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('''Background ''' Mitochondrial dysfunction is one of the most characte)

Krebiehl 2010 PLoS One + ('''Background''' Mitochondrial dysfunction … '''Background''' Mitochondrial dysfunction and degradation takes a central role in current paradigms of neurodegeneration in Parkinson's disease (PD). Loss of DJ-1 function is a rare cause of familial PD. Although a critical role of DJ-1 in oxidative stress response and mitochondrial function has been recognized, the effects on mitochondrial dynamics and downstream consequences remain to be determined.'''Methodology/Principal Findings''' Using DJ-1 loss of function cellular models from knockout (KO) mice and human carriers of the E64D mutation in the DJ-1 gene we define a novel role of DJ-1 in the integrity of both cellular organelles, mitochondria and lysosomes. We show that loss of DJ-1 caused impaired mitochondrial respiration, increased intramitochondrial reactive oxygen species, reduced mitochondrial membrane potential and characteristic alterations of mitochondrial shape as shown by quantitative morphology. Importantly, ultrastructural imaging and subsequent detailed lysosomal activity analyses revealed reduced basal autophagic degradation and the accumulation of defective mitochondria in DJ-1 KO cells, that was linked with decreased levels of phospho-activated ERK2.'''Conclusions/Significance''' We show that loss of DJ-1 leads to impaired autophagy and accumulation of dysfunctional mitochondria that under physiological conditions would be compensated via lysosomal clearance. Our study provides evidence for a critical role of DJ-1 in mitochondrial homeostasis by connecting basal autophagy and mitochondrial integrity in Parkinson's disease.hondrial integrity in Parkinson's disease.)
Ross-Hellauer 2017 F1000Res + ('''Background''': "Open peer review" (OPR) … '''Background''': "Open peer review" (OPR), despite being a major pillar of Open Science, has neither a standardized definition nor an agreed schema of its features and implementations. The literature reflects this, with numerous overlapping and contradictory definitions. While for some the term refers to peer review where the identities of both author and reviewer are disclosed to each other, for others it signifies systems where reviewer reports are published alongside articles. For others it signifies both of these conditions, and for yet others it describes systems where not only "invited experts" are able to comment. For still others, it includes a variety of combinations of these and other novel methods. '''Methods''': Recognising the absence of a consensus view on what open peer review is, this article undertakes a systematic review of definitions of "open peer review" or "open review", to create a corpus of 122 definitions. These definitions are systematically analysed to build a coherent typology of the various innovations in peer review signified by the term, and hence provide the precise technical definition currently lacking. '''Results''': This quantifiable data yields rich information on the range and extent of differing definitions over time and by broad subject area. Quantifying definitions in this way allows us to accurately portray exactly how ambiguously the phrase "open peer review" has been used thus far, for the literature offers 22 distinct configurations of seven traits, effectively meaning that there are 22 different definitions of OPR in the literature reviewed. '''Conclusions''': I propose a pragmatic definition of open peer review as an umbrella term for a number of overlapping ways that peer review models can be adapted in line with the aims of Open Science, including making reviewer and author identities open, publishing review reports and enabling greater participation in the peer review process. participation in the peer review process.)
Ahn 2010 Biochim Biophys Acta + ('''Background''': Atherosclerosis is one o … '''Background''': Atherosclerosis is one of the major complications of diabetes, which may result from insulin resistance via mitochondrial dysfunction. Although a strong association between insulin resistance and cardiovascular disease has been suggested, it is not clear yet whether stress-inducing factors damage mitochondria and insulin signaling pathway in cardiovascular tissues.'''Methods''': We investigated whether stress-induced mitochondrial dysfunction might alter the insulin/Akt signaling pathway in A10 rat vascular smooth muscle cells (VSMC).'''Results''': The treatment of oxidized low density lipoprotein (oxLDL) decreased ATP contents, mitochondrial respiration activity, mRNA expressions of OXPHOS subunits and IRS-1/2 and insulin-mediated phosphorylations of Akt and AMP-activated protein kinase (AMPK). Similarly, dideoxycytidine (ddC), the mtDNA replication inhibitor, or rotenone, OXPHOS complex I inhibitor, inhibited the insulin-mediated pAkt while increased pAMPK regardless of insulin. Reciprocally, an inhibitor of Akt, triciribine (TCN), decreased cellular ATP contents. Overexpression of Akt dominant positive reversed the oxLDL- or ddC-mediated ATP decrease but AMPK activator did not. Akt activation also normalized the aberrant VSMC migration induced by ddC.'''Conclusions''': Defective insulin signaling and mitochondrial function may collectively contribute to developing cardiovascular disease.'''General significance''': Akt may be a possible therapeutic target for treating insulin resistance-associated atherosclerosis.lin resistance-associated atherosclerosis.)
