many claims about the health benefits of pomegranates - including their supposed anti-aging properties. However, the authors note that a lack of conclusive evidence - plus controversial marketing - has led to much skepticism. So they decided to take a closer look.)

As we age, an important process that our cells rely on for energy slows down and begins to malfunction. This process - called "mitophagy" - recycles worn-out mitochondria, the tiny powerhouses inside cells that make the chemical units of energy that fuel their work.

Dersom utslitte mitokondrier ikke blir resirkulert, bygger de og deres oppløste komponenter seg opp inne i cellene, og etter hvert forårsaker problemer i mange vev, inkludert muskler, som gradvis blir svakere. (If worn-out mitochondria are not recycled, they and their decomposing components build up inside cells, eventually causing problems in many tissues, including muscle, which gradually becomes weaker.)

There is also evidence that build-up of faulty or worn-out mitochondria plays a role in the diseases of aging, such as Parkinson's disease. Scientists have also found that defects in the Parkinson's gene Fbxo7 also disrupt mitophagy. (…)

(Anm: Regular exercise may help muscle repair in older adults The study, from McMaster University in Hamilton, Ontario, Canada, was published in The FASEB Journal. (medicalnewstoday.com 20.6.2016).)

(Anm: Get to Know Your Lymph Nodes (webmd.com 18.5.2016).)

- Hypoksiterapi - et nytt håp for behandling av mitokondrielle dysfunksjoner.

Hypoxia therapy--a new hope for the treatment of mitochondrial dysfunctions.
Med Gas Res. 2016 Oct 14;6(3):174-176.
Abstract Mitochondrial dysfunctions are characteristic features of numerous diseases and play a critical role in disease pathogenesis. Despite intensive research in this area, there are no approved therapies that directly target mitochondria. Recently a study by Jain et al. from Massachusetts General Hospital, USA reported the effectiveness of hypoxia for treatment of mitochondrial disease in mice. In this commentary, we summarized the potential mechanisms underlying the therapeutic effects of hypoxia on mitochondrial dysfunction, and clinical limitations of hypoxia as a therapy for human patients. We hope that our concerns will be helpful for further clinical studies addressing moderate hypoxia in mitochondrial dysfunction. (…)

(Anm: Hypoxia. Hypoksi (av hypo- og oksygen), tilstand hvor organismen, eller deler av den, får for lite oksygen. Hypoksi kan f.eks. skyldes at den luft (eller gassblanding) som pustes inn, ikke inneholder nok oksygen eller at den innpustede luft ikke i stor nok grad kommer frem til de fine lungeblærene (lungealveolene). Kilde: Store norske leksikon.)

(Anm: Exercise Training Alleviates Hypoxia-induced Mitochondrial Dysfunction in the Lymphocytes of Sedentary Males. Abstract This study elucidates how interval and continuous exercise regimens affect the mitochondrial functionality of lymphocytes under hypoxic stress. (…) Thus, we concluded that either HIIT or MICT effectively improves lymphocyte mitochondrial functionality by enhancing oxidative phosphorylation and suppressing oxidative damage under hypoxic conditions. Sci Rep. 2016 Oct 12;6:35170.)

(Anm: Antibiotika (tarmbakterier, probiotika, mikrobiota etc.) (Dysbiose; dysbiosis (also called dysbacteriosis (dysbakteriose)). (mintankesmie.no).)

(Anm: Signaler fra tarmens mikrobiotika til fjerntliggende organer mht. fysiologi og sykdom. (Signals from the gut microbiota to distant organs in physiology and disease.) (Nat Med. 2016 Oct 6;22(10):1079-1089.)

(Anm: - Hadde medisinerne på et tidligere tidspunkt hatt et evolusjonært perspektiv på sin medisinering, ville vi ikke vært i den kritiske situasjon vi er kommet i med hensyn til resistens. (aftenposten.no 22.8.2016).)

(Anm: Antibiotika kan gi flere kroniske sykdommer. (…) Folkehelseinstituttet: – Faren er underkommunisert. – Advarslene er høyst betimelige, sier lege og seniorforsker Merete Eggesbø ved Folkehelseinstituttet. (…) Ifølge Blaser viser ny forskning at det er en sammenheng mellom endringen av den naturlige tarmfloraen vår og utvikling av nye sykdommer som fedme, diabetes, astma,(...) Advarslene er høyst betimelige, sier lege og seniorforsker Merete Eggesbø ved Folkehelseinstituttet. (…) Ifølge Blaser viser ny forskning at det er en sammenheng mellom endringen av den naturlige tarmfloraen vår og utvikling av nye sykdommer som fedme, diabetes, astma, allergi, autisme og mageinfeksjoner. (nrk.no 30.10.2016).)

(Anm: Researchers explore link between gut microbiome and nutrition in autism spectrum disorder. (…) Sharon Donovan, a professor of nutrition at the University of Illinois explains that researchers have started to look at more specific disease states and the microbiome. "We are starting to see links with autism, obesity, diabetes, cardiovascular disease, and almost every disease that is looked at. (news-medical.net 28.4.2017).)

(Anm: Researchers discover new mechanism that causes chronic intestinal inflammation. Researchers at the University Medical Center of Johannes Gutenberg University Mainz and the German Research Center for Environmental Health, Helmholtz Zentrum München have discovered that too much of the oncogene Bcl-3 leads to chronic intestinal diseases. They describe in Nature Communications exactly how it throws the immune system off-balance. Chronic intestinal disorders such as ulcerative colitis and Crohn's disease are caused by the body's own immune defense system. (news-medical.net 28.5.2017).)

(Anm: Forsiktighet kreves ved samtidig forskrivning av antibiotika med psykofarmaka hos eldre pasienter. (…) Antibiotika har flere legemiddelinteraksjoner med psykofarmaka som kan føre til bivirkninger eller behandlingssvikt og betydelig øke kostnadene for behandlinger. (dgnews.docguide.com 3.4.2017).)

(Anm: Antibiotika associeras med högre risk för tarmcancer. (…) Det här är första studien som visar på sambandet mellan antibiotikaanvändning och utveckling av adenom i tjock- och ändtarmen. Studien publiceras i den vetenskapliga tidskriften Gut. (…) Resultatet visade att långvarig antibiotikaanvändning tidigare i livet, i åldern 20 till 59 år, hade samband med diagnostiserade adenom. (lakemedelsvarlden.se 5.4.2017.)

(Anm: Ny forskning viser hvor raskt bakterien blir motstandsdyktig mot antibiotika. E. coli bakterien muteres raskt i kraftig antibiotikadose. Forskere ved Harvard-universitetet har registrert hvor raskt E. coli bakterien klarer å bli motstandsdyktig og overleve antibiotika. I Harvards pressemelding står det at på ti dager overlevde bakterien en antibiotikadose som var 1000 ganger sterkere enn det som vanligvis dreper bakterien. (dagbladet.no 12.9.2016).)

(Anm: Prebiotika kan hjelpe å behandle anstrengelsesutløst astma (Prebiotics could help treat exercise-induced asthma) (medicalnewstoday.com 6.8.2016).)

(Anm: Mitokondriesyndrom. Mitokondriesykdommer er en gruppe sykdommer knyttet til forstyrrelser i cellenes energiproduksjon. Mitokontdriesykdom kan gi symptomer fra flere deler av kroppen. (helsenorge.no 18.2.2013).)

(Anm: Granateple er godt og sunt. Tidsskr Nor Lægeforen (28.12.2005).)

(Anm: Dag Kristen Solberg. Psykofarmakologisk avdeling Diakonhjemmet sykehus. Herlig, herlig – men farlig, farlig. Tidsskr Nor Lægeforen 2006; 126:638 (23.2.2006).)

(Anm: Risperdal (risperidone) (mintankesmie.no).)

(Anm: Bivirkninger av antipsykotika - Related Editorial (Relatert lederartikkel) (…) Bruken av antipsykotika innebærer en vanskelig avveining mellom nytte for å lindre psykotiske symptomer og noen ganger risikoen for problematiske bivirkninger som forkorter levetiden. (…) Alle antipsykotika er forbundet med en økt sannsynlighet for sedasjon, seksuell dysfunksjon, postural hypotensjon, hjertearytmi og plutselig hjertedød. (…) Antikolinerge effekter inkluderer forstoppelse, urinretensjon, tørr munn, uklart syn og, til tider, kognitiv svekkelse. Disse symptomene kan føre til andre problemer som tannforråtnelse, fall eller gastrointestinal obstruksjon. Am Fam Physician. 2010 Mar 1;81(5):617-622).)

(Anm: Antidepressiva (inkl. SSRI-preparater) og antipsykotika har skadelige effekter på mitokondrier (Mol Cell Biochem 1999;199:103-9).)

(Anm: Mitokondriell dysfunksjon ligger bak kognitive defekter som et resultat av nevral stamcelleutarmning og nedsatt neurogenese. Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis. Hum Mol Genet. 2017 Jun 8.)

(Anm: Adenosintrifosfat (ATP) er en energirik kjemisk forbindelse som er involvert i alle energikrevende prosesser i menneskekroppen, som muskelsammentrekning, overføring av signaler i nerver, oppbygging av proteiner, kopiering av arvestoffer med mer. (…) ATP kan oppfattes som en universell energileverandør i alle celler og vev. Livet ville ikke vært mulig uten ATP. Forbindelsen er blitt kalt «livets molekyl». Kilde: Store norske leksikon.)

- Mitokondriell dysfunksjon ved lungepatogenese.

Mitochondrial Dysfunction in Lung Pathogenesis.
Annu Rev Physiol. 2016 Dec 7. [Epub ahead of print]
Abstract Remarkable new roles for mitochondria in calcium handling, apoptosis, heme turnover, inflammation, and oxygen and nutrient sensing have been discovered for organelles that were once thought to be simple energy converters. Although deficits in mitochondrial function are often associated with energy failure and apoptosis, working cells maintain a mitochondrial reserve that affords the organelles distinct homeostatic-sensing and regulatory abilities in lung cells. As primary intracellular sources of oxidants, mitochondria serve as critical monitors and modulators of vital oxidation-reduction processes, including mitochondrial biogenesis, mitophagy, inflammasome activation, cell proliferation, and prevention of fibrosis. These processes participate in disease pathogenesis in all lung regions mainly when interference with mitochondrial quality control mechanisms impedes their roles in maintenance of lung health. Sharper identification of mitochondrial-driven signaling mechanisms in specific lung cell types will better refine our understanding of respiratory pathogenesis and lead to new diagnostic and therapeutic measures to support mitochondrial quality. Expected final online publication date for the Annual Review of Physiology Volume 79 is February 10, 2017. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates. Annu Rev Physiol. 2016 Dec 7. [Epub ahead of print].)

- Defekte mitokondrier og Alzheimers demens. (- Sammenheng mellom mitokondrieskade og nevrodegenerative sykdommer.)

Defekte mitokondrier og Alzheimers demens
Tidsskr Nor Legeforen 2016; 136:1074 (12.7.2016)
En defekt i et mitokondrielt protein fører til nevrodegenerasjon og bekrefter derved en forbindelse mellom mitokondrier og Alzheimers demens.

Det har lenge vært diskutert om det er en sammenheng mellom mitokondrieskade og nevrodegenerative sykdommer, men denne forbindelsen har vært vanskelig å bevise. En norsk studie, publisert i tidsskriftet EMBO Molecular Medicine, viser at en defekt i et mitokondrielt protein fører til både nevrodegenerasjon og opphopning av β-amyloid (1). (…)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose, til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis- the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.) (medicalnewstoday.com 19.3.2017).)

(Anm: Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? Are Mitochondria the Key to Cracking Parkinson’s Disease? European Medical Journal 2017 (Februar 20, 2017).)

(Anm: Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer's Disease. (…) The understanding of the role of mitochondrial dysfunction in synaptic stress may lead to novel therapeutic strategies for the treatment of AD through the protection of synaptic transmission by targeting to mitochondrial deficits.J Alzheimers Dis. 2016 Sep 20. [Epub ahead of print].)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Aging: it's SIRTainly possible to restore mitochondrial dysfunction. Abstract. Mitochondrial dysfunction is strongly associated with aging. A recent study shows that reduced nuclear SIRT1 activity initiates age-related mitochondrial decline through a signaling pathway that perturbs expression of genes encoded by mitochondrial DNA. This reversible pathway has potential anti-aging therapeutic value. Curr Biol. 2014 Mar 3;24(5):R206-8.)

(Anm: Unchecked mitochondrial DNA mutations could be a problem for stem cell therapies (medicalnewstoday.com 14.4.2016).)

(Anm: Three Alzheimer's genetic risk factors linked to immune cell dysfunction. People with a variant copy of the TREM2 gene have an increased risk of developing Alzheimer's disease, but researchers are only beginning to understand why. (medicalnewstoday.com 21.7.2016).)

(Anm: Pink Light on Mitochondria in Autoimmunity and Parkinson Disease. Abstract. Mitochondrial dysfunction and T cell autoimmunity have been independently implicated in Parkinson disease pathogenesis. In a recent publication in Cell, Matheoud et al. (2016) link them by describing a new mechanism, activated in familial forms of Parkinson disease, in which mitochondrial proteins are processed for recognition by CD8+ T cells. Cell Metab. 2016 Jul 12;24(1):11-2.)

- Kognitiv svekkelse linket til Parkinsons sykdom: Mitokondrienes rolle

Cognitive Impairment Associated with Parkinson's Disease: Role of Mitochondria.
Curr Neuropharmacol. 2016 Jan 4. [Epub ahead of print]
Abstract Parkinson's disease (PD) is a movement disorder and is associated with some of the intellectual disabilities like cognitive dysfunctions. PD associated cognitive dysfunctions have been proved well in both in preclinical and clinical set ups. Like other neurodegenerative diseases, insults to mitochondria have a significant role in the pathobiology of PD associated dementia (PDD). Neurotoxins like MPTP, mutations of the mitochondrial genes, oxidative stress, imbalanced redox mechanisms and dysregulated mitochondrial dynamics have been implicated in mitochondrial dysfunctions and have paramount importance in the pathobiology of PDD. However, the extent of contribution of mitochondrial dysfunctions towards cognitive deficits in PD has not been characterized completely. In this review we highlight on the contribution of mitochondrial dysfunction to PDD. We also highlight different behavioural tests used in both nonhuman primate and rodent models for assessing cognitive deficits and some common techniques for evaluation of mitochondrial dysfunction in PDD. (…)

(Anm: Systems biology analysis of the proteomic alterations induced by MPP+, a Parkinson's disease-related mitochondrial toxin. Front. Cell. Neurosci., 2015 (02 February 2015).)

(Anm: Gene therapy targeting mitochondrial pathway in Parkinson's disease. J Neural Transm (Vienna). 2016 Sep 16. [Epub ahead of print].)

(Anm: Parkinson's connection to faulty mitochondria investigated. (…) One marker that is always present in PD are Lewy bodies. (…) They demonstrated that the alpha-synuclein within Lewy bodies attaches to a protein called TOM20. (…) "The effects of alpha-synuclein on mitochondria are like making a perfectly good coal-fueled power plant extremely inefficient, so it not only fails to make enough electricity but also creates too much toxic pollution." (medicalnewstoday.com 10.6.2016).)

- Mitokondriell complex I-linket sykdom

Mitochondrial complex I-linked disease.
Biochim Biophys Acta. 2016 Jul;1857(7):938-45. Epub 2016 Feb 22
Abstract Complex I deficiency is the most frequently encountered single mitochondrial single enzyme deficiency in patients with a mitochondrial disorder. Although specific genotype-phenotype correlations are very difficult to identify, the majority of patients present with symptoms caused by leukodystrophy. The poor genotype-phenotype correlations can make establishing a diagnosis a challenge. The classical way to establish a complex I deficiency in patients is by performing spectrophotometric measurements of the enzyme in a muscle biopsy or other patient-derived material (liver or heart biopsy, cultured skin fibroblasts). Complex I is encoded by both the mtDNA and nuclear DNA and pathogenic mutations have been identified in the majority of the 44 genes encoding the structural subunits of complex I. In recent years, the increasing possibilities for diagnostic molecular genetic tests of large gene panels, exomes, and even entire genomes has led to the identification of many novel genetic defects causing complex I deficiency. Complex I mutations not only result in a reduced enzyme activity but also induce secondary effects at the cellular level, such as elevated reactive oxygen species production, altered membrane potential and mitochondrial morphology. At this moment there is no cure for complex I deficiency and the treatment options for complex I patients are restricted to symptomatic treatment. Recent developments, amongst others based on the treatment of the secondary effects of complex I deficiency, have shown to be promising as new therapeutic strategies in vitro and have entered clinical trials. This article is part of a Special Issue entitled Respiratory complex I, edited by Volker Zickermann and Ulrich Brandt. (…)

(Anm: Mitochondrial protein interactome elucidated by chemical cross-linking mass spectrometry  (…) These data established direct physical evidence of the assembly of the complex I–III respirasome and enabled prediction of in situ interfacial regions of the complexes. Finally, we established a database and tools to harness the cross-linked interactions we observed as molecular probes, allowing quantification of conformation-dependent protein interfaces and dynamic protein complex assembly. PNAS (Proceedings of the National Academy of Sciences) 2017 (January 24, 2017).)

(Anm: Scientists make significant anti-aging breakthrough. A breakthrough in understanding human skin cells offers a pathway for new anti-ageing treatments. (…) A study, published online in the Journal of Investigative Dermatology, has found that the activity of mitochondrial complex II significantly decreases in older skin. (…) Findings may also lead to a greater understanding of how other organs in the body age, which could pave the way for drug developments in a number of age-related diseases, including cancer. (medicalnewstoday.com 26.2.2016).)

(Anm: Mitochondria and Cancer. Mitochondria are bioenergetic, biosynthetic, and signaling organelles that are integral in stress sensing to allow for cellular adaptation to the environment. Therefore, it is not surprising that mitochondria are important mediators of tumorigenesis, as this process requires flexibility to adapt to cellular and environmental alterations in addition to cancer treatments. Multiple aspects of mitochondrial biology beyond bioenergetics support transformation, including mitochondrial biogenesis and turnover, fission and fusion dynamics, cell death susceptibility, oxidative stress regulation, metabolism, and signaling. Thus, understanding mechanisms of mitochondrial function during tumorigenesis will be critical for the next generation of cancer therapeutics.Cell. 2016 Jul 28;166(3):555-566).)

(Anm: Newly discovered proteins may protect against aging's illnesses. Tested in both mice and human cells and produced in the energy-producing mitochondria of cells, the proteins may lead to greater understanding of aging-related diseases from diabetes to Alzheimer's to cancer. (…) This latest finding builds upon prior research by Cohen and his team that uncovered two significant proteins, humanin and MOTS-c, hormones that appear to have significant roles in metabolism and diseases of aging. Unlike most other proteins, humanin and MOTS-c are encoded in mitochondria, the structure within cells that produces energy from food, instead of in the cell's nucleus where most genes are contained. (medicalnewstoday.com 12.4.2016).)

(Anm: Same immune-system proteins may first giveth, then taketh away motor control. (…) The researchers reported in the journal Brain, Behavior, and Immunity that proteins in the family MHCI, or major histocompatibility complex class I, "prune" the connections, or synapses, between motor neurons and muscle fibers (medicalnewstoday.com 12.4.2016).)

