Search results for "mitochondria"

showing 6 items of 1306 documents

The oxidative capacity of skeletal muscle : effects of genotype, high-fat diet and physical activity

2016

sopeutuminenmitochondrial biogenesisrasvatexerciselihaksetliikuntafysiologiaadaptationhiiretruokavaliotgenotyyppiangiogenesishigh-fat dietgene expressionmetabolinen oireyhtymäfyysinen aktiivisuushapenotto
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The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and Cilia to Regulate Ciliogenesis and Ciliary Protein Traffic

2021

ABSTRACTELMODs are a family of three mammalian paralogs that display GTPase activating protein (GAP) activity towards a uniquely broad array of ADP-ribosylation factor (ARF) family GTPases that includes ARF-like (ARL) proteins. ELMODs are ubiquitously expressed in mammalian tissues, highly conserved across eukaryotes, and ancient in origin, being present in the last eukaryotic common ancestor. We described functions of ELMOD2 in immortalized mouse embryonic fibroblasts (MEFs) in the regulation of cell division, microtubules, ciliogenesis, and mitochondrial fusion. Here, using similar strategies with the paralogs ELMOD1 and ELMOD3, we identify novel functions and locations of these cell regu…

symbols.namesakeCell divisionGTPase-activating proteinmitochondrial fusionMicrotubuleCiliogenesisCiliumsymbolsGTPaseBiologyGolgi apparatusCell biology
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Prenatal thyroid hormones accelerate postnatal growth and telomere shortening in wild great tits

2021

AbstractEarly-life environment is known to affect later-life health and disease, which could be mediated by the early-life programming of telomere length, a key hallmark of ageing. According to thefetal programming of telomere biology hypothesis, variation in prenatal exposure to hormones is likely to influence telomere length. Yet the contribution of key metabolic hormones,i.e. thyroid hormones (THs), has been largely ignored. We recently showed that in contrast to predictions, exposure to elevated prenatal THs increased postnatal telomere length in wild collared flycatchers, but the generality of such effect, its underlying proximate mechanisms and consequences on survival have not been i…

telomerePhysiologymitokondriottalitiainenAquatic Sciencethyroid hormonemitochondriaikääntyminendevelopmental programmingageingInsect Scienceoxidative stressmaternal effectstelomeeritAnimal Science and Zoologymetabolismoksidatiivinen stressiaineenvaihduntaMolecular BiologyEcology Evolution Behavior and SystematicsJournal of Experimental Biology
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Randomized Trial : D-Glyceric Acid Activates Mitochondrial Metabolism in 50–60-Year-Old Healthy Humans

2021

Background: Based on earlier studies, natural metabolite D-glyceric acid (DGA) does not seem to play any role in whole-body metabolism. Nevertheless, one ethanol oxidation-related rat study with controversial results raised our interest. According to preparatory studies for the regulatory approval of DGA, some highly conserved mechanism seems to subtly activate the cellular energy metabolism. Therefore, the present 25-days double-blind human study with placebo control was initiated. Purpose: The main target in the present study with 27 healthy 50–60-year-old human volunteers was to find out whether an “acute” 4-days and a longer 21-days exogenous DGA regimen caused moderate activation of th…

tulehdusmitokondriotRC952-954.6mitochondrial activationre-oxidationsatunnaistetut vertailukokeetDGA activationsolutsubclinical inflammationGeriatricsmembrane integrityaineenvaihduntaD-glyseriinihappoenergiankulutus (aineenvaihdunta)
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Real-world experience with obeticholic acid in patients with primary biliary cholangitis

2021

Background & aims Obeticholic acid (OCA) is the second-line treatment approved for patients with primary biliary cholangitis (PBC) and an inadequate response or intolerance to ursodeoxycholic acid. We aimed to evaluate the effectiveness and safety of OCA under real-world conditions. Methods Patients were recruited into the Italian PBC Registry, a multicentre, observational cohort study that monitors patients with PBC at national level. The primary endpoint was the biochemical response according to Poise criteria; the secondary endpoint was the biochemical response according to normal range criteria, defined as normal levels of bilirubin, alkaline phosphatase (ALP), and alanine aminotransfer…

upper limit of normalCirrhosisALTAMAAutoimmunityantinuclear antibodiesULNPBCGastroenterologyUDCASettore MED/12ULN upper limit of normalobeticholic acidaRR adjusted risk ratio.CRFs case record formAST aspartate transferaseClinical endpointGGT gamma-glutamyl transferaseQCprimary biliary cholangitisGastroenterologyUrsodeoxycholic acidANATCCCirrhosisCholestasiTIPSTreatment Completer CohortANA antinuclear antibodiemedicine.medical_specialtyRRUDCA ursodeoxycholic acidTIPS transjugular intrahepatic portosystemic shuntOCACirrhosiALP alkaline phosphataseautoimmune hepatitismedicine.diseasedigestive system diseasesDiscontinuationKeywords: AIH autoimmune hepatitiQC quality controlchemistrygamma-glutamyl transferaserandomised controlled trialelectronic data captureantimitochondrial antibodiesaspartate transferaseAutoimmune hepatitischemistry.chemical_compoundAIHCRFsImmunology and Allergyadjusted risk ratioANA antinuclear antibodiesRR risk ratioOverall cohortALT alanine transferaseAMA antimitochondrial antibodieCholestasisCRFs case record formsObeticholic acidOverlap PBC-AIHursodeoxycholic acidOCA obeticholic acidTolerabilityalkaline phosphataseRCTResearch Articlemedicine.drugcase record formsContext (language use)AMA antimitochondrial antibodiesInternal medicineEDC electronic data capturetransjugular intrahepatic portosystemic shuntInternal MedicinemedicineRCT randomised controlled trialaRR adjusted risk ratioOClcsh:RC799-869quality controlalanine transferaseASTaRRHepatologybusiness.industryAutoimmunity; Cholestasis; Cirrhosis; Overlap PBC-AIHAIH autoimmune hepatitisTCC Treatment Completer CohortPBC primary biliary cholangitiGGTrisk ratioOC Overall cohortALPlcsh:Diseases of the digestive system. GastroenterologyPBC primary biliary cholangitisbusinessEDC
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Virus-cell interactions as a pathological mechanism of parvovirus infection

2014

vauriotreplikaatiovuorovaikutusisäntäsolutviruksetCPVpatogeneesimitokondriotapoptosiscanine parvovirussolutuhocell signallinginfektiotmitochondriacell cycle arrestpathologyparvoviruksetapoptoosi
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