Trimmer 2009 Mol Neurodegener + ('''Background''': It has been hypothesized … '''Background''': It has been hypothesized that reduced axonal transport contributes to the degeneration of neuronal processes in Parkinson's disease (PD). Mitochondria supply the adenosine triphosphate (ATP) needed to support axonal transport and contribute to many other cellular functions essential for the survival of neuronal cells. Furthermore, mitochondria in PD tissues are metabolically and functionally compromised. To address this hypothesis, we measured the velocity of mitochondrial movement in human transmitochondrial cybrid "cytoplasmic hybrid" neuronal cells bearing mitochondrial DNA from patients with sporadic PD and disease-free age-matched volunteer controls (CNT). The absorption of low level, near-infrared laser light by components of the mitochondrial electron transport chain (mtETC) enhancesmitochondrial metabolism, stimulates oxidative phosphorylation and improves redox capacity. PD and CNT cybrid neuronal cells were exposed to near-infrared laser light to determine if the velocity of mitochondrial movement can be restored by low level light therapy (LLLT). Axonal transport of labeled mitochondria was documented by time lapse microscopy in dopaminergic PD and CNT cybrid neuronal cells before and after illumination with an 810 nm diode laser (50 mW/cm2) for 40 s. Oxygen utilization and assembly of mtETS complexes were also determined.'''Results''': The velocity of mitochondrial movement in PD cybrid neuronal cells (0.175 +/- 0.005 SEM) was significantly reduced (p < 0.02) compared to mitochondrial movement in disease free CNT cybrid neuronal cells (0.232 +/- 0.017 SEM). For two hours after LLLT, the average velocity of mitochondrial movement in PD cybrid neurites was significantly (p < 0.003) increased (to 0.224 +/- 0.02 SEM) and restored to levels comparable to CNT. Mitochondrial movement in CNT cybrid neurites was unaltered by LLLT (0.232 +/- 0.017 SEM). Assembly of complexes in the mtETC was reduced and oxygen utilization was altered in PD cybrid neuronal cells. PD cybrid neuronal cell lines with the most dysfunctional mtETC assembly and oxygen utilization profiles were least responsive to LLLT.'''Conclusion''': The results from this study support our proposal that axonal transport is reduced in sporadic PD and that a single, brief treatment with near-infrared light can restore axonal transport to control levels. These results are the first demonstration that LLLT can increase axonal transport in model human dopaminergic neuronal cells and they suggest that LLLT could be developed as a novel treatmentto improve neuronal function in patients with PD. treatment to improve neuronal function in patients with PD.)
Droese 2009 Biochim Biophys Acta + ('''Background''': Reactive oxygen species … '''Background''': Reactive oxygen species (ROS) are among the main determinants of cellular damage during ischemia and reperfusion. There is also ample evidence that mitochondrial ROS production is involved in signaling during ischemic and pharmacological preconditioning. In a previous study we analyzed the mitochondrial effects of the efficient preconditioning drug diazoxide and found that it increased the mitochondrial oxidation of the ROS-sensitive fluorescent dye 2′,7′-dichlorodihydrofluorescein (H2DCF) but had no direct impact on the H2O2 production of submitochondrial particles (SMP) or intact rat heart mitochondria (RHM).'''Methods''': H2O2 generation of bovine SMP and tightly coupled RHM was monitored under different conditions using the amplex red/horseradish peroxidase assay in response to diazoxide and a number of inhibitors.'''Results''': We show that diazoxide reduces ROS production by mitochondrial Complex I under conditions of reverse electron transfer in tightly coupled RHM, but stimulates mitochondrial ROS production at the Qo site of Complex III under conditions of oxidant-induced reduction; this stimulation is greatly enhanced by uncoupling. These opposing effects can both be explained by inhibition of Complex II by diazoxide. 5-Hydroxydecanoate had no effect, and the results were essentially identical in the presence of Na+ or K+ excluding a role for putative mitochondrial KATP-channels.'''General significance''': A straightforward rationale is presented to mechanistically explain the ambivalent effects of diazoxide reported in the literature. Depending on the metabolic state and the membrane potential of mitochondria, diazoxide-mediated inhibition of Complex II promotes transient generation of signaling ROS at Complex III (during preconditioning) or attenuates the production of deleterious ROS at Complex I (during ischemia and reperfusion).x III (during preconditioning) or attenuates the production of deleterious ROS at Complex I (during ischemia and reperfusion).)