(Anm: Powering senescence: The ugly side of mitochondria. Cell Cycle. 2016 Jul 11:0. [Epub ahead of print].)

(Anm: Senescence, apoptosis or autophagy? When a damaged cell must decide its path--a mini-review. Many features of aging result from the incapacity of cells to adapt to stress conditions. When damage accumulates irreversibly, mitotic cells from renewable tissues rely on either of two mechanisms to avoid replication. They can permanently arrest the cell cycle (cellular senescence) or trigger cell death programs. Apoptosis (self-killing) is the best-described form of programmed cell death, but autophagy (self-eating), which is a lysosomal degradation pathway essential for homeostasis, reportedly contributes to cell death as well. Unlike mitotic cells, postmitotic cells like neurons or cardiomyocytes cannot become senescent since they are already terminally differentiated. The fate of these cells entirely depends on their ability to cope with stress. Autophagy then operates as a major homeostatic mechanism to eliminate damaged organelles, long-lived or aberrant proteins and superfluous portions of the cytoplasm. In this mini-review, we briefly summarize the molecular networks that allow damaged cells either to adapt to stress or to engage in programmed-cell-death pathways. Gerontology. 2008;54(2):92-9. Epub 2008 May 2.)

(Anm: Mitochondrial roles in disease: a box full of surprises EMBO Mol Med. 2015 Jul 20;7(10):1245-7. doi: 10.15252/emmm.201505350.)

- Alzheimers sykdom (AD) er en ødeleggende nevrodegenerativ lidelse preget av progressivt tap av kolinerge nevroner, som fører til utbrudd av alvorlig atferd, motorikk og kognitiv svekkelse.

Mitochondrial Dysfunction in Alzheimer's Disease and the Rationale for Bioenergetics Based Therapies.
Aging Dis. 2016 Mar 15;7(2):201-14. doi: 10.14336/AD.2015.1007. eCollection 2016.
Abstract Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by the progressive loss of cholinergic neurons, leading to the onset of severe behavioral, motor and cognitive impairments. It is a pressing public health problem with no effective treatment. Existing therapies only provide symptomatic relief without being able to prevent, stop or reverse the pathologic process. While the molecular basis underlying this multifactorial neurodegenerative disorder remains a significant challenge, mitochondrial dysfunction appears to be a critical factor in the pathogenesis of this disease. It is therefore important to target mitochondrial dysfunction in the prodromal phase of AD to slow or prevent the neurodegenerative process and restore neuronal function. In this review, we discuss mechanisms of action and translational potential of current mitochondrial and bioenergetic therapeutics for AD including: mitochondrial enhancers to potentiate energy production; antioxidants to scavenge reactive oxygen species and reduce oxidative damage; glucose metabolism and substrate supply; and candidates that target apoptotic and mitophagy pathways to remove damaged mitochondria. While mitochondrial therapeutic strategies have shown promise at the preclinical stage, there has been little progress in clinical trials thus far. Aging Dis. 2016 Mar 15;7(2):201-14. doi: 10.14336/AD.2015.1007. eCollection 2016. (…)

 It is a pressing public health problem with no effective treatment. Existing therapies only provide symptomatic relief without being able to prevent, stop or reverse the pathologic process. While the molecular basis underlying this multifactorial neurodegenerative disorder remains a significant challenge, mitochondrial dysfunction appears to be a critical factor in the pathogenesis of this disease. It is therefore important to target mitochondrial dysfunction in the prodromal phase of AD to slow or prevent the neurodegenerative process and restore neuronal function. In this review, we discuss mechanisms of action and translational potential of current mitochondrial and bioenergetic therapeutics for AD including: mitochondrial enhancers to potentiate energy production; antioxidants to scavenge reactive oxygen species and reduce oxidative damage; glucose metabolism and substrate supply; and candidates that target apoptotic and mitophagy pathways to remove damaged mitochondria. While mitochondrial therapeutic strategies have shown promise at the preclinical stage, there has been little progress in clinical trials thus far. . (…)

(Anm: - Antikolinerge effekter av vanlige legemidler knyttet til økt dødelighet (BMJ 2011; 342:d4037 (28 June).)

(Anm: Drugs on the Anticholinergic Burden (ACB) scale. (A total ACB scale score of three or more is considered clinically relevant) (uea.ac.uk).)

(Anm: Anticholinergic Medication Use and Cognitive Impairment in the Older Population: The Medical Research Council Cognitive Function and Ageing Study. Journal of the American Geriatrics Society 2011 (24 JUN).)

(Anm: Worsening Depression Linked to Higher Dementia Risk. —Ongoing study finds 'worsening' trajectory the only one tied to dementia. (…) "Indeed, depressive symptoms might appear as a reaction to underlying subclinical cognitive impairment, and lie in a continuum between subclinical cognitive impairment and overt dementia," they wrote. (medpagetoday.com 1.5.2016).)

(Anm: Cerebrovascular disease linked to Alzheimer's. While strokes are known to increase risk for dementia, much less is known about diseases of large and small blood vessels in the brain, separate from stroke, and how they relate to dementia. Diseased blood vessels in the brain itself, which commonly is found in elderly people, may contribute more significantly to Alzheimer's disease dementia than was previously believed, according to new study results published in June in The Lancet Neurology, a British medical journal.  (medicalxpress.com 1.7.2016).)

- Mitokondriell dysfunksjon: moderne aspekter av behandlingen (GJENNOMGANG)]

[MITOCHONDRIAL DYSFUNCTION: MODERN ASPECTS OF THERAPY (REVIEW)].
Georgian Med News. 2015 Jul-Aug;(244-245):78-84.
Abstract Mitochondrial diseases are considered as one of the major problems of modern interdisciplinary neonatology and pediatrics. Mitochondrial pathology can be revealed as refractory myoclonic or multifocal seizures, craniofacial dysostosis, dysmetabolic manifestations and respiratory disorders. Central nervous system (CNS), muscles, heart, liver and kidneys is involved in this pathological process. An important criterion for diagnosis of mitochondrial dysfunction is increases in blood lactate and pyruvate levels; the absolute criterion - molecular genetic diagnostic studies of mitochondrial DNA. Polymorphism of clinical symptoms complicates the process of early diagnostics, the lack clear recommendations complicates therapy. Modern aspects of treatment of mitochondrial dysfunction in various neurological syndromes are based primarily in improving the efficiency of the processes of oxidative phosphorylation at the system level. Dietary carbohydrate restriction, and medication (Coenzyme Q10, Idebenonum, Cofactors, drugs which reduce lactic acidosis- Dimephosphon, Dichloroacetate, Antioxidants, Anticonvulsants and Antidiabetic agents, vitamins C, E, K, hemotransfusions) is prescribed. Such complex approach allows us to achieve a reduction in lactate-acidosis, and improve the condition of patients in 70% of cases. (…)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose, til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis- the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.) (medicalnewstoday.com 19.3.2017).)

(Anm: Vitamins - Building the Body and Fighting Disease. Get your vitamins. Who has not heard the words "You need your vitamins!" as a child? Vitamins help us grow up healthy and strong, so our parents told us, as they recited the vitamins' own peculiar version of the alphabet, which starts with 'A', and has a letter (sometimes with a number) to represent each of these essential nutrients. The Nobel Prize has acknowledged the importance of vitamins by awarding the seven scientists below. Several Nobel Laureates who have been awarded for other achievements have also performed research on the substances that continue to be as vital to our health today as they were hundreds of years ago. Read about some important breakthroughs in vitamin research (nobelprize.org).)

(Anm: Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? Are Mitochondria the Key to Cracking Parkinson’s Disease? European Medical Journal 2017 (Februar 20, 2017).)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Mitokondriesyndrom. Mitokondriesykdommer er en gruppe sykdommer knyttet til forstyrrelser i cellenes energiproduksjon. Mitokontdriesykdom kan gi symptomer fra flere deler av kroppen. (helsenorge.no 18.2.2013).)

- The Antidepressant Sertraline (Zoloft) Targets Intracellular Vesiculogenic Membranes in Yeast

The Antidepressant Sertraline Targets Intracellular Vesiculogenic Membranes in Yeast.
Genetics. 2010 May 10. [Epub ahead of print]
Abstract Numerous studies have shown that the clinical antidepressant sertraline (Zoloft((R))) is biologically active in model systems, including fungi, which do not express its putative protein target, the serotonin/5-HT transporter, thus demonstrating the existence of one or more secondary targets. Here we show that in the absence of its putative protein target, sertraline targets phospholipid membranes that comprise the acidic organelles of the intracellular vesicle transport system by a mechanism consistent with the bilayer couple hypothesis. Based on a combination of drug-resistance selection and chemical-genomic screening, we hypothesize that loss of vacuolar ATPase activity reduces uptake of sertraline into cells, whereas dysregulation of clathrin function reduces the affinity of membranes for sertraline. Remarkably, sub-lethal doses of sertraline stimulate growth of mutants with impaired clathrin function. Ultrastructural studies of sertraline-treated cells revealed a phenotype that resembles phospholipidosis induced by cationic amphiphilic drugs in mammalian cells. Using reconstituted enzyme assays, we also demonstrated that sertraline inhibits phospholipase A1 and phospholipase D, exhibits mixed effects on phospholipase C and activates phospholipase A2. Overall, our study identifies two evolutionarily conserved membrane-active processes-vacuolar acidification and clathrin-coat formation-as modulators of sertraline's action at membranes. (...)

(Anm: Antidepressants encounter autophagy in neural cells..Autophagy. 2011 Oct;7(10):1247-8. Epub 2011 Oct 1.)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Effekten av tramadol, klonazepam og deres kombinasjoner på hjernens mitokondrielle komplekser. (Effects of tramadol, clonazepam, and their combination on brain mitochondrial complexes.) (…) Dette resultatet forklarer de kliniske og deres respektive histopatologiske effekter av tramadol, for eksempel anfall og røde nevroner (markør for apoptose). (The results showed that groups that received tramadol (therapeutic and abuse) suffered from weight loss.) (Toxicol Ind Health. 2015 Dec;31(12):1325-33).)

(Anm: Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR. Semin Cancer Biol. 2017 May 9. pii: S1044-579X(17)30125-6. [Epub ahead of print].)

- Mitokondriell dysfunksjon i okulær sykdom: Fokus på glaukom

Mitochondrial dysfunction in ocular disease: Focus on glaucoma.
Mitochondrion. 2017 May 9. pii: S1567-7249(17)30128-9. doi: 10.1016/j.mito.2017.05.004. [Epub ahead of print]
Abstract Mitochondrial dysfunction commonly presents with ocular findings as a part of a systemic disorder. These ophthalmic manifestations can be the first sign of a mitochondrial abnormality, which highlights the key role of a comprehensive ophthalmic assessment. On the other hand, a number of visually disabling genetic and acquired eye diseases with no curative treatment show abnormal mitochondrial function. Recent advances in mitochondrial research have improved our understanding of previously unexplained ocular disorders utilising better diagnostic approaches. Further studies on mitochondrial dysfunction and novel modalities of treatment will help to improve outcomes of these conditions. In this review article we discuss the clinical picture of common mitochondrial-related eye diseases, diagnostic approaches and possible treatment options including a very recent interesting report about gene therapy, with a particular focus on glaucoma. (…)

(Anm: Simple eye test can diagnose early signs of glaucoma. (…) Results of first clinical trials with glaucoma patients are published today (28/04/17) in the journal BRAIN. (…) The technique developed is called DARC, which stands for detection of apoptosing retinal cells. (news-medical.net 27.4.2017).)

(Anm: Antidepressiva (øyesykdommer). (mintankesmie.no).)

(Anm: High Glucose Induces Mitochondrial Dysfunction in Retinal Müller Cells: Implications for Diabetic Retinopathy. (…) Conclusions: Findings indicate that HG-induced mitochondrial morphology changes and subsequent mitochondrial dysfunction may contribute to retinal Müller cell loss associated with diabetic retinopathy. Invest Ophthalmol Vis Sci. 2017 Jun 1;58(7):2915-2921.)

(Anm: Antibiotika kan utløse mitokondriell dysfunksjon som induserer psykiatriske lidelser. (Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders. Med Sci Monit. 2017 Jan 7;23:101-106.)

(Anm: Mitochondrial Complex 1 Activity Measured by Spectrophotometry Is Reduced across All Brain Regions in Ageing and More Specifically in Neurodegeneration.PLoS One. 2016 Jun 22;11(6):e0157405.)

(Anm: Acute ketamine impairs mitochondrial function and promotes superoxide dismutase activity in the rat brain. (…) CONCLUSIONS: Acute ketamine administration impaired the function of mitochondrial complex I leading to increased mtNOS activity, increased generation of hydrogen peroxide and NO, resulting in superoxide dismutase triggering, and improved antioxidant activity. The present findings clarify the role of NO modulation in ketamine anesthesia, providing new data on a relevant clinical mechanism. Anesth Analg. 2015 Feb;120(2):320-8.)

(Anm: Depresjonsstudie på Ketamin- trukket tilbake etter granskning ved Yale. Ketamine-depression paper retracted following investigation at Yale. A psychiatry journal has retracted a 2011 paper exploring the use of ketamine to treat patients with severe depression following an investigation at Yale University. According to the retraction notice, Yale determined that the paper, published in the International Journal of Neuropsychopharmacology, did not accurately describe the research. But the study’s lead author, Gregory Larkin, says he believes the retraction “is wholly unnecessary, serving neither patients nor science.” (retractionwatch.com 28.8.2017).)

(Anm: Ketamine-Induced Toxicity in Neurons Differentiated from Neural Stem Cells. Mol Neurobiol. 2015 Oct;52(2):959-69. Epub 2015 Jun 9.)

(Anm: PYRUVATE (webmd).)

(Anm: Pyruvat dehydrogenase mangel (Pyruvate Dehydrogenase Deficiency) (rarelink.no).)

(Anm: UiB-forskning: ME-syke har defekt i stoffskiftet. Forskere ved Universitetet i Bergen er ett skritt nærmere forklaring på ME-gåten. (…) Cellene våre benytter normalt karbohydrater, fett og protein (aminosyrer) som energikilder. Dette forbrennes i mitokondriene, som kalles cellenes kraftverk. Når vi trener hardt, får ikke mitokondriene i musklene nok oksygen og det dannes melkesyre. Et spesielt enzym spiller en viktig rolle for cellenes evne til å forbrenne karbohydrater. Akkurat dette enzymet, som heter pyruvat dehydrogenase (PDH), er hemmet i ME-pasienter, noe som kan forklare både energimangel og økt melkesyreproduksjon. Når PDH-enzymet ikke fungerer optimalt, går kroppen løs på andre energikilder i stedet for sukker. Nivået av aminosyrer i cellene blir derfor lavere. Cellene blir også dårligere til å justere forbrenningen ut fra energibehov. (bt.no 1.1.2017).)

(Anm: Magnesium, terapi. Magnesium er et viktig mineral i kroppen. Hos noen personer kan det oppstå situasjoner med magnesiummangel. (…) Magnesium er det fjerde hyppigst forekommende mineralet i kroppen1. Det er fordelt med ca. halvparten i skjelettet og den andre halvparten i muskulatur og annet bløtvev. Mindre enn 1% finnes i blodet. (…) Magnesiums rolle i kroppen. Magnesium deltar i mer enn 300 ulike metabolske reaksjoner i kroppen4-5. Disse prosessene inkluderer proteinsyntese, produksjon og lagring av celleenergi, cellevekst og reproduksjon, DNA og RNA syntese og stabilisering av mitokondrienes membraner6-7. (nhi.no 28.4.2014).)

(Anm: Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells. BACKGROUND: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. (…) CONCLUSION: These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance. BMC Neurosci. 2017 Jan 19;18(1):15.)

(Anm: The Use of Antioxidants in the Treatment of Traumatic Brain Injury. AIMS: To discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. (…) CONCLUSION: The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury. J Adv Nurs. 2017 Jan 19. [Epub ahead of print].)

- Soppdrepende legemiddel knyttet til legemiddelindusert hjertesykdom. (- Mitokondriell legemiddelindusert sykdom.)

Antifungal-Associated Drug-Induced Cardiac Disease. (Soppdrepende legemiddel knyttet til legemiddelindusert hjertesykdom)
Clin Infect Dis. 2015 Dec 1;61 Suppl 6:S662-8.
Abstract The etiology of cardiomyopathies are classified into 4 main groupings (dilated, hypertrophic, restrictive, and idiopathic) and can be mechanistically caused by myocarditis, conduction abnormalities, focal direct injury, or nutritional deficiency. Based on our review of this topic, evidence suggests that echinocandin-related cardiac dysfunction is a mitochondrial drug-induced disease caused by focal direct myocyte injury. With caspofungin or anidulafungin administration into the heart via central line, exposure is likely extreme enough to induce the acute toxicity. Chronic or low-dose exposure may lead to hypertrophic cardiomyopathy; however, only acute exposures have been explored to date. (…)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Effekten av tramadol, klonazepam og deres kombinasjoner på hjernens mitokondrielle komplekser. (Effects of tramadol, clonazepam, and their combination on brain mitochondrial complexes.) (…) Dette resultatet forklarer de kliniske og deres respektive histopatologiske effekter av tramadol, for eksempel anfall og røde nevroner (markør for apoptose). (The results showed that groups that received tramadol (therapeutic and abuse) suffered from weight loss.) (Toxicol Ind Health. 2015 Dec;31(12):1325-33).)

(Anm: Antibiotika kan utløse mitokondriell dysfunksjon som induserer psykiatriske lidelser. (Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders. Med Sci Monit. 2017 Jan 7;23:101-106.)

(Anm: Mitochondrial Dynamics: Coupling Mitochondrial Fitness with Healthy Aging. Aging is associated with a decline in mitochondrial function and the accumulation of abnormal mitochondria. However, the precise mechanisms by which aging promotes these mitochondrial alterations and the role of the latter in aging are still not fully understood. Mitochondrial dynamics is a key process regulating mitochondrial function and quality. Altered expression of some mitochondrial dynamics proteins has been recently associated with aging and with age-related alterations in yeast, Caenorhabditis elegans, mice, and humans. Here, we review the link between alterations in mitochondrial dynamics, aging, and age-related impairment. We propose that the dysregulation of mitochondrial dynamics leads to age-induced accumulation of unhealthy mitochondria and contributes to alterations linked to aging, such as diabetes and neurodegeneration. Trends Mol Med. 2017 Feb 7. pii: S1471-4914(17)30003-5.)

(Anm: Drug-induced mitochondrial dysfunction and cardiotoxicity. Am J Physiol Heart Circ Physiol. 2015 Sep 18:ajpheart.00554.2015. [Epub ahead of print].)

(Anm: A mitochondria-targeted antioxidant can inhibit peroxidase activity of cytochrome c by detachment of the protein from liposomes. FEBS Lett. 2016 Jul 21.)

(Anm: PET Imaging of Mitochondrial Complex I with 18F-BCPP-EF in Brain of Parkinson's Disease Model Monkey. (…) CONCLUSION: 18F-BCPP-EF has potential as a PET probe for the quantitative imaging of MC-1 damage in the living brains of PD model monkeys using PET. J Nucl Med. 2016 Feb 11. pii: jnumed.115.169615. [Epub ahead of print].)

(Anm: The Emerging Role of Mitochondrial Targeting in Kidney Disease. (…) This chapter provides an overview of the involvement of mitochondrial dysfunction in renal disease and summarizes the current knowledge on mitochondria-targeted strategies to attenuate renal disease. Handb Exp Pharmacol. 2016 Jun 18. [Epub ahead of print].)

(Anm: Parkinson's connection to faulty mitochondria investigated. (…) One marker that is always present in PD are Lewy bodies. (…) They demonstrated that the alpha-synuclein within Lewy bodies attaches to a protein called TOM20. (…) "The effects of alpha-synuclein on mitochondria are like making a perfectly good coal-fueled power plant extremely inefficient, so it not only fails to make enough electricity but also creates too much toxic pollution." (medicalnewstoday.com 10.6.2016).)

(Anm: Leder i Mitokondrieforenigen. Anne Hansen Når livskraften svikter. Ny behandling kan hindre en genetisk arvelig sykdom som påfører barn smerte, lidelse og tidlig død. Men metoden er forbudt i Norge. (…) Norge sier nei. Bioteknologirådet sier nei, med unntak av ett medlem. Se også reportasjen i NRK Nett-TV: Magnus (11) lever på overtid. (nrk.no 21.5.2016).)

(Anm: Mitochondrial Transplantation Attenuates Airway Hyperresponsiveness by Inhibition of Cholinergic Hyperactivity. Theranostics. 2016 May 24;6(8):1244-60. doi: 10.7150/thno.13804. eCollection 2016.)

(Anm: Mitochondrial functions in stem cells. Curr Opin Genet Dev. 2016 Jun 4;38:110-117. [Epub ahead of print].)

- Mitokondrielt DNA, mitokondriell dysfunksjon og hjertemanifestasjoner.

Mitochondrial DNA, mitochondrial dysfunction, and cardiac manifestations.
Front Biosci (Landmark Ed). 2016 Jun 1;21:1410-26.
Abstract Mitochondria, the powerhouses of cells, have their own DNA (mtDNA). They regulate the transport of metabolites and ions, which determine cell physiology, survival, and death. Mitochondrial dysfunction, including impaired oxidative phosphorylation, preferentially affects heart function via imbalance of energy supply and demand. Recently, mitochondrial mutations and associated mitochondrial dysfunction were suggested as a causal factor of cardiac manifestations. Oxidative stress largely influences mtDNA stability due to oxidative modifications of mtDNA. Furthermore, the continuous replicative state of mtDNA and presence of minimal nucleoid structure render mitochondria vulnerable to oxidative damage and subsequent mutations, which impair mitochondrial functions. However, the occurrence of mtDNA heteroplasmy in the same mitochondrion or cell and presence of nuclear DNA-encoded mtDNA repair systems raise questions regarding whether oxidative stress-mediated mtDNA mutations are the major driving force in accumulation of mtDNA mutations. Here, we address the possible causes of mitochondrial DNA mutations and their involvement in cardiac manifestations. Current strategies for treatment related to mitochondrial mutations and/or dysfunction in cardiac manifestations are briefly discussed. (…)

(Anm: The Mitochondrial Basis of Aging. Mol Cell. 2016 Mar 3;61(5):654-666.)

(Anm: Akutt hjerteinfarkt og mitokondrielt DNA. Mitokondrielt DNA kan detekteres i blodstrømmen etter hjerteinfarkt og kan utløse potensielt skadelig immunreaksjon i hjertet. Tidsskr Nor Legeforen 2016; 136:648 (19.4.2016).)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose, til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis- the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.) (medicalnewstoday.com 19.3.2017).)

(Anm: Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? Are Mitochondria the Key to Cracking Parkinson’s Disease? European Medical Journal 2017 (Februar 20, 2017).)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Mitochondria: "Mood Altering Organelles" that Impact Disease Throughout the Nervous System. Curr Neurovasc Res. 2015 Aug 7. [Epub ahead of print].)

(Anm: RE: Psykisk syke lever kortere. Tidsskr Nor Legeforen Tidsskr Nor Legeforen 2015; 135:246 – 8 (8.09.2015).)

(Anm: RE: Psykisk syke lever kortere. Tidsskr Nor Legeforen 2015; 135:1534 – 5 (22.9.2015).)

(Anm: RE: Psykisk syke lever kortere. Tidsskr Nor Legeforen Tidsskr Nor Legeforen 2015; 135:1923-4 (17.11.2015).)

(Anm: Uriktig fremstilling av skader i studier på antidepressiva. Nye bevis fra kliniske studierapporter avdekker feilklassifisering, feiltolkning, og underrapportering av alvorlige skader. BMJ 2016;352:i217 (Published 28 January 2016).)

(Anm: Offentligt betalte forskere pynter på resultater af forsøg på mennesker. (videnskab.dk 14.3.2016).)

(Anm: Helsevesenet bruker ikke ny forskning. Norske pasienter får medisiner og behandling de ikke har bruk for fordi nye forskningsresultater ikke tas i bruk. Større problem enn unyttig forskning, mener eksperter. (forskning.no 2.1.2016).)

(Anm: Forvaltningsmakt og kunnskapspolitikk. Sammendrag. Helse- og omsorgsdepartementet benekter at de ønsker å styre forskninga i underliggende etater, og ser ingen problemer med at forskninga ligger under forvaltninga. Rus & Samfunn 05 / 2016 (Volum 9) Side: 33-35.)

(Anm: Frie forskere eller maktens lakeier? Abstrakt. Det går et skisma gjennom den samfunnsvitenskapelige rusforskningen. Ved første øyekast er det vanskelig å forstå hvorfor. Rus & Samfunn 05 / 2016 (Volum 9) Side: 36-40.)

(Anm: Lederartikler (Editorials) Tid for kunnskapsbasert forskningspolitikk Og offentlig finansierte forskere må være åpne om den sannsynlige betydningen av forskningen. (Time for evidence based research policy. And publicly funded researchers need to be candid about the likely impact of research). BMJ 2016;353:i3146 (Published 13 June 2016).)

(Anm: Kronikk: Kari Sollien, leder i allmennlegeforeningen. Hvorfor bruker ikke kommunene legenes kunnskap? Kunnskap skal redde velferdsstaten. I kommunene har ledelsen en lang vei å gå for å involvere helsepersonell i arbeidet med å utvikle helsetjenesten. (dagensmedisin.no 15.8.2016).)

(Anm: Leger ivaretar din mentale helse, men hvem ivaretas deres? (Doctors look after our mental health but who looks after theirs?) (theconversation.com 26.4.2016).)

(Anm: Dorothea Dix: Redefining mental illness. During the 19th century, mental health disorders were not recognized as treatable conditions. They were perceived as a sign of madness, warranting imprisonment in merciless conditions. One woman set out to change such perceptions: Dorothea Lynde Dix. (…) Dix - a teacher and nurse during the American Civil War - tirelessly campaigned for the fair treatment of patients with mental health disorders, after being appalled by the conditions in which they were confined. (medicalnewstoday.com 5.5.2017).)

(Anm: Tor K. Larsen, professor i psykiatri, Stavanger universitetssykehus: - Den valgfriheten som helseministeren nå ønsker å påtvinge helsevesenet vil føre til at mange svært alvorlig syke mennesker i praksis fratas retten til best mulig behandling. Innføring av medikamentfrie poster i psykiatrien er et gigantisk feilgrep. (dagensmedisin.no 29.7.2016).)

(Anm: Tre av 60.000 studenter ble tvunget til å slutte. Medstudenter og lærere varsler for sjelden om personer som ikke egner seg til yrket de utdanner seg til, mener fagfolk. Studenter som skal jobbe med mennesker og sårbare grupper, bør ikke ha rusproblemer, psykiske problemer, dårlige kommunikasjonsevner eller holdninger som ikke er forenlig med yrket. (aftenposten.no 18.8.2016).)

(Anm: - Hvorfor legers mentale helse bør være en bekymring for oss alle. (- Noen av de mer alarmerende resultater av å ha stressede og deprimerte leger er patologisk kynisme, en uvilje mot å ta vare på kronisk syke og redusert empati.)  (newstatesman.com 16.4.2016).)

(Anm: 27% of Medical Students Are Depressed. In the new research published in the Journal of the American Medical Association, researchers analyzed nearly 200 studies of 129,000 medical students in 47 countries. They found that 27% of medical students had depression or symptoms of it, and 11% reported suicidal thoughts during medical school. (time.com 10.12.2016).)

(Anm: LEDER. Ville du like å gå til en lege som er psykopat? Tidsskr Nor Legeforen 2008; 128:1805 (28.8. 2008).)

(Anm: Psychopathy of 1,800 prisoners leads to novel diagnostic tool for criminals and non-criminals alike (medicalnewstoday.com 12.8.2016).)

(Anm: Introduction and validation of Psychopathic Personality Traits Scale (PPTS) in a large prison sample. Conclusion. This brief measure of psychopathic traits uncontaminated with behavioral items can be used in the same way among participants with and without criminal history. Journal of Criminal Justice 2016;46: 9–17 (September 2016).)

(Anm: Mitochondrial involvement in myocyte death and heart failure. Heart Fail Rev. 2016 Feb 17. [Epub ahead of print].)

(Anm: Magnus (11) lever på overtid. (…) – Som mor må jeg se at barnet mitt må gå gjennom umenneskelige påkjenninger og smerter. Personlig synes jeg det hadde vært fint å ha muligheten til å være sikker på at barnet ikke får denne diagnosen, sier Anne Hansen. Hun har nettopp fått vite at Bioteknologirådet ikke ønsker å åpne for mitokondriedonasjon i Norge. (nrk.no 10.3.2016).)

(Anm: Leder, Bioteknologirådet. Kristin Halvorsen. Mitokondriedonasjon er komplisert. Det var ikke frykten for «supermennesker» som gjorde at flertallet i Bioteknologirådet stemte imot å tillate mitokondriedonasjon for å hindre sykdom. (nrk.no 27.5.2016).)

(Anm: Vil ikke blande gener fra tre personer. Friske mitokondrier fra en eggdonor kan hindre at livstruende sykdommer overføres fra mor til barn. Denne nye formen for assistert befruktning blir ikke tillatt i Norge. Ennå. (nrk.no 15.3.2016).)

(Anm: Mitochondrial Replacement Techniques - Implications for the Clinical Community. N Engl J Med. 2016 Mar 24;374(12):1103-1106. Epub 2016 Feb 24.)

(Anm: Effects of Air Pollution and Blood Mitochondrial DNA Methylation on Markers of Heart Rate Variability. BACKGROUND: (…)  The mtDNA damage induced by oxidative stress can cause mitochondrial dysfunction and is implicated in human diseases; however, mtDNA methylation has been largely overlooked in environmental studies relating to human disease. (…) CONCLUSIONS: Blood mtDNA methylation levels were negatively associated with PM2.5 exposure and modified the adverse relationships between PM2.5 exposure and heart rate variability outcomes.J Am Heart Assoc. 2016 Apr 22;5(4). pii: e003218.)

- MITOKONDRIELL DYSFUNKSJON VED DEPRESJON

MITOCHONDRIAL DYSFUNCTION IN DEPRESSION. (MITOKONDRIELL DYSFUNKSJON VED DEPRESJON)
Curr Neuropharmacol. 2016 Feb 28. [Epub ahead of print]
Mitokondriell dysfunksjon, en påkrevd faktor som spiller en nøkkelrolle i patofysiologien for ulike nevropsykiatriske sykdommer. Den temporale gåten om hvorvidt mitokondriell dysfunksjon aktiverer de ulike intracellulære kaskader som fører til økning av depressive symptomer forblir gåtefull. Det finnes bevis som viser seg å kunne være mitokondriell dysfunksjon i forskjellige hjerneområder som er knyttet til depresjon. Nylige funn har gitt fornyet innsikt i rollen til mitokondriene i mange intracellulære prosesser koblet til synaptisk plastisitet og cellulær elastisitet. Ved depresjon er forskjellige intracellulære prosesser oppregulert som følge av stress som er nært knyttet til overholdelse av energibehovet og metabolsk integritet for mitokondrier og til slutt cellestabilitet. Ny innsikt i patofysiologi ved depresjon dreier seg om svekkelse av nevroplastisitet. Mitokondrier har en potensiell rolle for ATP-produksjon, intracellulær Ca2 + signalering for å etablere membranstabilitet, reaktive oksygenarters (ROS) balanse og for å utføre de komplekse prosesser av nevrotransmisjon og plastisitet. Så forståelse av de ulike konsepter for mitokondriell dysfunksjon i patogenesen ved depresjon bidrar utvilsomt til nye og mer målrettede terapeutiske tilnærminger for depresjonsbehandling. (…) (Mitochondrial dysfunction, an imperative factor plays a key role in the pathophysiology of various neuropsychiatric diseases. The temporal conundrum of whether mitochondrial dysfunction activates the different intracellular cascades that leads to the exaggeration of depressive symptoms remains enigmatic. There are evidences showing that might be mitochondrial dysfunction in various brain regions are associated with the depression. Recent findings have sparked renewed appreciation for the role of mitochondria in many intracellular processes coupled to synaptic plasticity and cellular resilience. In depression various intracellular processes are up-regulated as a consequence of stress which intimately associated with the compliance of energy requirement and metabolic integrity by mitochondria and ultimately to cellular stability. New insights in depression pathophysiology are revolving around the impairment of neuroplasticity. Mitochondria has potential role in ATP production, intracellular Ca2+ signalling to establish membrane stability, reactive oxygen species (ROS) balance and to execute the complex processes of neurotransmission and plasticity. So understanding the various concepts of mitochondrial dysfunction in pathogenesis of depression indubitably helps to novel and more targeted therapeutic approaches for depression treatment.)

(Anm: Loss of Mitochondrial Function Impairs Lysosomes. J Biol Chem. 2016 Mar 17. pii: jbc.M115.695825. [Epub ahead of print].)

(Anm: ATP: The crucial component of secretory vesicles. Abstract. (…) To our knowledge, our data provide the first demonstration that ATP, in addition to serving as an energy source and purinergic transmitter, is an essential element in the concentration of catecholamines in secretory vesicles. In this way, cells can use ATP to accumulate neurotransmitters and other secreted substances at high concentrations, supporting quantal transmission. PNAS (Proceedings of the National Academy of Sciences) 2016 (May 20, 2016).)

(Anm: Ny, norsk forskning: Genfeil peker mot Alzheimers-løsning. (…) – Funnet vi har gjort er både spennende og viktig, fordi denne studien for første gang bekrefter at det faktisk er en sammenheng mellom mitokondrier og avleiringsprosesser i hjernen som er typisk for Alzheimer, sier professor Laurence A. Bindoffsom. (vg.no 1.4.2016).)

(Anm: Mitokondrienes funksjon i hjernen kobler angst med sosial underkastelse. (Mitochondrial function in the brain links anxiety with social subordination.) (…) These findings highlight a role for cerebral energy metabolism in social behavior and point to mitochondrial function in the nucleus accumbens as a potential marker and avenue of treatment for mood disorders. PNAS (Proceedings of the National Academy of Sciences) 2015;112(50):15486–15491.)

(Anm: Antidepressiva - deprimert, litt trist, angst, stresset eller utbrent? (mintankesmie.no).)

Transport på cellenivået. (…) Denne transporten skjer på spesielle transportvegar, såkalla mikrotubuli, ved hjelp av to energidrivne proteinmotorar av typen kinesin og dynein. Desse to transportørane ber bokstaveleg tala, på celleorganellar, medan dei går på mikrotubuli. Til og med mitokondria synest å bli transporterte på dette viset i cellene, i alle høve i nerveceller. Naturen 02 / 2016.)

- Mitokondrier ved lungesykdommer, hjertesykdom, Alzheimers sykdom, kreft etc.

Mitochondria in lung disease.
J Clin Invest. 2016 Mar 1;126(3):809-20. Epub 2016 Mar 1.
Abstract Mitochondria are a distinguishing feature of eukaryotic cells. Best known for their critical function in energy production via oxidative phosphorylation (OXPHOS), mitochondria are essential for nutrient and oxygen sensing and for the regulation of critical cellular processes, including cell death and inflammation. Such diverse functional roles for organelles that were once thought to be simple may be attributed to their distinct heteroplasmic genome, exclusive maternal lineage of inheritance, and ability to generate signals to communicate with other cellular organelles. Mitochondria are now thought of as one of the cell's most sophisticated and dynamic responsive sensing systems. Specific signatures of mitochondrial dysfunction that are associated with disease pathogenesis and/or progression are becoming increasingly important. In particular, the centrality of mitochondria in the pathological processes and clinical phenotypes associated with a range of lung diseases is emerging. Understanding the molecular mechanisms regulating the mitochondrial processes of lung cells will help to better define phenotypes and clinical manifestations associated with respiratory disease and to identify potential diagnostic and therapeutic targets. (…)

(Anm: Mitochondrial dysfunction in inflammatory responses and cellular senescence: pathogenesis and pharmacological targets for chronic lung diseases. Br J Pharmacol. 2016 May 17. [Epub ahead of print].)

(Anm: Sugar rush shrinks brain cell powerhouse. The spike in blood sugar levels that can come after a meal is controlled by the brain's neuronal mitochondria, which are considered the "powerhouse of cells," Yale School of Medicine researchers found in a new study. Published in the Feb. 25 issue of the journal Cell, the findings could provide a better understanding of how type 2 diabetes develops. (medicalnewstoday.com 26.2.2016).)

(Anm: Motion giver mental gevinst. (…) Regelmæssig træning øger antallet af mitokondrier i hjernecellerne hos mus. (videnskab.dk 28.9.2011).)

(Anm: Mitochondrial dysfunction in liver failure requiring transplantation. (…) Furthermore, improving mitochondrial function may be targeted as part of a complex therapy approach in different forms of liver diseases. J Inherit Metab Dis. 2016 Apr 6. [Epub ahead of print]).)

(Anm: Key brain receptor sheds light on neurological conditions, CU Anschutz researchers say. (…) For years, scientists believed that a special calcium permeable subtype of AMPA-type glutamate receptor only strengthened synapses, which send signals between brain cells. But Professor Mark Dell'Acqua, vice-chair of the Dept. of Pharmacology at the University of Colorado School of Medicine, and his team of researchers found that it also weakened synapses. (…) (medicalnewstoday.com 4.3.2016).)

(Anm: Ny, norsk forskning: Genfeil peker mot Alzheimers-løsning. (…) – Funnet vi har gjort er både spennende og viktig, fordi denne studien for første gang bekrefter at det faktisk er en sammenheng mellom mitokondrier og avleiringsprosesser i hjernen som er typisk for Alzheimer, sier professor Laurence A. Bindoffsom. (vg.no 1.4.2016).)

(Anm: Blocking transfer of calcium to cell's powerhouse selectively kills cancer cells. Inhibiting the transfer of calcium ions into the cell's powerhouse is specifically toxic to cancer cells, according to an article published this week in Cell Reports by researchers from the Perelman School of Medicine at the University of Pennsylvania. (medicalnewstoday.com 4.3.2016).)

(Anm: Stress pushes cells to die when gatekeeper of calcium use in mitochondria is dysfunctional. Search is now on for agent that can inhibit the calcium overload and cell death that causes damage during heart attacks and strokes. Malfunctioning mitochondria -- the power plants in cells -- are behind the damage caused by strokes, heart attacks, and neurodegenerative diseases, but little has been known about how to stop these reactors from melting down, destroying cells and tissue. Mitochondria also take up calcium, which regulates energy production. Now, online in Nature Communications, researchers at Thomas Jefferson University report important insights into how mitochondria are naturally protected against taking up too much calcium, which can force cells to die. (medicalnewstoday.com 9.3.2016).)

- Mitokondriell dysfunksjon: Et nytt terapeutisk mål i patologisk lungeremodulering eller tilskuer?

Mitochondria dysfunction: A novel therapeutic target in pathological lung remodeling or bystander?
Pharmacol Ther. 2016 Jul 1. pii: S0163-7258(16)30109-7. doi: 10.1016/j.pharmthera.2016.06.019. [Epub ahead of print]
Abstract The renascence in mitochondrial research has fueled breakthroughs in our understanding of mitochondrial biology identifying major roles in biological processes ranging from cellular oxygen sensing and regulation of intracellular calcium levels through to initiation of apoptosis or a shift in cell phenotype. Chronic respiratory diseases are no exception to the resurgent interest in mitochondrial biology. Microscopic observations of lungs from patients with chronic respiratory diseases such as pulmonary arterial hypertension, asthma and COPD show accumulation of dysmorphic mitochondria provide the first evidence of mitochondrial dysfunction in diseased lungs. Recent mechanistic insights have established links between mitochondrial dysfunction or aberrant biogenesis and the pathogenesis of chronic respiratory diseases through playing a causative role in structural remodeling of the lung. The aim here is to discuss the case for a mitochondrial basis of lung remodeling in patients with chronic respiratory diseases. The present article will focus on the question of whether currently available data supports mitochondrial mechanisms as a viable point of therapeutic intervention in respiratory diseases and suggestions for future avenues of research in this rapidly evolving field. (…)  

(Anm: Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics. Am J Physiol Heart Circ Physiol. 2016 Mar 4:ajpheart.00858.2015. doi: 10.1152/ajpheart.00858.2015. [Epub ahead of print].)

(Anm: Exercise-induced hormone irisin linked to new mechanisms for bone metabolism. Two weeks of voluntary wheel running induces higher expression of irisin - a fat-burning hormone that is released during exercise - in bone tissue in mice. In addition, systemic administration of irisin increased bone formation and thickness, mimicking the effects of exercise on the mouse skeletal system. The findings demonstrate a potential new mechanism for the regulation of bone metabolism. (medicalnewstoday.com 7.3.2017).)

(Anm: Infertility and recurrent miscarriage with complex II deficiency-dependent mitochondrial oxidative stress in animal models.Mech Ageing Dev. 2016 Mar 1. pii: S0047-6374(16)30018-5. doi: 10.1016/j.mad.2016.02.013. [Epub ahead of print].)

(Anm: Mitochondrial Regulation of the Muscle Microenvironment in Critical Limb IschemiaCritical limb ischemia (CLI) is the most severe clinical presentation of peripheral arterial disease and manifests as chronic limb pain at rest and/or tissue necrosis. Front. Physiol. 2016 (18 November 2015).)

(Anm: Critical limb ischemia (CLI), also referred to as limb threat, is an advanced stage of peripheral artery disease. It includes ischemic rest pain, arterial insufficiency ulcers, and gangrene. (en.wikipedia.org).)

(Anm: The Measurement of Reversible Redox Dependent Post-translational Modifications and Their Regulation of Mitochondrial and Skeletal Muscle Function. Front. Physiol. 2016 (25 November 2015).)

(Anm: Hypothesis on Skeletal Muscle Aging: Mitochondrial Adenine Nucleotide Translocator Decreases Reactive Oxygen Species Production While Preserving Coupling Efficiency. Front. Physiol. 2016 (16 December 2015).)

(Anm: Mitochondrial Bioenergetics and Fiber Type Assessments in Microbiopsy vs. Bergstrom Percutaneous Sampling of Human Skeletal Muscle. Front. Physiol. (18 December 2015).)

(Anm: Barth Syndrome: From Mitochondrial Dysfunctions Associated with Aberrant Production of Reactive Oxygen Species to Pluripotent Stem Cell Studies. Front. Genet. 2016 (20 January 2016).)

(Anm: Unchecked mitochondrial DNA mutations could be a problem for stem cell therapies (medicalnewstoday.com 14.4.2016).)

- Mitokodriesykdommer

Mitokodriesykdommer
nevro.legehandboka.no 17.11.2014
Se Frambu (senter for sjelden diagnoser) sine sider
Kort om
Mitokondriesykdommer er betegnelsen på en gruppe sykdommer knyttet til organismens energiomsetning ved forstyrrelser i mitokondrienes oxydative forsforylering (OXPHOS).

Som regel skyldes tilstandene genfeil i form av punktmutasjoner. Mutasjonen kan sitte i cellekjernens DNA-struktur (nDNA) eller i mitokondrienes eget arvestoff (mtDNA) som arves nesten utelukkende fra mor. Mutasjoner i mtDNA finnes sjeldnere hos barn enn hos voksne. Mitokondriefeilen trenger ikke finnes i alle vev/organer i samme grad. Sykdommen kan derfor komme til varierende uttrykk og risikoen for arv kan variere sterkt. Det kan også være vanskelig å finne mutasjonene i blodprøver.

Mitokondriesykdommer kan 

  • affisere alle vev 
  • presenteres i alle aldre
  • ha alle slags arvemønstre

Diagnostikk
Kliniske kjennetegn
Alle kroppens organer og funksjoner er avhengige av energi i vekslende grad og mitokondriesykdommer er karakterisert ved sammensatte sykdomsbilder fra flere organsystemer.

  • Muskelsystemet (myopati)
  • Hjertet (nedsatt slagkraft, redusert pumpeevne tross fortykket vegg)
  • CNS (encefalopati, ataxi, slagliknende episoder, myoklonus epilepsi)
  • PNS (polynevropati)
  • Syn (netthinneskade, optikusnevropati)
  • Øyemotoriske forstyrrelser
  • Hørsel (nevrogent hørselstap)
  • Muskel (svakhet)
  • Autonom svikt
  • Lever, pancreas, nyrer
  • Endokrine forstyrrelser (diabetes)
  • Benmarg (anemi) (…)

Supplerende undersøkelser
Diagnosen stilles på bakgrunn av de kliniske bildene kombinert med:

  • Markert forhøyet laktat i blod (kan ha mange årsaker) og/eller CSF og forhøyet ratio mellom laktat og puryvat (>25)
  • Abnorm utskillelse av organiske syrer i urinen Link til remisse
  • MR caput kan vise forandringer; hyperintense lesjoner lokalisert til basalganglier (særlig putamen), cerebellum, thalamus, medulla, leukodystrofiliknende foranndringer, kortikal eller cerebellar atrofi.
  • MR spektroskopi kan vise laktat topp i parenchym eller spinalvæske.
  • Muskelbiopsi. Mulige analyser:
  • Ragged red fibers
  • Spesialfarging for succinate dehydrogenase (SDH) og cytokrom c oxygenase (COX).
  • Elektronmikroskopi
  • Biokjemiske us
  • Gentest: Det finnes over 100 mutasjoner, og genetisk testing er en spesialistoppgave. Kfr Laurence Bindoff eller Rikshospitalet og se Norsk portal for Medisinske genetiske analyser .
  • Familiemedlem med overbevisende mitokondriesykdom

Undergrupper

Det pågår mye forskning på mitokondriesykdommer og listen over diagnoser som kommer inn under sykdomsgruppen øker stadig. Noen ganger regnes de samme diagnosene også med i andre sykdomsgrupper. (…)

(Anm: Legemiddelinduserte mitokondrielle skader og sykdom. (Medication-induced mitochondrial damage and disease.) (mintankesmie.no).)

(Anm: Laktat er et biprodukt av den kjemiske prosess som er kjent som glykolyse - å bryte ned av sukker eller glukose, til mindre molekyler med det formål å frembringe energi. Under intens fysisk aktivitet, akkumuleres laktat i vevet og blod, som noen ganger kan føre til dårligere fysisk ytelse og muskelstivhet. (Lactate is a byproduct of the chemical process known as glycolysis- the breaking down of sugar, or glucose, into smaller molecules with the purpose of producing energy. During intense physical activity, lactate accumulates in the tissue and blood, which can sometimes lead to poorer physical performance and muscle stiffness.) (medicalnewstoday.com 19.3.2017).)

(Anm: Er Mitokondrier nøkkelen til å finne en løsning på Parkinsons sykdom? Are Mitochondria the Key to Cracking Parkinson’s Disease? European Medical Journal 2017 (Februar 20, 2017).)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Mitokondriesyndrom. Mitokondriesykdommer er en gruppe sykdommer knyttet til forstyrrelser i cellenes energiproduksjon. Mitokontdriesykdom kan gi symptomer fra flere deler av kroppen. (helsenorge.no 18.2.2013).)

(Anm: Mitochondria affect stress responses. CHOP scientist: Cell's powerhouse plays role in mind-body interactions, with long-term health effects. Mitochondria, the tiny structures inside our cells that generate energy, may also play a previously unrecognized role in mind-body interactions. Based on new studies of stress responses, this insight may have broad implications for human psychology and for the biology of psychiatric and neurological diseases. A pioneering scientist in mitochondrial medicine has led research in animals showing how alterations in mitochondrial function lead to distinct physiological changes in hormonal, metabolic and behavioral systems in response to mild stress. (medicalnewstoday.com 3.12.2015).)

(Anm: Mitokondrienes funksjon i hjernen kobler angst med sosial underkastelse. (Mitochondrial function in the brain links anxiety with social subordination.) (…) These findings highlight a role for cerebral energy metabolism in social behavior and point to mitochondrial function in the nucleus accumbens as a potential marker and avenue of treatment for mood disorders. PNAS (Proceedings of the National Academy of Sciences) 2015;112(50):15486–15491.)

(Anm: Hardtrener syke hjerter. (…) Nitroglyserin med på fjelltur. (…) Tilstanden Angina Pectoris betyr smerter i brystet. Smertene kan også oppstå i skuldre og rygg når hjertet ikke får nok blod og oksygen, gjerne i sammenheng med fysisk anstrengelse. Tilstanden kan behandles, men operasjonen kan i seg selv gi skader. (…) Heldigvis kan mange hjertesyke få hjelp. Angina Pectoris er et symptom på at hjertemuskelen ikke får nok blod og oksygen. Det kan være en forløper til infarkt. (…) – Vi ønsker å se om vi kan få selve kraftverket i cellene, mitokondriene, til å fortsette å bruke energi fra oksygen også mens hjertet er stoppet. (nrk.no 15.1.2016).)

(Anm: Mitochondrial Quality Control as a Therapeutic Target. (…) The goals of such therapies extend beyond amelioration of energy insufficiency and tissue loss and entail cell repair, cell replacement, and the prevention of fibrosis. This review summarizes current concepts of mitochondria as disease elements and outlines novel strategies to address mitochondrial dysfunction through the stimulation of mitochondrial biogenesis and quality control. Pharmacol Rev. 2016 Jan;68(1):20-48.)

(Anm: Mitochondrial oxidative stress and dysfunction in arsenic neurotoxicity: A review. (…) The understanding of molecular mechanism of mitochondrial dysfunction may be helpful to develop therapeutic strategies against arsenic-induced neurotoxicity.J Appl Toxicol. 2015 Oct 29. [Epub ahead of print].)

(Anm: Role of mitochondria, ROS, and DNA damage in arsenic induced carcinogenesis. Front Biosci (Schol Ed). 2016 Jun 1;8:312-20.)

(Anm: Statlig legemiddelkontroll (Statens legemiddelverk etc.) (mintankesmie.no).)

(Anm: Statlig hvitvasking av legemiddelinformasjon (Tidsskr Nor Legeforen 2010; 130:368 (25.2.2010).)

(Anm: Forskning bliver farlig, når de negative resultater glemmes. (…) Nyt dansk studie viser problemet. (...) For få negative resultater leder til falske konklusioner. (…) Manglende negative resultater har kostet liv. (…) Vores model viser, at vi er nødt til at få publiceret mindst 20 procent af de negative resultater, der produceres inden for hvert forskningsfelt, hvis vi skal undgå at lave falske antagelser om videnskabelig fakta. (videnskab.dk 5.1.2017).)

(Anm: Legemiddelindustriens fortjeneste var nesten det dobbelte av utgifter til forskning og utvikling (FoU-utgifter) i 2013, 2014 og 2015. (Pharmaceutical Industry Profits Are Nearly Double R&D Costs in 2013, 2014 and 2015) (…) En primær unnskyldning som legemiddelindustrien bruker for «prisøkning» er de høye kostnadene for forskning og utvikling (FoU) som disse firmaene betaler for å få nye legemidler på markedet. (citizen.org 27.3.2017).)

- Dette skjoldet av patenter beskytter verdens bestselgende legemiddel.

(Anm: Dette skjoldet av patenter beskytter verdens bestselgende legemiddel. (- Produktet med 16 milliarder dollar i årsomsetning. (...) - Det har dessuten vært tilgjengelig i nærmere 15 år. (…) Den virkelige utfordringen var den tilsynelatende ugjennomtrengelige festningen av patenter som AbbVie metodisk har bygget rundt sin verdsatte pengemaskin. (…) Humira, som står for mer enn 60 prosent av AbbVies inntekter har en listepris på mer enn 50 000 dollar per pasient. (bloomberg.com 7.9.2017).)

(Anm: Myten om mediers åpenhet. Hvorfor er virkelig fordomsfri og frisinnet debatt uvanlig? Hvorfor så få nye, uavhengige meningsytrere? Hvorfor møter mediene dem dels med motstand, dels med taushet? (aftenposten.no 7.9.2006).)

(Anm: Er det en reproduserbarhetskrise i vitenskapelig forskning? (Is there a reproducibility crisis in science?) (…) Nyere studier, som undersøkte en rekke publiserte legemiddelstudier, klarte å gjenskape resultatene for mindre enn 25 % av dem - og tilsvarende resultater er blitt funnet i andre vitenskapelige disipliner. Hvordan bekjemper vi denne krisen for vitenskapelig ikke-reproduserbarhet? (ed.ted.com).)

(Anm: Spinn i randomiserte kontrollerte studier (RCT) på angstlegemidler (antidepressiva) med et positivt opprinnelig resultat: en sammenligning av bekymringer uttrykt av den amerikanske legemiddelkontrollen FDA og den publiserte litteratur. (Spin in RCTs of anxiety medication with a positive primary outcome: a comparison of concerns expressed by the US FDA and in the published literature.) BMJ Open. 2017 Mar 29;7(3):e012886.)

(Anm: LEGEMIDDELPENGER – FDA er avhengig av industrifinansiering; penger kommer «festet med strikk» (DRUG MONEY. FDA Depends on Industry Funding; Money Comes with “Strings Attached”) (pogo.org 1.12.2016).)

(Anm: LEGEMIDDELPENGER - I FDA-møter er "pasientstemmene" ofte finansiert av legemiddelfirmaer (DRUG MONEY - In FDA Meetings, "Voice" of the Patient Often Funded by Drug Companies) (pogo.org 3.12.2016).)

(Anm: Recommendations to improve adverse event reporting in clinical trial publications: a joint pharmaceutical industry/journal editor perspective. BMJ 2016;355:i5078 (Published 03 October 2016).)

(Anm: - Hadde medisinerne på et tidligere tidspunkt hatt et evolusjonært perspektiv på sin medisinering, ville vi ikke vært i den kritiske situasjon vi er kommet i med hensyn til resistens. (aftenposten.no 22.8.2016).)

(Anm: Antibiotika kan gi flere kroniske sykdommer. (…) Folkehelseinstituttet: – Faren er underkommunisert. – Advarslene er høyst betimelige, sier lege og seniorforsker Merete Eggesbø ved Folkehelseinstituttet. (…) Ifølge Blaser viser ny forskning at det er en sammenheng mellom endringen av den naturlige tarmfloraen vår og utvikling av nye sykdommer som fedme, diabetes, astma,(...) Advarslene er høyst betimelige, sier lege og seniorforsker Merete Eggesbø ved Folkehelseinstituttet. (…) Ifølge Blaser viser ny forskning at det er en sammenheng mellom endringen av den naturlige tarmfloraen vår og utvikling av nye sykdommer som fedme, diabetes, astma, allergi, autisme og mageinfeksjoner. (nrk.no 30.10.2016).)

(Anm: Researchers explore link between gut microbiome and nutrition in autism spectrum disorder. (…) Sharon Donovan, a professor of nutrition at the University of Illinois explains that researchers have started to look at more specific disease states and the microbiome. "We are starting to see links with autism, obesity, diabetes, cardiovascular disease, and almost every disease that is looked at. (news-medical.net 28.4.2017).)

(Anm: Researchers discover new mechanism that causes chronic intestinal inflammation. Researchers at the University Medical Center of Johannes Gutenberg University Mainz and the German Research Center for Environmental Health, Helmholtz Zentrum München have discovered that too much of the oncogene Bcl-3 leads to chronic intestinal diseases. They describe in Nature Communications exactly how it throws the immune system off-balance. Chronic intestinal disorders such as ulcerative colitis and Crohn's disease are caused by the body's own immune defense system. (news-medical.net 28.5.2017).)

(Anm: Forsiktighet kreves ved samtidig forskrivning av antibiotika med psykofarmaka hos eldre pasienter. (…) Antibiotika har flere legemiddelinteraksjoner med psykofarmaka som kan føre til bivirkninger eller behandlingssvikt og betydelig øke kostnadene for behandlinger. (dgnews.docguide.com 3.4.2017).)

(Anm: Antibiotika associeras med högre risk för tarmcancer. (…) Det här är första studien som visar på sambandet mellan antibiotikaanvändning och utveckling av adenom i tjock- och ändtarmen. Studien publiceras i den vetenskapliga tidskriften Gut. (…) Resultatet visade att långvarig antibiotikaanvändning tidigare i livet, i åldern 20 till 59 år, hade samband med diagnostiserade adenom. (lakemedelsvarlden.se 5.4.2017.)

(Anm: For mange retningslinjer for behandlinger er skrevet av eksperter med finansielle konflikter, viser studien. (statnews.com 22.8.2016).)

(Anm: Mange kliniske studier på barn forblir upubliserte eller uferdige. (Many pediatric clinical trials go unpublished or unfinished.) (- Selv om ulike statlige lover ble utformet for å fremme kliniske studier for å teste produkter på barn blir en bemerkelsesverdig stor mengde forskning enten ikke publisert eller ikke fullført, ifølge en ny studie.) (statnews.com 4.8.2016).)

- Toxic and Endocrine Myopathies.

Toxic and Endocrine Myopathies.
Continuum (Minneap Minn). 2016 Dec;22(6, Muscle and Neuromuscular Junction Disorders):1815-1828.
PURPOSE OF REVIEW: This article discusses the clinical features, pathophysiology, and management of toxic and endocrine myopathies.
RECENT FINDINGS: Early detection and expeditious correction of metabolic disturbances in endocrinopathies such as Cushing syndrome, thyroid and parathyroid diseases, and acromegaly can minimize and prevent neurologic complications including myopathy. Recently proposed mechanisms of injury in patients with critical illness myopathy include inhibition of protein synthesis, mitochondrial dysfunction, disruption of the ubiquitin-proteasome system, oxidative stress, and disruption of intramuscular calcium homeostasis, which can cause a myosin-loss myopathy. Mechanisms underlying toxic myopathies include myosin loss; damage to cellular structures, including myofibrils and organelles such as lysosomes and mitochondria; inflammation; and necrosis. Presentations range anywhere from acute, painful, and necrotic myopathies, as can occur in statin myopathy, to more insidious presentations such as steroid myopathy.

SUMMARY: Endocrinopathies known to cause myopathy include thyroid and parathyroid diseases, disorders of the adrenal axis such as Cushing syndrome, and acromegaly. Patients in the intensive care unit are at risk for developing critical illness myopathy, also known as myosin-loss myopathy, which should be considered if intensive care unit acquired weakness develops. The most common toxic agents associated with myopathy include statins and other lipid-lowering medications, corticosteroids, colchicine, amiodarone, hydroxychloroquine, and chloroquine. (…)

(Anm: Alvorlige bivirkninger skjules helt lovlig. Lægemiddelvirksomhederne tegner ikke altid et sandfærdigt billede af den medicin, de har udviklet - hverken over for myndighederne eller i de videnskabelige tidsskrifter. (videnskab.dk 25.1.2011).)

(Anm: Manisk svitsj forårsaket av antidepressiva: en sammenfattende sammenlignende gjennomgang av randomiserte kontrollerte studier og observasjonsstudier Manic switches induced by antidepressants: an umbrella review comparing randomized controlled trials and observational studies.(...) Conclusion. Our results highlight an underestimation of the rates of manic switch under antidepressants in RCTs compared to the rates observed in observational studies. Acta Psychiatrica Scandinavica 2016 (First published: 23 November 2016).)

(Anm: Markant flere bivirkninger i upublicerede kliniske studier. (…) Den mediane procentdel af offentliggjort dokumenter med information om bivirkninger var 46 pct., sammenlignet med 95 pct. i de tilsvarende, upublicerede dokumenter. (dagenspharma.dk 23.9.2016).)

(Anm: Fiona Godlee, editor in chief. Editor's Choice (Redaktørens valg). Hvorfor legemiddelgodkjenninger trenger bedre bevis (Why drug approval needs better evidence). (…) Begge artiklene konkluderer at legemiddelkontrollen har et straksbehov for å kreve høyere standarder på bevis før og etter godkjenning. Økte kostnader for evaluering vil mer enn oppveies av lavere kostnader for ineffektive behandlinger, med bedre resultater og færre pasientskader. I mellomtiden trenger pasienter og deres leger å ha en ærlig og åpen kommunikasjon om den virkelige styrken på bevisene bak beslutninger om godkjenninger.) BMJ 2016;353:i3483 (Published 23 June 2016).)

(Anm: Folk dør av hemmelige bivirkninger. Over 90 prosent av alle bivirkninger fra legemidler rapporteres ikke - selv ikke dødelige og livstruende bivirkninger. (...) Slik kan du hjelpe andre: (bt.no 9.3.2015).)

(Anm: For mange retningslinjer for behandlinger er skrevet av eksperter med finansielle konflikter, viser studien. (statnews.com 22.8.2016).)

(Anm: Autisme: tidlig dødsrisiko en "skjult krise" (- Den ulikhet i utfall for autistiske mennesker vist i disse data er skammelige. Vi kan ikke akseptere en situasjon hvor mange autistiske mennesker aldri vil oppleve sin 40-årsdag.) (- Alle som er involvert i å støtte folk med autismespekteret fra regjeringen rett ned til lokalt helsepersonell har et ansvar for å stå opp og begynne å redde liv så snart som mulig.) (medicalnewstoday.com 21.3.2016).)

(Anm: Association of anticholinergic burden with adverse effects in older people with intellectual disabilities: an observational cross-sectional study. Conclusions Older people with intellectual disabilities and with mental health conditions were exposed to high anticholinergic burden. This was associated with daytime dozing and constipation. The British Journal of Psychiatry Dec 2016, 209 (6) 504-510.)

(Anm: New study links autism to mutations in mitochondrial DNA (medicalnewstoday.com 31.10.2016).)

(Anm: Økning i dødsfall blant pasienter med psykiske lidelser må etterforskes, sier parlamentsmedlem. (Rise in deaths of mental health patients needs investigating, says MP.) BMJ 2016;352:i518 (Published 26 January 2016).)

(Anm: Medisinske feil — den tredje største dødsårsaken i USA. Medisinske feil inkluderes ikke i dødsattester eller i rangeringen av dødsårsaker. (...) Medisinske feil "fører til mer enn 250 000 dødsfall i USA årlig". (Medical error—the third leading cause of death in the US. Medical error is not included on death certificates or in rankings of cause of death. (...) Medical error 'causes more than 250,000 deaths in the U.S. annually.) BMJ 2016;353:i2139 (Published 03 May 2016).)

(Anm: Forskere: Medisinske feil nå tredje største dødsårsak i USA (Researchers: Medical errors now third leading cause of death in United States) (washingtonpost.com 3.7.2016).)

(Anm: Legemiddelfirmaer har inngått forlik om påstander om villeding av leger om overlevelsesdata for kreft. (Drug companies settle claim of misleading doctors on cancer survival data) (- Medisinsk svindel sto for mer enn halvparten av 3,5 milliarder dollar som ble utbetalt i erstatninger i fjor. Vanligvis involverte dette beskyldninger om bestikkelser betalt for å generere falske pasienter eller unødvendige behandlinger og resepter som er belastet Medicare.) BMJ 2016;353:i3361 (Published 15 June 2016).)

(Anm: Den britiske regjeringen har drevet lobbyvirksomhet overfor EU-kommisjonen for å få vedtatt en mer avslappet tilnærming til reguleringer av legemidler, medisinsk utstyr og mat, ifølge et brev som BMJ har fått tilgang til. (The UK government has been lobbying the European Commission to adopt a more relaxed approach to regulating drugs, devices, and food, a letter seen by The BMJ has shown.) BMJ 2016;353:i3357 (Published 15 June 2016).)

(Anm: Gruppe (Transparency International) ber om flere tiltak for å takle korrupsjonen innen legemiddelindustrien. (Group calls for more to be done to tackle corruption in the pharmaceutical industry) (…) På begynnelsen av 2016 har én av 10 korrupsjonsundersøkelser i USA involvert legemiddelfirmaer, hvilket ifølge rapporten er et langt høyere antall saker enn det som involverer banksektoren. BMJ 2016;353:i3099 (Published 02 June 2016).)

(Anm: Finanschef beskyldt for insiderhandel med pharma-tips. (- Sanjay Valvani er anklaget for at have handlet på tips fra en tidligere ansat i den amerikanske FDA-myndighed, som bl.a. godkender lægemidler, samt for at sende informationerne videre til kollegaen Christopher Plaford. (medwatch.dk 16.6.2016).)

(Anm: TEST UTVIKLET FOR Å OPPDAGE FARLIGE BIVIRKNINGER SLIK AT FÆRRE PASIENTER GIS UTRYGGE LEGEMIDLER (Test aims to detect dangerous side effects so that fewer patients are given unsafe drugs) (medicalnewstoday.com 19.12.2014).)

(Anm: Mitochondria: "Mood Altering Organelles" that Impact Disease Throughout the Nervous System. Curr Neurovasc Res. 2015 Aug 7. [Epub ahead of print].)

(Anm: Microbiota-mitochondria inter-talk: consequence for microbiota-host interaction. Pathog Dis. 2015 Oct 23. pii: ftv096. [Epub ahead of print].)

(Anm: SSRI-preparater og antipsykotika har uheldige effekter på mitokondrier (mintankesmie.no).)

(Anm: Ørsmå mitokondrier spiller en svært stor rolle mht. menneskets evolusjon og sykdom (Tiny mitochondria play outsized role in human evolution and disease.) (medicalnewstoday.com 25.9.2015).)

(Anm: Oxidative stress, mitochondrial damage and diabetic retinopathy.Biochim Biophys Acta. 2015 Aug 4. pii: S0925-4439(15)00222-7. [Epub ahead of print].)

(Anm: mtDNA Damage in the Development of Heart Failure.Am J Physiol Heart Circ Physiol. 2015 Jun 19:ajpheart.00475.2015. [Epub ahead of print].)

(Anm: The growing importance of mitochondrial calcium in health and disease. PNAS (Proceedings of the National Academy of Sciences) 2015.) 

(Anm: Three toxic gases meet in the mitochondria. Front. Physiol. 2015 (20 August 2015).)

- Våre data viser således at T(3) har en viktig rolle i å åpne mitokondrie-membranpermeabilitet-pore og aktiverer funksjonen av de to viktige fysiologiske svellende induserende, kalsium- og fosfationer

In vitro and in vivo activation of mitochondrial membrane permeability transition pore using triiodothyronine.
Physiol Res. 2016 Jun 20;65(2):321-31. Epub 2015 Oct 8.
Abstract Using a novel method for evaluating mitochondrial swelling (Drahota et al. 2012a) we studied the effect of calcium (Ca(2+)), phosphate (P(i)), and triiodothyronine (T(3)) on the opening of mitochondrial membrane permeability transition pore and how they interact in the activation of swelling process. We found that 0.1 mM P(i), 50 microM Ca(2+) and 25 microM T(3) when added separately increase the swelling rate to about 10 % of maximal values when all three factors are applied simultaneously. Our findings document that under experimental conditions in which Ca(2+) and P(i) are used as activating factors, the addition of T(3) doubled the rate of swelling. T(3) has also an activating effect on mitochondrial membrane potential. The T(3) activating effect was also found after in vivo application of T(3). Our data thus demonstrate that T(3) has an important role in opening the mitochondrial membrane permeability pore and activates the function of the two key physiological swelling inducers, calcium and phosphate ions. (…)

(Anm: Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the “old” triiodothyronine and the “emerging” 3,5-diiodothyronine. Front. Physiol.2015 (21 August 2015).)

(Anm: Implications of mitochondrial dynamics on neurodegeneration and on hypothalamic dysfunction. Front. Aging Neurosci. 2015 (10 June 2015).)

(Anm: Mitochondrial flash as a novel biomarker of mitochondrial respiration in the heart. (…) Limiting electron entrance at Complex I by knocking out Ndufs4, an assembling subunit of Complex I, suppresses mitochondrial flash activity. These results suggest that mitochondrial electron flow can be monitored by real-time imaging of mitochondrial flash.  Am J Physiol Heart Circ Physiol. 2015 Aug 14:ajpheart.00462.2015. [Epub ahead of print].)

- Legemidler indisert for mitokondriell dysfunksjon som behandlinger for akutt encefalopati med utbrudd av feberkramper/ febril status epileptikus.

Drugs indicated for mitochondrial dysfunction as treatments for acute encephalopathy with onset of febrile convulsive status epileptics.
J Neurol Sci. 2016 Jan 15;360:57-60. doi: 10.1016/j.jns.2015.11.043. Epub 2015 Nov 24.
Abstract We studied the efficacy of drugs indicated for mitochondrial dysfunction in the treatment of 21 patients with acute encephalopathy with onset of febrile convulsive status epilepticus at our hospital from January 2006 to December 2014. Among them, 11 patients had been treated with a mitochondrial drug cocktail consisting of vitamin B1, vitamin C, biotin, vitamin E, coenzyme Q10, and l-carnitine (prescription group) and 10 patients were not treated with the cocktail (non-prescription group). We retrospectively reviewed age, trigger, clinical form, treatment start time, and sequelae. Clinical form was classified into a biphasic group presenting acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) and a monophasic group. Sequelae were classified as (A) no sequelae group or (B) sequelae group, and differences in the interval between diagnosis and treatment were also evaluated. The sequelae were not different between the mitochondrial drug cocktail prescription and non-prescription groups, but significantly better in the group administered the mitochondrial drug cocktail within 24h (P=0.035). We expect that early treatment with a mitochondrial drug cocktail could prevent sequelae in acute encephalopathy with onset of febrile convulsive status epilepticus. (…)

(Anm: Coenzyme Q-10 in Human Health: Supporting Evidence? (…) This review is an attempt to actualize the available information on CoQ10 and define its potential benefit and appropriate usage.South Med J. 2016 Jan;109(1):17-21.)

(Anm: Vitamin C can target and kill cancer stem cells, study shows. Cancer is currently one of the top killers worldwide, and the number of cancer cases is only expected to rise. Although there are a number of therapies available, most of them are toxic and cause serious side effects. New research examines the impact of the natural vitamin C on cancer cell growth. (…) New research, published in the journal Oncotarget, examines the effectiveness of three natural substances, three experimental drugs, and one clinical drug in stopping the growth of these cancer stem cells (CSCs.) (…) Vitamin C up to 10 times more effective than experimental drugs. (…) "We have been looking at how to target cancer stem cells with a range of natural substances including silibinin (milk thistle) and CAPE, a honey-bee derivative, but by far the most exciting are the results with vitamin C. Vitamin C is cheap, natural, nontoxic and readily available so to have it as a potential weapon in the fight against cancer would be a significant step." (medicalnewstoday.com 13.3.2017).)

(Anm: How Vitamin C May Help Cancer Treatments Work Better. Cancer treatments are often hard on patients, but the side effects and challenges are necessary to control or even destroy tumor cells. Now researchers say there may be a way to make those treatments work even better. In a study published in Cancer Cell, scientists say that giving people high doses of vitamin C during treatment may weaken cancer cells and make them more vulnerable to the effects of chemotherapy and radiation. (time.com 5.4.2017).)

(Anm: What can you do to make your nails grow faster? (…) Fingernails grow an average of 3.5 millimeters (mm) per month. (…) Like the rest of the body, the nails need a balanced diet to grow, including protein, water, fruits, vegetables, and a wide array of vitamins and minerals. People who do not get enough iron, for instance, may have brittle nails, or nails with dents. Protein deficiency may cause ridges in the nails. (…) Biotin is a B-complex vitamin that proponents say can promote healthy hair and nail growth. Biotin may strengthen brittle nails, preventing them from breaking, but there is little evidence that biotin supplements will help the nails grow faster. (medicalnewstoday.com 18.11.2017).)

(Anm: Forsker: Hjerneceller kan påvirke hinanden uden at have kontakt. Nerveceller kan sende bølger af aktivitet gennem hjernen via elektriske felter uden at være forbundne, viser ny forskning. Det kan åbne op for en ny forståelse af sygdomme som epilepsi, vurderer forskere. (…) Det er en vigtig opdagelse, da det giver os en mere komplet forståelse af, hvordan hjerneceller kommunikerer og påvirker hinanden, konkluderer forskerne bag undersøgelsen. (videnskab.dk 23.2.2016).)

- Fungerer biotin for hårvekst? Dosering og bivirkninger. Biotin, eller B7, er et essensielt B-vitamin som hjelper kroppen til å få energi og næringsstoffer fra karbohydrater, proteiner og fettstoffer.

(Anm: Does biotin for hair growth work? Dosage and side effects. Biotin, or B7, is an essential B vitamin that helps the body get energy and nutrients from carbohydrates, proteins, and fats. Gastrointestinal bacteria usually produce enough biotin to meet bodily needs. Many foods also contain small amounts of biotin, including whole wheat, egg yolks, nuts, and legumes. (medicalnewstoday.com 16.9.2017).)

- Vitamin B-3-mangel: Symptomer, årsaker og behandling. Vitamin B-3 mangel kan forstyrre dusinvis av prosesser i kroppen og kan føre til en sykdom kalt pellagra.

(Anm: Vitamin B-3 deficiency: Symptoms, causes, and treatment. Vitamin B-3 deficiency can disrupt dozens of processes in the body and can lead to a disease called pellagra. Vitamin B-3, also known as niacin, plays a key role in skin, digestive, and mental health, and supports the functions of more than 200 enzymes in the body. Vitamin B-3 is a combination of two chemicals: nicotinic acid and nicotinamide. The body breaks these chemicals down to produce two additional chemicals: NAD and NADP. NAD and NADP play a role in a variety of chemical reactions inside the body and also support cell metabolism. So, people who don't get enough vitamin B-3 can experience a range of health problems and symptoms, ranging from minor to life-threatening. (medicalnewstoday.com 16.9.2017).)

(Anm: Pellagra er en sjelden mangelsykdom, forårsaket av mangel på niacin (Vitamin B3) i kroppen. Dette kan skyldes redusert inntak av niacin eller aminosyrene tryptofan og leucin. Sykdommen kan ses blant annet ved ensidig kosthold med mais, og ved langvarig alkoholisme. (no.wikipedia.org).)

(Anm: High doses of vitamin C to improve cancer treatment passes human safety trial Clinical trials found that it is safe to regularly infuse brain and lung cancer patients with 800 - 1000 times the daily recommended amount of vitamin C as a potential strategy to improve outcomes of standard cancer treatments. In a work presented in Cancer Cell, University of Iowa researchers also show pathways by which altered iron metabolism in cancer cells, and not normal cells, lead to increased sensitivity to cancer cell death caused by high dose vitamin C. (worldpharmanews.com 31.3.2017).)

(Anm: Vitamin C modulates the immunotoxic effect of 17 alpha-methyltestosterone in Nile tilapia. Abstract. The synthetic androgen, 17 alpha-methyltestosterone (MT), is profusely used and practically needed in the production of all-male Nile tilapia fry; however, such androgenic hormones badly disrupt the immune system. This study aimed to alleviate or counteract the immunotoxic effect of MT using vitamin C (ascorbic acid, vit C). Biochemistry. 2017 Mar 21.)

(Anm: How does broccoli help prevent cancer? Study sheds light. Researchers from Oregon State University (OSU) found that sulforaphane reduced the expression of long noncoding RNAs (lncRNAs) in prostate cancer cells, which disrupted the cells' ability to form colonies - a hallmark of metastatic cancer. Previously believed to be "junk DNA" with no significant function, lncRNAs have increasingly emerged as key players in the development of numerous cancers, including prostate, breast, stomach, and lung cancers. (medicalnewstoday.com 18.3.2017).)

(Anm: Low Vitamin B6 Linked to Inflammation. Chronic Inflammation Tied to Low Blood Levels of Vitamin B6 (webmd.com 19.5.2012).)

(Anm: Symptoms of Vitamin B12 Deficiency (news-medical.net 20.2.2017).)  

(Anm: Vitamin B12 tabletter - et godt alternativ til injeksjoner. Vitamin B12 tabletter, Cyankobalamin 1 mg (Behepan) fikk nylig markedsføringstillatelse og refunderes på blå resept fra 1. juni. Ubehandlet B12 mangel kan gi pernisiøs anemi, beinmargssvikt og alvorlige, irreversible skader på nervesystemet. I Norge har B12-mangel nesten utelukkende vært behandlet med injeksjoner til tross for god dokumentasjon for at tablettbehandling kan være like effektivt (1). (...) Det anbefales ikke alminnelig screening for B12 mangel, men lav terskel for å måle B12 hos pasienter med anemi, såre munnslimhinner, polynevropati, demens, asteni eller uklare nevrologiske eller psykiatriske symptomer. (legemiddelverket.no 31.5.2017).)

(Anm: Study reveals link between vitamin B supplementation and lung cancer. A new study has shown that taking high-dose vitamin B supplements over a long period is associated with an increased risk of lung cancer among men. The study, which analysed data for 77,000 people, showed that long-term use of the supplements increased the cancer risk among men by between two and four times, compared with non-use. No such effect was observed for women. This risk was further increased among male smokers who took more than 20 mg of B6 or 55 mg of B12 every day for ten years. Taking B6 at this dose increased the lung cancer risk by three times and taking B12 at this dose increased it by four times. Taking these supplements has previously been shown to have a protective effect against lung cancer, but the authors of the current study say this appears to be a double-edged sword. (news-medical.net 23.8.2017).)

(Anm: Sneaky Depression Triggers as You Age (medicinenet.com 7.5.2016).)

(Anm: B Vitamins May Ward off Air Pollution Effects. Study demonstrates epigenetic impact of dirty air on health. B vitamins, such as folic acid and vitamins B6 and B12, may play an important role in reducing the impact of air pollution on the epigenome, according to results from a small, placebo-controlled trial. (medpagetoday.com 16.3.2017).)

(Anm: B vitamins attenuate the epigenetic effects of ambient fine particles in a pilot human intervention trial. PNAS (Proceedings of the National Academy of Sciences) 2017 (Mar 13).)

(Anm: Beskytter B-vitaminer mod luftforurening? Det lyder måske helt hen i vejret, men svaret er formodentlig ja, hvis man spørger forskerne bag et nyt studie, beskrevet i Proceedings of the National Academy of Sciences (PNAS). I studiet kunne forskerne via indgift af høje doser b-vitamin til 10 personer sandsynliggøre, at vitaminerne kunne afværge den skade, som forårsages af luftforurening. Forskerne understreger dog, at yderligere studier med flere interviewpersoner og i mere tungt forurenede byer så som Beijing eller Mexico, er påkrævede, før de endeligt tør svare ja til spørgsmålet i overskriften. (pharmadanmark.dk 17.3.2017).)

(Anm: Oxidative damage and mitochondrial decay in aging. Abstract We argue for the critical role of oxidative damage in causing the mitochondrial dysfunction of aging. Oxidants generated by mitochondria appear to be the major source of the oxidative lesions that accumulate with age. Several mitochondrial functions decline with age. The contributing factors include the intrinsic rate of proton leakage across the inner mitochondrial membrane (a correlate of oxidant formation), decreased membrane fluidity, and decreased levels and function of cardiolipin, which supports the function of many of the proteins of the inner mitochondrial membrane. Acetyl-L-carnitine, a high-energy mitochondrial substrate, appears to reverse many age-associated deficits in cellular function, in part by increasing cellular ATP production. Such evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging. Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):10771-8.)

(Anm: [ACTION OF L-CARNITINE, CORVITIN AND THEIR COMBINATION ON FUNCTIONAL STATE OF LIVER IN EXPERIMENTAL MODEL OF REYE SYNDROME IN RATS]. Administration of Aacetylsalicylic acid in children with viral infections (influence B, chickenpox) can be related with development of Reye syndrome - severe encephalopathy and liver insufficiency with mortality in 50% of cases. (…) The most pronounced hepatoprotective effect of concurrent administration of L-Carnitine and Corvitin may be due to synergic action of these drugs and such regime can be recommended for correction of liver function during Reye syndrome. Georgian Med News. 2017 Feb;(263):105-111.)

(Anm: Magnesium, terapi. Magnesium er et viktig mineral i kroppen. Hos noen personer kan det oppstå situasjoner med magnesiummangel. (…) Magnesium er det fjerde hyppigst forekommende mineralet i kroppen1. Det er fordelt med ca. halvparten i skjelettet og den andre halvparten i muskulatur og annet bløtvev. Mindre enn 1% finnes i blodet. (…) Magnesiums rolle i kroppen. Magnesium deltar i mer enn 300 ulike metabolske reaksjoner i kroppen4-5. Disse prosessene inkluderer proteinsyntese, produksjon og lagring av celleenergi, cellevekst og reproduksjon, DNA og RNA syntese og stabilisering av mitokondrienes membraner6-7. (nhi.no 28.4.2014).)

(Anm: Omega-3 fatty acids regulate NLRP3 inflammasome activation and prevent behavior deficits after traumatic brain injury. Abstract Omega-3 fatty acids (ω-3 FAs) attenuate inflammation and improve neurological outcome in response to traumatic brain injury (TBI), but the specific anti-inflammatory mechanisms remain to be elucidated. Here we found that NLRP3 inflammasome and subsequent pro-inflammatory cytokines were activated in human brains after TBI. Rats treated with ω-3 FAs had significantly less TBI-induced caspase-1 cleavage and IL-1β secretion than those with vehicle. G protein-coupled receptor 40 (GPR40) was observed to be involved in this anti-inflammation. GW1100, a GPR40 inhibitor, eliminated the anti-inflammatory effect of ω-3 FAs after TBI. β-Arrestin-2 (ARRB2), a downstream scaffold protein of GPR40, was activated to inhibit inflammation via directly binding with NLRP3 in the ω-3 FAs treatment group. Interestingly, we also observed that ω-3 FAs prevented NLRP3 mitochondrial localization, which was reversed by GW1100. Furthermore, ω-3 FAs markedly ameliorated neuronal death and behavioral deficits after TBI, while GW1100 significantly suppressed this effect. Collectively, these data indicate that the GPR40-mediated pathway is involved in the inhibitory effects of ω-3 FAs on TBI-induced inflammation and ARRB2 is activated to interact with NLRP3. Exp Neurol. 2017 Apr;290:115-122 Epub 2017 Jan 8.)

(Anm: Butyrate (also known as butanoate) is the traditional name for the conjugate base of butyric acid (also known as butanoic acid). The formula of the butyrate ion is C4H7O2−. The name is used as part of the name of esters and salts of butyric acid, a short chain fatty acid. (en.wikipedia.org).)

(Anm: Potential beneficial effects of butyrate in intestinal and extraintestinal diseases. Abstract The multiple beneficial effects on human health of the short-chain fatty acid butyrate, synthesized from non-absorbed carbohydrate by colonic microbiota, are well documented. At the intestinal level, butyrate plays a regulatory role on the transepithelial fluid transport, ameliorates mucosal inflammation and oxidative status, reinforces the epithelial defense barrier, and modulates visceral sensitivity and intestinal motility. In addition, a growing number of studies have stressed the role of butyrate in the prevention and inhibition of colorectal cancer. (…) These data suggest a wide spectrum of positive effects exerted by butyrate, with a high potential for a therapeutic use in human medicine. World J Gastroenterol. 2011 Mar 28; 17(12): 1519–1528.)

(Anm: Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells. BACKGROUND: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. (…) CONCLUSION: These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance. BMC Neurosci. 2017 Jan 19;18(1):15.)

(Anm: The Use of Antioxidants in the Treatment of Traumatic Brain Injury. AIMS: To discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. (…) CONCLUSION: The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury. J Adv Nurs. 2017 Jan 19. [Epub ahead of print].)

(Anm: AZT-induced mitochondrial toxicity: an epigenetic paradigm for dysregulation of gene expression through mitochondrial oxidative stress. Abstract Mitochondrial dysfunction causes oxidative stress and cardiomyopathy. Oxidative stress also is a side effect of dideoxynucleoside antiretrovirals (NRTI) and is observed in NRTI-induced cardiomyopathy. We show here that treatment with the NRTI AZT {1-[(2R,4S,5S)-4-azido-5-(hydroxymethyl)oxolan-2-yl]-5-methylpyrimidine-2,4-dione} modulates cardiac gene expression epigenetically through production of mitochondrially derived reactive oxygen species. Physiol Genomics. 2015 Oct;47(10):447-54. Epub 2015 Jul 21.)

(Anm: Chronic treatment with coenzyme Q10 reverses restraint stress-induced anhedonia and enhances brain mitochondrial respiratory chain and creatine kinase activities in rats. Behav Pharmacol. 2013 Oct;24(7):552-60.)

(Anm: Genetic rescue of Mitochondrial and Skeletal Muscle Impairment in an IPSCs Model of Coenzyme Q10 Deficiency. The COQ4 mutation in iPSC was associated with CoQ10 deficiency, metabolic dysfunction, and respiration defects. iPSC differentiation into SkM was compromised, and the resulting SkM also displayed respiration defects. Remarkably, iPSC differentiation in dopaminergic or motor neurons was unaffected. This study offers an unprecedented iPSC model recapitulating CoQ10 deficiency-associated functional and metabolic phenotypes caused by COQ4 mutation. Stem Cells. 2017 May 4.)

(Anm: Dysfunction of cellular powerplant shakes B-vitamin metabolism and causes genetic damage. Mitochondria are the cellular powerplant, but their functions in conjunction with B-vitamins are only starting to be revealed. When nutrient status is good, vitamin B9, folate, turns mitochondria to cellular builders. Through folate, mitochondria produce substances to make ingredients for genome replication and repair, cell membrane renewal and synthesis of antioxidants. The mechanism also includes other B-vitamins. (medicalnewstoday.com 7.3.2016).)

(Anm: Impaired Exercise Performance and Skeletal Muscle Mitochondrial Function in Rats with Secondary Carnitine Deficiency. Front. Physiol., 10 August 2016.)

(Anm: Coenzyme Q10 in the Treatment of Corneal Edema in Kearns-Sayre: Is There an Application in Fuchs Endothelial Corneal Dystrophy? Cornea. 2016 Jul 20. [Epub ahead of print].)

(Anm: The Use of Antioxidants in the Treatment of Traumatic Brain Injury. (…) Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defense mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species. (…) CONCLUSION: The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury. This article is protected by copyright. All rights reserved. J Adv Nurs. 2017 Jan 19.)

(Anm: Vitamin B1 (thiamine) and dementia. The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine (vitamin B1). Throughout the last century, research showed that thiamine deficiency is associated with neurological problems, including cognitive deficits and encephalopathy. Multiple similarities exist between classical thiamine deficiency and Alzheimer's disease (AD) in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients and by thiamine decline, and a decrease in their levels could account for the reduction in glucose metabolism. Ann N Y Acad Sci. 2016 Mar 11. [Epub ahead of print].)

Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment. (Forebygging av Alzheimers sykdom-relaterte grå materie atrofi med B-vitaminbehandling.)
Proc Natl Acad Sci U S A. 2013 May 20. [Epub ahead of print]
Abstract Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented. (...)

(Anm: Taking B vitamins may reduce epigenetic effects of air pollution. A new study by researchers at Columbia University's Mailman School of Public Health showed that B vitamins may play a critical role in reducing the impact of air pollution on the epigenome, further demonstrating the epigenetic effects of air pollution on health. This is the first study to detail a course of research for developing interventions that prevent or minimize the adverse effects of air pollution on potential automatic markers. The results will be published online in the journal PNAS. (…) The researchers administered one placebo or B-vitamin supplement (2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12) daily to each adult recruited for the trial. To take part in the intervention, volunteers were required to be healthy non-smokers, 18 to 60 years old, who were not taking any medicines or vitamin supplements. (medicalnewstoday.com 15.3.2017).)

(Anm: Beskytter B-vitaminer mod luftforurening? Det lyder måske helt hen i vejret, men svaret er formodentlig ja, hvis man spørger forskerne bag et nyt studie, beskrevet i Proceedings of the National Academy of Sciences (PNAS). I studiet kunne forskerne via indgift af høje doser b-vitamin til 10 personer sandsynliggøre, at vitaminerne kunne afværge den skade, som forårsages af luftforurening. Forskerne understreger dog, at yderligere studier med flere interviewpersoner og i mere tungt forurenede byer så som Beijing eller Mexico, er påkrævede, før de endeligt tør svare ja til spørgsmålet i overskriften. (pharmadanmark.dk 17.3.2017).)

(Anm: Gray matter loss and the inflamed brain in the development of psychosis (medicalnewstoday.com 15.1.2015).)

(Anm: Stress hormone link with psychosis. JCU Associate Professor Zoltan Sarnyai said it was the first meta-analysis study to compare the level of cortisol in a waking patient's body with the stage of schizophrenia they are suffering. Dr Sarnyai said it means doctors may be able to eventually identify those who will develop full-blown psychosis from amongst those who present with early stages of the disease. (medicalnewstoday.com 3.6.2016).)

(Anm: High folic acid level in pregnancy may decrease high blood pressure in children. A new article published in the American Journal of Hypertension finds that babies born to mothers with cardiometabolic risk factors were less likely to develop high blood pressure if their mothers had higher levels of folate during pregnancy. (medicalnewstoday.com 10.3.2017).)

(Anm: Mitochondrial dysfunction and seizures: the neuronal energy crisis. (…) An understanding of the reciprocal relation between mitochondrial dysfunction and epilepsy is crucial to select appropriate anticonvulsant treatment and has the potential to open up new therapeutic approaches in the subset of epileptic disorders caused by mitochondrial dysfunction. Lancet Neurol. 2015 Sep;14(9):956-66.)

(Anm: Mitochondrial Dysfunction, Disruption of F-actin Polymerization, and Transcriptomic Alterations in Zebrafish Larvae Exposed to Trichloroethylene. Chem. (…) Trichloroethylene (TCE) is primarily used as an industrial degreasing agent and has been in use since the 1940s. (…) Current literature links TCE exposure to various adverse health effects including cardiovascular toxicity. (...) Overall, results from our study support TCE as a developmental cardiovascular toxicant, provide molecular targets and pathways for investigation in future studies, and indicate a need for continued priority for environmental regulation. Res. Toxicol. 2016 (January 8, 2016).)

(Anm: Mitochondrial calcium overload is a key determinant in heart failure. Our data demonstrate that leaky RyR2, but not IP3R2, channels cause mitochondrial Ca2+ overload and dysfunction in HF. PNAS (Proceedings of the National Academy of Sciences) 2015 (July 6, 2015).)

(Anm: Disrupting mitochondrial-nuclear coevolution affects OXPHOS complex I integrity and impacts human health. Genome Biol Evol. 2014 Sep 22;6(10):2665-80.)

(Anm: The Red Queen in mitochondria: cyto-nuclear co-evolution, hybrid breakdown and human disease. Front. Genet. 2015 (19 May 2015).)

(Anm: Coenzyme Q10 Supplementation Modulates NFκB and Nrf2 Pathways in Exercise Training. (…) In conclusion, these results suggest that Q10 modulates the expression of NFκB, IκB, Nrf2 and HO-1 in exercise training, indicating an anti-inflammatory effect of Q10 and emphasizes its role in antioxidant defense. Key pointsCoenzyme Q10 is a component of the electron transport chain in mitochondria which is linked to the generation of energy in the cell.Coenzyme Q10 may inhibit the peroxidation of lipids, thus acting as an antioxidant and protects tissue against oxidative injury.Using of coenzyme Q10 can significantly elevate IκB, Nrf2 and HO-1 and reduce NFκB during exercise training. J Sports Sci Med. 2016 Feb 23;15(1):196-203. eCollection 2016.)

(Anm: Coenzyme Q biosynthesis and its role in the respiratory chain structure. Biochim Biophys Acta. 2016 Mar 9. pii: S0005-2728(16)30057-3.)

(Anm: Depletion of mitochondrial enzyme system in liver, lung, brain, stomach and kidney induced by benzo(a)pyrene. Environ Toxicol Pharmacol. 2016 Mar 4;43:83-93. [Epub ahead of print].)

(Anm: Nuclear DNA damage signalling to mitochondria in ageing. Mitochondrial dysfunction is a hallmark of ageing, and mitochondrial maintenance may lead to increased healthspan. Emerging evidence suggests a crucial role for signalling from the nucleus to mitochondria (NM signalling) in regulating mitochondrial function and ageing. Nat Rev Mol Cell Biol. 2016 Mar 9. [Epub ahead of print].)

(Anm: Altered Mitochondrial Signalling and Metabolism in Cancer. Abstract. Mitochondria being the central organelle for metabolism and other cell signalling pathways have remained the topic of interest to tumour biologists. In spite of the wide acceptance of Warburg's hypothesis, role of mitochondrial metabolism in cancer is still unclear. Uncontrolled growth and proliferation, hallmarks of tumour cells, are maintained when the cells adapt to metabolic reprogramming with the help of altered metabolism of mitochondria. This review has focussed on different aspects of mitochondrial metabolism and inter-related signalling pathways which have been found to be modified in cancer. Front Oncol. 2017 Mar 20;7:43. eCollection 2017.)

(Anm: Mitochondrial Dynamics: In Cell Reprogramming as It Is in Cancer. (…) Accordingly, mitochondrial fission, the process whereby the mitochondria divide, plays an important role in the cell reprogramming process. Here, we present an overview of the importance of mitochondrial fission in both cell reprogramming and cellular transformation. Stem Cells Int. 2017;2017:8073721. Epub 2017 Apr 17.)

(Anm: Nuclear gene mutations as the cause of mitochondrial complex III deficiency Front. Genet. 2015 (1 April 2015).)

(Anm: How the Wnt signaling pathway protects from neurodegeneration: the mitochondrial scenario Front. Cell. Neurosci. 2015 (5 May 2015).)

(Anm: Premature aging: Scientists identify and correct defects in diseased cells (…) 3D reconstruction of a primary fibroblast from the skin of a patient with Cockayne syndrome: mitochondria are shown in green and the nucleus in blue. (medicalnewstoday.com 22.5.2015).)

(Anm: Polynevropati betyr at flere av de perifere nervene i kroppen (særlig i føttene) ikke fungerer som de skal. (nhi.no 11.11.2013).)

(Anm: Kokain og ecstasy forårsaker ikke bare avhengighet og øker risikoen for kreft, men forårsaker også genmutasjoner (Cocaine and ecstasy cause DNA mutation: study.) (...) "Kokain og ecstasy har vist seg å være farligere enn vi hadde forestilt oss," sa Giorgio Bronzetti, sjefsforsker ved bioteknologisk avdeling ved National Centre for Research's (CNR) . ("Cocaine and ecstasy have proved to be more dangerous than we had imagined," said Giorgio Bronzetti, chief scientist at the National Centre for Research's (CNR) biotechnology department.) Disse midlene, med sine sterke toksikologiske effekter, angriper DNA, utløser mutasjoner og endrer arvematerialet. Dette er svært bekymringsfullt for den effekten de kan ha på fremtidige generasjoner," sa han. ("These drugs, on top of their toxicological effects, attack DNA, provoking mutations and altering the hereditary material. This is very worrying for the effects it could have on future generations," he said.) (Reuters Health 5.12.2003).)

(Anm: Kardiovaskulær mitokondriell dysfunksjon indusert av kokain: Biomarkører og mulige fordelaktige effekter av modulatorer av oksidativ stress. Cardiovascular Mitochondrial Dysfunction Induced by Cocaine: Biomarkers and Possible Beneficial Effects of Modulators of Oxidative Stress. Abstract Cocaine abuse has long been known to cause morbidity and mortality due to its cardiovascular toxic effects. The pathogenesis of the cardiovascular toxicity of cocaine use has been largely reviewed, and the most recent data indicate a fundamental role of oxidative stress in cocaine-induced cardiovascular toxicity, indicating that mitochondrial dysfunction is involved in the mechanisms of oxidative stress. The comprehension of the mechanisms involving mitochondrial dysfunction could help in selecting the most appropriate mitochondria injury biological marker, such as superoxide dismutase-2 activity and glutathionylated hemoglobin. The potential use of modulators of oxidative stress (mitoubiquinone, the short-chain quinone idebenone, and allopurinol) in the treatment of cocaine cardiotoxic effects is also suggested to promote further investigations on these potential mitochondria-targeted antioxidant strategies. Oxid Med Cell Longev. 2017;2017:3034245.)

(Anm: Common cancers hijack powerhouses of cells (medicalnewstoday.com 9.4.2015).)

(Anm: Key brain receptor sheds light on neurological conditions, CU Anschutz researchers say. (…) For years, scientists believed that a special calcium permeable subtype of AMPA-type glutamate receptor only strengthened synapses, which send signals between brain cells. But Professor Mark Dell'Acqua, vice-chair of the Dept. of Pharmacology at the University of Colorado School of Medicine, and his team of researchers found that it also weakened synapses. (…) (medicalnewstoday.com 4.3.2016).)

(Anm: Blocking transfer of calcium to cell's powerhouse selectively kills cancer cells. Inhibiting the transfer of calcium ions into the cell's powerhouse is specifically toxic to cancer cells, according to an article published this week in Cell Reports by researchers from the Perelman School of Medicine at the University of Pennsylvania. (medicalnewstoday.com 4.3.2016).)

(Anm: Mitochondrial dysfunction in DDR-related cancer predisposition syndromes. Biochim Biophys Acta. 2016 Feb 26. pii: S0304-419X(16)30022-1. [Epub ahead of print].)

(Anm: Cancer cells exploit adaptive mitochondrial dynamics to increase tumor cell invasion. Cell Cycle. 2015 Aug 28:0. [Epub ahead of print].)

(Anm: The role of mitochondria in cancer induction, progression and changes in metabolism. Mini Rev Med Chem. 2015 Oct 16. [Epub ahead of print]).)

(Anm: Cancer as a mitochondrial metabolic disease. Front Cell Dev Biol. 2015 Jul 7;3:43. eCollection 2015.)

(Anm: Cocaine may spur brain cells to destroy themselves. New research on mice shows that high doses of cocaine can cause brain cells to literally digest their own insides by sending a natural garbage-clearing process called autophagy into overdrive. In a new study about to be published in the Proceedings of the National Academy of Sciences, researchers from Johns Hopkins University in Baltimore, MD, describe how they found high doses of cocaine can cause autophagy in mouse brains to become hyperactive. (…) Dr. Prasun Guha, postdoctoral student at Johns Hopkins, says: "Autophagy is the housekeeper that takes out the trash - it's usually a good thing. But cocaine makes the housekeeper throw away really important things, like mitochondria, which produce energy for the cell." (medicalnewstoday.com 19.1.2016).)

(Anm: Relationship Between Mitochondrial DNA Mutations and Aging. Estimation of Age-at-death. J Gerontol A Biol Sci Med Sci. 2015 Aug 18. pii: glv115. [Epub ahead of print].)

(Anm: Coenzyme Q and Its Role in the Dietary Therapy against Aging. Molecules. 2016 Mar 18;21(3). pii: E373.)

(Anm: How the Cell Got Its Mitochondria. Microbes Infect. 2015 Aug 17. pii: S1286-4579(15)00159-8. [Epub ahead of print].)

- Britisk firma prøvde HIV-legemiddel på foreldreløse

UK firm tried HIV drug on orphans (Britisk firma prøvde HIV-legemiddel på foreldreløse)
guardian.co.uk 4.4.2006
GlaxoSmithKline trukket inn i skandale hvor babyer og barn angivelig er brukt som "laboratoriedyr". (GlaxoSmithKline embroiled in scandal in which babies and children were allegedly used as ‘laboratory animals’.)

Foreldreløse og babyer så unge som tre måneder er blitt brukt som forsøkskaniner i potensielt farlige medisinske eksperimenter sponset av farmasøytiske firmaer, har en undersøkelse av Observer avslørt. (Orphans and babies as young as three months old have been used as guinea pigs in potentially dangerous medical experiments sponsored by pharmaceutical companies, an Observer investigation has revealed.)

Den britiske legemiddelgiganten GlaxoSmithKline er trukket inn i skandalen. Firmaet sponset eksperimenter på barn fra Incarnation Childrens Centre, et omsorgshjem i New York som spesialiserer seg på behandling av HIV-lidelser drevet av katolsk velgjørenhet. (British drug giant GlaxoSmithKline is embroiled in the scandal. The firm sponsored experiments on the children from Incarnation Children’s Centre, a New York care home that specialises in treating HIV sufferers and is run by Catholic charities.)

Barna var enten infisert med HIV eller født av HIV-positive mødre. Deres foreldre var døde, ikke lot seg oppspore eller ansett som uskikket til å ta seg av dem. (...) (The children had either been infected with HIV or born to HIV-positive mothers. Their parents were dead, untraceable or deemed unfit to look after them.)

Helsedirektoratet i byen har innledet en etterforsking av påstander om at mer enn 100 barn ved Incarnation ble brukt i 36 eksperimenter - i det minste fire sponset av Glaxo. Noen av disse forsøk ble designet for å teste "giftigheten" av AIDS-legemidler. En involverte det å gi barn så unge som fire år en høydose cocktail på syv legemidler samtidig. En annen så på reaksjonen hos seks måneder gamle babyer som fikk dobbel dose meslingvaksine. (The city health department has launched an investigation into claims that more than 100 children at Incarnation were used in 36 experiments - at least four co-sponsored by Glaxo. Some of these trials were designed to test the ‘toxicity’ of Aids medications. One involved giving children as young as four a high-dosage cocktail of seven drugs at one time. Another looked at the reaction in six-month-old babies to a double dose of measles vaccine.)

De fleste eksperimenter ble finansiert av statlige etater som National Institute of Allergy og Infectious Diseases. Inntil nå hadde ikke Glaxos rolle kommet frem. (Most experiments were funded by federal agencies like the National Institute of Allergy and Infectious Diseases. Until now Glaxo’s role had not emerged.)

I et co-sponset eksperiment i 1997 brukte av Glaxo barn fra Incarnation for å "oppnå toleranse, sikkerhet og farmakokinetiske" data for legemidler mot herpes. I et mer nylig eksperiment, ble barn brukt til å teste AZT. Et tredje eksperiment sponset av Glaxo og det amerikanske legemiddelfirmaet Pfizer utforsket "langsiktig sikkerhet" for antibakterielle legemidler på tre måneder gamle babyer. (...) (In 1997 an experiment co-sponsored by Glaxo used children from Incarnation to ’obtain tolerance, safety and pharmacokinetic’ data for Herpes drugs. In a more recent experiment, the children were used to test AZT. A third experiment sponsored by Glaxo and US drug firm Pfizer investigated the ’long-term safety’ of anti-bacterial drugs on three-month-old babies.)

(Anm: AZT-induced mitochondrial toxicity: an epigenetic paradigm for dysregulation of gene expression through mitochondrial oxidative stress. Abstract Mitochondrial dysfunction causes oxidative stress and cardiomyopathy. Oxidative stress also is a side effect of dideoxynucleoside antiretrovirals (NRTI) and is observed in NRTI-induced cardiomyopathy. We show here that treatment with the NRTI AZT {1-[(2R,4S,5S)-4-azido-5-(hydroxymethyl)oxolan-2-yl]-5-methylpyrimidine-2,4-dione} modulates cardiac gene expression epigenetically through production of mitochondrially derived reactive oxygen species. Physiol Genomics. 2015 Oct;47(10):447-54. Epub 2015 Jul 21.)

- Forstyrrelser av cellenes "kraftstasjoner" (mitokondrier) kan føre til tumorvekst, ifølge Penn-studie

Disrupting cells' 'powerhouses' can lead to tumor growth, Penn study finds (Forstyrrelser av cellenes "kraftstasjoner" kan føre til tumorvekst, ifølge Penn-studie)
medicalnewstoday.com 11.7.2015
Kreftceller trosser regler som normale celler holde. De kan dele uten å opphøre, invadere fjerne vev og forbruker glukose ved unormale overholder. (Cancer cells defy the rules by which normal cells abide. They can divide without cease, invade distant tissues and consume glucose at abnormal rates.)

Nå indikerer en studie utført av forskere ved University of Pennsylvania forskere at defekter i mitokondriene, de energiproduksjonssentrene i celler, som spiller en nøkkelrolle ved overgangen fra normaltilstand til kreft. Når Penn-forskerne forstyrrer en nøkkelkomponent i mitokondriene fikk ellers normale celler til egenskapene til kreftkreftceller. (Now a study by University of Pennsylvania researchers implicates defects in mitochondria, the energy-production centers of cells, as playing a key role in the transition from normal to cancerous. When the Penn scientists disrupted a key component of mitochondria, otherwise normal cells took on characteristics of cancerous tumor cells.)

Forskningen er publisert I tidsskriftet Oncogene og ble ledet av medlemmer av laboratoriet  til Narayan G. Avadhani, Harriet Ellison Woodward, professor i biokjemi ved Penn's School of Veterinary Medicine's Department of Biomedical Sciences, I samarbeid med laboratoriet til Hiroshi Nakagawa ved Gastroenterology Division ved Penn's Perelman School of Medicine. Satish Srinivasan, forskningsgransker ved Avadhani's lab, var førsteforfatter. Manti Guha, Dawei Dong and Gordon Ruthel ved Penn Vet and Kelly A. Whelan of Penn Medicine bidro også, sammen med Yasuto Uchikado og Shoji Natsugoe det japanske Kagoshima University. (The research is published in the journal Oncogene and was led by members of the lab of Narayan G. Avadhani, the Harriet Ellison Woodward Professor of Biochemistry in Penn's School of Veterinary Medicine's Department of Biomedical Sciences, in collaboration with the lab of Hiroshi Nakagawa from the Gastroenterology Division in Penn's Perelman School of Medicine. Satish Srinivasan, a research investigator in Avadhani's lab, was the lead author. Manti Guha, Dawei Dong and Gordon Ruthel of Penn Vet and Kelly A. Whelan of Penn Medicine also contributed, along with Yasuto Uchikado and Shoji Natsugoe of Japan's Kagoshima University.)

I 1924 observerte den tyske biologen Otto Heinrich Warburg at kreftceller forforbruker glukose med en høyere rate enn normale celler og hadde feil i deres "grana," de organeller som nå er kjent som mitokondrier. Han hevdet at mitokondrielle defekter førte til problemer i prosessen ved hvilken cellen produserer energi, kalt oksidativ fosforylering, og at disse defekter bidro til cellene blir kreftlignende. (In 1924, German biologist Otto Heinrich Warburg observed that cancerous cells consumed glucose at a higher rate than normal cells and had defects in their "grana," the organelles that are now known as mitochondria. He postulated that the mitochondrial defects led to problems in the process by which the cell produces energy, called oxidative phosphorylation, and that these defects contributed to the cells becoming cancerous.)

"Den første delen av Warburghypotesen om at de fleste prolifererende svulster viser høy avhengighet av glukose som energikilde har vært solid, og at de frigjør store mengder melkesyre," uttalte Avadhani . "Men den andre delen, om den defekte mitokondrienes funksjon forårsaker celler blir tumorigente, har vært svært omstridt."  (…) ("The first part of the Warburg hypothesis has held up solidly in that most proliferating tumors show high dependence on glucose as an energy source and they release large amounts of lactic acid," Avadhani said. "But the second part, about the defective mitochondrial function causing cells to be tumorigenic, has been highly contentious.")

(Anm: Disruption of cytochrome c oxidase function induces the Warburg effect and metabolic reprogramming. Oncogene 2015 (6 July 2015).)

(Anm: Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage Front. Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Immunol. 2016 (20 July 2016).)

(Anm: Cancer as a mitochondrial metabolic disease. Front Cell Dev Biol. 2015 Jul 7;3:43. eCollection 2015.)

(Anm: Aggressive lymphoma linked to disruption in cell energy production (medicalnewstoday.com 20.7.2015).)

(Anm: Mitokondriell dysfunksjon (mitokondriedysfunksjon) indusert av sertraline (Zoloft), et antidepressiva (Mitochondrial dysfunction induced by sertraline, an antidepressant agent) Toxicol Sci. 2012 Jun;127(2):582-91. Epub 2012 Mar 2.)

(Anm: Kan Lupus øke risikoen for demens? Could lupus raise dementia risk? People living with lupus may be at significantly greater risk of developing dementia than those without the autoimmune disease, a new study suggests. (…) Study co-author Daniela Amital, of the Sackler Faculty of Medicine at Tel Aviv University in Israel, and colleagues recently reported their results in the International Journal of Geriatric Psychiatry. (medicalnewstoday.com 9.11.2017).)

(Anm: Effekten av tramadol, klonazepam og deres kombinasjoner på hjernens mitokondrielle komplekser. (Effects of tramadol, clonazepam, and their combination on brain mitochondrial complexes.) (…) Dette resultatet forklarer de kliniske og deres respektive histopatologiske effekter av tramadol, for eksempel anfall og røde nevroner (markør for apoptose). (The results showed that groups that received tramadol (therapeutic and abuse) suffered from weight loss.) (Toxicol Ind Health. 2015 Dec;31(12):1325-33).)

(Anm: Antibiotika kan utløse mitokondriell dysfunksjon som induserer psykiatriske lidelser. (Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders. Med Sci Monit. 2017 Jan 7;23:101-106.)

(Anm: PET Imaging of Mitochondrial Complex I with 18F-BCPP-EF in Brain of Parkinson's Disease Model Monkey. (…) CONCLUSION: 18F-BCPP-EF has potential as a PET probe for the quantitative imaging of MC-1 damage in the living brains of PD model monkeys using PET. J Nucl Med. 2016 Feb 11. pii: jnumed.115.169615. [Epub ahead of print].)

(Anm: Drug-induced mitochondrial dysfunction and cardiotoxicity. Am J Physiol Heart Circ Physiol. 2015 Sep 18:ajpheart.00554.2015. [Epub ahead of print].)

- Forskere oppdager mekanisme som styrer frigjøring av molekyler involvert i inflammatoriske sykdommer.

(Anm: Researchers discover mechanism that controls release of molecules involved in inflammatory diseases. In a recent study published in Cell Reports, a research team led by Colin Adrain, from the Instituto Gulbenkian de Ciência (IGC, Portugal), discovered the mechanism that controls the release of important molecules that trigger the inflammatory response during the clearance of infections. When this machinery is deregulated it can contribute to important chronic diseases such as inflammatory bowel disease, arthritis, and cancer. (…) An important feature of the newly identified mechanism is that the same protein, iRhom2, is important for controlling the release of growth factors that trigger cellular growth associated with many serious epithelial cancers. (news-medical.net 2.11.2017).)

(Anm: Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus.Lupus. 2015 Sep 18. pii: 0961203315605370. [Epub ahead of print].)

(Anm: Sykdommen som får kroppen til å angripe seg selv. Lupus rammer kvinner ni ganger så ofte som menn. (…) - Tilstanden er vanligst blant kvinner som er i 20- til 40-årene, sier Eide. Menn med lupus kan se ut til å bli oftere angrepet i nyrene enn kvinner med sykdommen, og man kan også oftere se endringer i blodbildet (hemolytisk anemi, lavere antall blodplater eller lavere antall lymfocytter) hos menn. (klikk.no 17.4.2017).)

(Anm: Mitochondrial troublemakers unmasked in lupus. Drivers of autoimmune disease. Inflammation discovered in the traps of pathogen-capturing white blood cells. New findings expose how mitochondria might instigate lupus-like inflammation. (medicalnewstoday.com 23.1.2016).)

- Fluoksetin (Prozac) og mitokondriene: En gjennomgang av de toksikologiske aspekter. (- Fluoksetin induserer også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser.) (- På den annen side har inntak av fluoxetin blitt assosiert med økt risiko for kreft. Likevel forblir data motstridende og ingen konklusjoner er trukket.) (- Flere studier har vist at fluoksetin interagerer med mitokondrier og trigger apoptose og / eller endring av mitokondriefunksjon ved å modulere aktiviteten av respiratoriske kjedekomponenter og enzymer i Krebs syklus. Videre påvirker fluoksetin mitokondriene relaterte redoks parametre i ulike eksperimentelle modeller.)

Fluoxetine and the mitochondria: A review of the toxicological aspects. (Fluoksetin og mitokondriene: En gjennomgang av de toksikologiske aspekter.)
Toxicol Lett. 2016 Jul 5. pii: S0378-4274(16)32264-0. [Epub ahead of print]
Abstrakt Fluoxetin (en selektiv serotonin-reopptaksinhibitor (SSRI)) brukes som antidepressiva ved å modulere nivåene av serotonin i den synaptiske spalten. Ikke desto mindre induserer fluoksetin også bivirkninger, som for eksempel angst, seksuell dysfunksjon, søvnforstyrrelser, og gastrointestinale svekkelser. Fluoksetin har blitt sett på som en substans som kan forstyrre celleforløpet ved å utløse apoptose. På den annen side er inntak av fluoxetin blitt assosiert med økt risiko for kreft. Til tross for dette forblir data motstridende og ingen konklusjoner er trukket. Flere studier har vist at fluoksetin interagerer med mitokondrier og trigger apoptose og / eller endring av mitokondriefunksjon ved å modulere aktiviteten av respiratoriske kjedekomponenter og enzymer i Krebs syklus. Videre påvirker fluoksetin mitokondriene relaterte redoks parametre i ulike eksperimentelle modeller. I denne gjennomgangen er data som viser effekten av fluoksetin på pattedyrs mitokondrier beskrevet og diskutert, samt flere uløste spørsmål i dette forskningsfeltet adressert. En egen del tar for seg fremtidige behov når det gjelder forskning som involverer effekten av fluoksetins påvirkninger på mitokondrier og mitokondrierelatert signalering. (...) (Abstract Fluoxetine (a selective serotonin reuptake inhibitor (SSRI)) is used as an antidepressant by modulating the levels of serotonin in the synaptic cleft. Nevertheless, fluoxetine also induces undesirable effects, such as anxiety, sexual dysfunction, sleep disturbances, and gastrointestinal impairments. Fluoxetine has been viewed as an agent that may interfere with cell fate by triggering apoptosis. On the other hand, fluoxetine intake has been associated with increased cancer risk. Nonetheless, data remain contradictory and no conclusions were taken. Several studies demonstrated that fluoxetine interacts with mitochondria triggering apoptosis and/or altering mitochondrial function by modulating the activity of respiratory chain components and enzymes of the Krebs cycle. Furthermore, fluoxetine affects mitochondria-related redox parameters in different experimental models. In this review, data demonstrating the effects of fluoxetine upon mammalian mitochondria are described and discussed, as well as several unsolved questions in this field of research are addressed. A separate section deals with future needs regarding the research involving the impact of fluoxetine treatment upon mitochondria and mitochondria-related signaling.)

(Anm: Mitochondrial dysfunction related to cell damage induced by 3-hydroxykynurenine and 3-hydroxyanthranilic acid: non dependent-effect of early reactive oxygen species production. Neurotoxicology. 2015 Aug 5. pii: S0161-813X(15)00118-7. [Epub ahead of print].)

- Sitronsyresyklus. Sitronsyresyklusen (også kjent som Krebs’ syklus og trikarboksylsyresyklus) er en serie kjemiske reaksjoner som er svært viktige i alle levende celler som nyttegjør seg av oksygen som en del av celleåndingen.

(Anm: Sitronsyresyklus. Sitronsyresyklusen (også kjent som Krebs’ syklus og trikarboksylsyresyklus) er en serie kjemiske reaksjoner som er svært viktige i alle levende celler som nyttegjør seg av oksygen som en del av celleåndingen. I denne syklusen blir det dannet energibærere i form av NADH, FADH2 og ATP. Hos aerobe organismer er sitronsyresyklusen en del av den metabolske prosessen som bryter ned karbohydrater, fett og proteiner til karbondioksid (CO2) og vann (H2O) for å generere energi. Den er den andre av tre metabolske prosesser som er involvert i katabolismen av næringsstoffer og produksjonen av ATP. (en.wikipedia.org).)

(Anm: Sertraline (Zoloft)-indusert systemisk lupus erythematosus (SLE) (Lupus) (Sertraline Induced Systemic Lupus Erythematosus) (The Internet Journal of Internal Medicine 2005;6(1).)

- Dødsrater for Lupus forblir høye i USA.

(Anm: Lupus Death Rates Remain High in U.S. Drop in SLE death rates less than non-lupus mortality. Despite improving trends in mortality, death rates from systemic lupus erythematosus (lupus) remain high compared with those in the general population, and disparities persist between subpopulations and geographic regions, according to a report in the Annals of Internal Medicine. (medpagetoday.com 6.11.2017).)

– Studien viser hvordan vanlig trening, stressreduksjon kan føre til bedre helse hos lupus pasienter.

(Anm: Study shows how regular exercise, stress reduction could lead to better health in lupus patients. Study shows how regular exercise, stress reduction could lead to better health in lupus patients (news-medical.net 19.9.2017).)

(Anm: Lupus Patients at Risk for Stroke. Risks high for women, the young, and during the year after diagnosis. Systemic lupus erythematosus (SLE) patients are more likely to experience ischemic and hemorrhagic stroke than the general population especially in the first year they are diagnosed, according to new research published in Annals of the Rheumatic Diseases. (medpagetoday.com 23.4.2017).)

(Anm: Lupus: Probiotics could help to reduce kidney inflammation. (…) Researchers have found that adding Lactobacillus to the diets of mice with lupus-induced kidney inflammation - also known as lupus nephritis - led to improvements in kidney function and increased their survival, but only in female mice. (…) Study co-author Xin Luo, from the Department of Biomedical Sciences and Pathobiology at Virginia-Maryland College of Veterinary Medicine at Virginia Tech, and colleagues recently reported their results in the journal Microbiome. (medicalnewstoday.com 3.10.2017).)

(Anm: Lupus: Low vitamin D may raise risk of kidney failure. (…) Dr. Michelle A. Petri, Ph.D., director of the Hopkins Lupus Center is the lead author of the study, and the findings were presented at the American College of Rheumatology/Association of Rheumatology Health Professionals (ACR/ARHP) Annual Meeting in San Diego, CA. Lupus is an autoimmune disease characterized by inflammation throughout the body. This occurs because the body does not recognize its own tissues and starts attacking them. The disease can affect various organ systems, from the cardiovascular and immune systems to vital organs such as the lungs and the kidneys. (medicalnewstoday.com 6.11.2017).)

(Anm: Lupus: Probiotics could help to reduce kidney inflammation. (…) Researchers have found that adding Lactobacillus to the diets of mice with lupus-induced kidney inflammation - also known as lupus nephritis - led to improvements in kidney function and increased their survival, but only in female mice. Lactobacillus are a type of "good" bacteria that reside in the digestive, urinary, and genital systems. These bacteria are also present in yogurt, kefir, and other fermented foods, as well as dietary supplements. While further studies are needed to confirm the possible benefits of Lactobacillus, the researchers believe that their findings indicate that women with lupus and kidney inflammation may benefit from taking probiotics. Study co-author Xin Luo, from the Department of Biomedical Sciences and Pathobiology at Virginia-Maryland College of Veterinary Medicine at Virginia Tech, and colleagues recently reported their results in the journal Microbiome. (medicalnewstoday.com 6.11.2017).)

(Anm: Researchers discover that beneficial bacteria in yogurt may affect severity of lupus (news-medical.net 3.10.2017).)

(Anm: Antifungals and probiotics could play critical role in potential new therapeutic approaches for IBD. (news-medical.net 5.10.2017).)

(Anm: Financial Strain Tied to Depression in Women with SLE. Survey: 40% of those reporting high money pressures developed depression. High financial strain nearly doubles the risk of incident depression in women with systemic lupus erythematosus (SLE). In an analysis of data from the Lupus Outcomes Study, financial strain was the only significant socioeconomic predictor of incident depression, reported Patricia P. Katz, PhD, from the University of California, San Francisco, and colleagues in Arthritis Care & Research. (medpagetoday.com 26.4.2017).)

(Anm: For lupus patients, anti-inflammatory immune cells are maturing Into wrong cell type (medicalnewstoday.com 9.3.2016).)

(Anm: Sertraline use during pregnancy and the risk of major malformations. OBJECTIVE: Given the current debate and growing public concerns on selective serotonin reuptake inhibitors (SSRIs) and birth defects generated by Food and Drug Administration warnings, we aim to quantify the association between first-trimester exposure to sertraline, a first-line treatment, and the risk of congenital malformations in a cohort of depressed women. (…) CONCLUSION: Sertraline use during the first trimester of pregnancy was associated with an increased risk of atrial/ventricular defects and craniosynostosis above and beyond the effect of maternal depression. Nonsertraline SSRIs were associated with an increased risk of craniosynostosis and musculoskeletal defects.Am J Obstet Gynecol. 2015 Jun;212(6):795.e1-795.e12. Epub 2015 Jan 28.)

(Anm: Fluoxetine (Prozac) interacts with the lipid bilayer of the inner membrane in isolated rat brain mitochondria, inhibiting electron transport and F1F0-ATPase activity (Fluoxetine interagerer med de lipide bilayer i det indre membram i isolerte mitokondrier i rottehjerner, hemmer elektrontransport og F1F0-ATPase aktivitet) Mol Cell Biochem 1999;199:103-9.)

(Anm: Effect of fluoxetine treatment on mitochondrial bioenergetics in central and peripheral rat tissues. (…) We observed an increase in glutathione S-transferase activity only in the hypothalamus of the Fx group. Taken together, our results suggest that chronic exposure to fluoxetine during the nursing phase of early rat development results in a positive modulation of mitochondrial respiration in the hypothalamus and skeletal muscle that persists into adulthood. Such long-lasting alterations in mitochondrial activity in the CNS, especially in areas regulating appetite, may contribute to permanent changes in energy balance in treated animals. Appl Physiol Nutr Metab. 2015 Jun;40(6):565-74. Epub 2015 Jan 22.)

- Svekket mitokondriefunksjon ved psykiatriske lidelser

Impaired mitochondrial function in psychiatric disorders. (Svekket mitokondriefunksjon ved psykiatriske lidelser)
Nat Rev Neurosci. 2012 Apr 18;13(5):293-307.
Abstakt Alvorlige psykiatriske sykdommer som stemningslidelser og schizofreni er kroniske tilbakevendende psykiske lidelser som påvirker livene til millioner av mennesker. Selv om disse lidelsene tradisjonelt er blitt sett på som "nevrokjemiske sykdommer" er det nå klart at de er knyttet til svekkelse av synaptisk plastisitet og cellulær elastisitet. Selv om de fleste pasienter med disse lidelsene ikke har klassiske mitokondrielidelser er det en økende mengde bevis som tyder på at svekket mitokondriefunksjon kan påvirke viktige cellulære prosesser, og dermed endre synaptisk funksjon og bidra til atrofiske endringer som ligger til grunn den forverrede langsiktige utvikling av disse sykdommene. Styrking av mitokondriefunksjon kan representere en viktig vei for utvikling av nye behandlingsformer og også representerer en mulighet for en potensielt mer effektiv utviklingsprosess for legemidler. (…) (Abstract Major psychiatric illnesses such as mood disorders and schizophrenia are chronic, recurrent mental illnesses that affect the lives of millions of individuals. Although these disorders have traditionally been viewed as 'neurochemical diseases', it is now clear that they are associated with impairments of synaptic plasticity and cellular resilience. Although most patients with these disorders do not have classic mitochondrial disorders, there is a growing body of evidence to suggest that impaired mitochondrial function may affect key cellular processes, thereby altering synaptic functioning and contributing to the atrophic changes that underlie the deteriorating long-term course of these illnesses. Enhancing mitochondrial function could represent an important avenue for the development of novel therapeutics and also presents an opportunity for a potentially more efficient drug-development process.)

- In schizophrenia, mitochondria are differentially affected depending on the brain region, cell type, subcellular location, treatment status, treatment response and symptoms.

Postmortem studies on mitochondria in schizophrenia.
Schizophr Res. 2017 Feb 9. pii: S0920-9964(17)30070-1. [Epub ahead of print]
Abstract The aim of this paper is to provide a brief review of mitochondrial structure as it relates to function and then present abnormalities in mitochondria in postmortem schizophrenia with a focus on ultrastructure. Function, morphology, fusion, fission, motility, ΔΨmem, ATP production, mitochondrial derived vesicles, and mitochondria-associated ER membranes will be briefly covered. Pathology in mitochondria has long been implicated in schizophrenia, as shown by genetic, proteomic, enzymatic and anatomical abnormalities. The cortex and basal ganglia will be reviewed. In the anterior cingulate cortex, the number of mitochondria per neuronal somata in layers 5/6 in schizophrenia is decreased by 43%. There are also fewer mitochondria in terminals forming axospinous synapses. In the caudate and putamen the number of mitochondria is abnormal in both glial cells and neurons in schizophrenia subjects, the extent of which depends on treatment, response and predominant lifetime symptoms. Treatment-responsive schizophrenia subjects had about a 40% decrease in the number of mitochondria per synapse in the caudate nucleus and putamen, while treatment resistant cases had normal values. A decrease in mitochondrial density in the neuropil distinguishes paranoid from undifferentiated schizophrenia. The appearance, size and density of mitochondria were normal in the nucleus accumbens. In the substantia nigra, COX subunits were affected in rostral regions. Mitochondrial hyperplasia occurs within axon terminals that synapse onto dopamine neurons, but mitochondria in dopamine neuronal somata are similar in size and number. In schizophrenia, mitochondria are differentially affected depending on the brain region, cell type, subcellular location, treatment status, treatment response and symptoms. (…)

(Anm: Altered Mitochondrial Function, Mitochondrial DNA and Reduced Metabolic Flexibility in Patients With Diabetic Nephropathy.EBioMedicine. 2015 Apr 11;2(6):499-512. eCollection 2015.)

(Anm: Building scaffolds in the cell's power stations. (…) Mitochondria are the powerhouses of cells and contain microscopic, strongly infolded membrane structures. These structures allow mitochondria to use the energy gained from food effectively. A large complex of several protein components, called the MICOS complex (the acronym for mitochondrial contact site and cristae organizing system), plays a key role in the inner structure of mitochondria and was discovered by the same group of scientists from the University of Freiburg several years ago. (medicalnewstoday.com 8.5.2015).)

(Anm: Slideshow: Thyroid Symptoms and Solutions (webmd.com 15.4..2014).)
(Anm: 15 Cancer Symptoms to Know (webmd 28.3.2016).)
(Anm: Slideshow: Causes of Fatigue and Sleepiness and How to Fight Them. (webmd).)
(Anm: Slideshow: A Visual Guide to Fibromyalgia (webmd.com 10.11.2014).)
(Anm: Slideshow: A Visual Guide to Understanding Lupus (webmd.com 2.2.2016).)
(Anm: Gout Pictures Slideshow: Causes, Symptoms, and Treatments of Gout (webmd.com 3.2.2016).)
(Anm: Slideshow: What Your Nails Say About Your Health (webmd.com 8.4.2014).)
(Anm: Sinusitis Slideshow: Symptoms, Diagnosis, Treatment (webmd 8.12.2014).)
(Anm: What Your Skin Says About Your Health Slideshow. (webmd.com 2.2.2016).)
(Anm: Type 2 Diabetes Overview (webmd.com 2.2.2016).)
(Anm: What Eye Problems Look Like (webmed).)

(Anm: Fibromyalgi: Fibromyalgi rammer over 100.000 norske kvinner. - En del tror sykdommen bare er tøys. Også blant leger er det en del som flirer av den, forteller professor. (…)   Når leger blir bedt om å rangere hvilke sykdommer det er mest prestisje å jobbe med, så havner alltid fibromyalgi nederst, forteller hun. Professor Egil Andreas Fors ved Institutt for samfunnsmedisin og allmennmedisinsk forskningsenhet ved NTNU er blant Norges fremste eksperter på sykdommen. Han bekrefter holdningene Slydal beskriver. (…) Sykdommen kjennetegnes gjerne ved at man har kroniske muskelsmerter, andre symptomer kan være utmattelse, hodepine, stivhet i kroppen, svimmelhet, kvalme, indre frost, depresjoner, angst og søvnproblemer. (kk.no 8.3.2016).)

(Anm: Lettere at diagnosticere fibromyalgi. På University of Colorado har forskere opdaget en speciel hjernesignatur, der med 93 pct. sikkerhed kan fastslå, hvorvidt en person lider af fibromyalgi eller ej. (pharmadanmark.anp.se 27.10.2016).)

(Anm: Management of interstitial lung disease associated with connective tissue disease. (…) Shrinking lung syndrome. (…) Systemic lupus erythematosus. BMJ 2016;352:h6819 (Published 24 February 2016).)

(Anm: Suicidal Thoughts Seen as Risk in Lupus. —Common among lupus patients with neuropsychiatric manifestations (medpagetoday.com 24.9.2015).)

(Anm: Antidepressiva - zimelidine (Zelmid) (SSRI) (mintankesmie.no).)

(Anm: Polynevropati betyr at flere av de perifere nervene i kroppen (særlig i føttene) ikke fungerer som de skal. (nhi.no 11.11.2013).)

(Anm: PET Imaging of Mitochondrial Complex I with 18F-BCPP-EF in Brain of Parkinson's Disease Model Monkey. (…) CONCLUSION: 18F-BCPP-EF has potential as a PET probe for the quantitative imaging of MC-1 damage in the living brains of PD model monkeys using PET. J Nucl Med. 2016 Feb 11. pii: jnumed.115.169615. [Epub ahead of print].)

- Translational Identification of Transcriptional Signatures of Major Depression and Antidepressant Response. (- Therefore, it was not surprising that the biological processes of the mitochondria are shared by the blood and the brain and are differentially regulated by chronic stress and fluoxetine treatment (Figure 3C).)

(Anm: Translational Identification of Transcriptional Signatures of Major Depression and Antidepressant Response. (…) Of the 13 identified genes that we tested for biomarker validation in human MDE patients, one of the genes HK1 has been previously linked to mood and psychotic disorders. HK1 encodes hexokinase 1, an initial and rate-limiting enzyme of glycolysis (Regenold et al., 2012). It has been known that genes associated with energy production are altered in postmortem brains as well as in peripheral tissues of MDD patients (Sibille et al., 2004; Klempan et al., 2009; Tobe, 2013; Garbett et al., 2015), and that molecular entities that are part of glycolysis pathway and the mitochondria in general serve as biomarkers and potential therapeutic targets for diagnosis and treatment of depression (Gormanns et al., 2011). Therefore, it was not surprising that the biological processes of the mitochondria are shared by the blood and the brain and are differentially regulated by chronic stress and fluoxetine treatment (Figure 3C). Front. Mol. Neurosci., 08 August 2017.)

(Anm: Pasienter behandlet med antipsykotika (nevroleptika) har signifikant senket platelet complex I aktivitet i mitokondrier i likhet med det som er observert ved idiopatisk Parkinsons sykdom. (...) Antipsykotika (nevroleptika) hemmer kompleks I i elektrontransportkjeden. (Neuroleptic medications inhibit complex I of the electron transport chain. (...) Neuroleptic treated patients have significant depression of platelet complex I activity similar to that seen in idiopathic Parkinson’s disease. Complex I inhibition may be associated with the extrapyramidal side effects of these drugs.) Ann Neurol. 1993;33:512-7).)

(Anm: Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes. (…) Highlights • Pancreatic mitochondrial complex I shows hyperactivity in diabetes. • Complex I hyperactivity is associated with increased NADH/NAD+ redox imbalance. • Complex I hyperactivity is associated with increased oxidative stress and cell death. • Complex I hyperactivity is linked with compromised cellular anti-oxidative stress capacity such as decreased sirt3 and NQO1 expressions. Biochem Biophys Rep. 2017 Sep;11:119-129.)

(Anm: Effekter av MPTP på serotonerge nevronale systemer og mitokondrie Complex I aktiviteten i den levende hjernen: En PET-studie på bevisste rhesusaper. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys. (Effects of MPTP on Serotonergic Neuronal Systems and Mitochondrial Complex I Activity in the Living Brain: A PET Study on Conscious Rhesus Monkeys.) J Nucl Med. 2017 Mar 9. pii: jnumed.116.189159.)

(Anm: Dysfunction of cellular powerplant shakes B-vitamin metabolism and causes genetic damage. Mitochondria are the cellular powerplant, but their functions in conjunction with B-vitamins are only starting to be revealed. When nutrient status is good, vitamin B9, folate, turns mitochondria to cellular builders. Through folate, mitochondria produce substances to make ingredients for genome replication and repair, cell membrane renewal and synthesis of antioxidants. The mechanism also includes other B-vitamins. (medicalnewstoday.com 7.3.2016).)

(Anm: Dementia in Parkinson's disease is associated with enhanced mitochondrial complex I deficiency. (…) CONCLUSIONS: Patients with PDD have a deficiency in mitochondrial complex I activity and reduced mitochondrial DNA levels in the prefrontal cortex without a change in mitochondrial protein quantity. Therefore, mitochondrial complex I deficiency and reduced mitochondrial DNA in the prefrontal cortex may be a hallmark of dementia in patients with PD. © 2016 International Parkinson and Movement Disorder Society.Mov Disord. 2016 Feb 8. [Epub ahead of print].)

(Anm: Antipsykotika (psykofarmaka etc.) (mintankesmie.no).)

(Anm: Lægemiddelstyrelsen opfordrer læger til at være opmærksomme på disse alvorlige bivirkninger hos børn og unge i behandling med aripiprazol (Abilify) (…) Gennemgangen viser også, at børn med ASD (autisme) der behandles med aripiprazol, kan udvikle alvorlige psykiatriske bivirkninger såsom svære kroniske søvnproblemer, aggressiv adfærd og hallucinationer. (…) Hårtab, depression og psykose, Vægtøgning, Hypercholesterolemi, Hypercholesterolemi. (LÆGEMIDDELSTYRELSEN - NYT OM BIVIRKNINGER 2016;7(9).)

(Anm: «Psykiatrien i Norge har hatt for svak ledelse. På alle nivåer. I alle år». KRONIKK: Helseminister Bent Høie (H). BENT HØIE, Helseminister. (vg.no 23.11.2016).)

(Anm: - Kan vi stole på forskningen? (...) - Er det ikke så nøye med sannheten fordi det lønner seg økonomisk og er lettvint bare å tro på forenklingene, halvsannhetene og de opplagt bløffene? (...) - Trass i all forskning. Trass i alle milliarder av kroner som var blitt investert, trass i alle gode intensjoner. Men «sannheten om de psykiske sykdommers natur, ubalansen i hjernens kjemi»