Sokolova 2009 BMC Cell Biol + ('''Background''': Restriction of intracell … '''Background''': Restriction of intracellular diffusion of adenine nucleotides has been studied intensively on adult rat cardiomyocytes. However, their cause and role ''in vivo'' is still uncertain. Intracellular membrane structures have been suggested to play a role. We therefore chose to study cardiomyocytes from rainbow trout (''Oncorhynchus mykiss''), which are thinner and have fewer intracellular membrane structures than adult rat cardiomyocytes. Previous studies suggest that trout permeabilized cardiac fibers also have diffusion restrictions. However, results from fibers may be affected by incomplete separation of the cells. This is avoided when studying permeabilized, isolated cardiomyocytes. The aim of this study was to verify the existence of diffusion restrictions in trout cardiomyocytes by comparing ADP-kinetics of mitochondrial respiration in permeabilized fibers, permeabilized cardiomyocytes and isolated mitochondria from rainbow trout heart. Experiments were performed at 10, 15 and 20°C in the absence and presence of creatine.'''Results''': Trout cardiomyocytes hypercontracted in the solutions used for mammalian cardiomyocytes. We developed a new solution in which they retained their shape and showed stable steady state respiration rates throughout an experiment. The apparent ADP-affinity of permeabilized cardiomyocytes was different from that of fibers. It was higher, independent of temperature and not increased by creatine. However, it was still about ten times lower than in isolated mitochondria.'''Conclusions''': The differences between fibers and cardiomyocytes suggest that results from trout heart fibers were affected by incomplete separation of the cells. However, the lower ADP-affinity of cardiomyocytes compared to isolated mitochondria indicate that intracellular diffusion restrictions are still present in trout cardiomyocytes despite their lower density of intracellular membrane structures. The lack of a creatine effect indicates that trout heart lacks mitochondrial creatine kinase tightly coupled to respiration. This argues against diffusion restriction by the outer mitochondrial membrane. These results from rainbow trout cardiomyocytes resemble those from other low-performance hearts such as neonatal rat and rabbit hearts. Thus, it seems that metabolic regulation is related to cardiac performance, and it is likely that rainbow trout can be used as a model animal for further studies of the localization and role of diffusion restrictions in lowperformance hearts.ion restrictions in lowperformance hearts.)
Amoedo 2011 PLoS One + ('''Background''': Tumor cells are characte … '''Background''': Tumor cells are characterized by accelerated growth usually accompanied by up-regulated pathways that ultimately increase the rate of ATP production. These cells can suffer metabolic reprogramming, resulting in distinct bioenergetic phenotypes, generally enhancing glycolysis channeled to lactate production. In the present work we showed metabolic reprogramming by means of inhibitors of histone deacetylase (HDACis), sodium butyrate and trichostatin. This treatment was able to shift energy metabolism by activating mitochondrial systems such as the respiratory chain and oxidative phosphorylation that were largely repressed in the untreated controls.'''Methodology/Principal Findings''': Various cellular and biochemical parameters were evaluated in lung cancer H460 cells treated with the histone deacetylase inhibitors (HDACis), sodium butyrate (NaB) and trichostatin A (TSA). NaB and TSA reduced glycolytic flux, assayed by lactate release by H460 cells in a concentration dependent manner. NaB inhibited the expression of glucose transporter type 1 (GLUT 1), but substantially increased mitochondria bound hexokinase (HK) activity. NaB induced increase in HK activity was associated to isoform HK I and was accompanied by 1.5 fold increase in HK I mRNA expression and cognate protein biosynthesis. Lactate dehydrogenase (LDH) and pyruvate kinase (PYK) activities were unchanged by HDACis suggesting that the increase in the HK activity was not coupled to glycolytic flux. High resolution respirometry of H460 cells revealed NaB-dependent increased rates of oxygen consumption coupled to ATP synthesis. Metabolomic analysis showed thatNaB altered the glycolytic metabolite profile of intact H460 cells. Concomitantly we detected an activation of the pentose phosphate pathway (PPP). The high O2 consumption in NaB-treated cells was shown to be unrelated to mitochondrial biogenesis since citrate synthase (CS) activity and the amount of mitochondrial DNA remained unchanged.'''Conclusion''': NaB and TSA induced an increase in mitochondrial function and oxidative metabolism in H460 lung tumor cells concomitant with a less proliferative cellular phenotype.h a less proliferative cellular phenotype.)
Gomez 2008 Circulation + ('''Background'''—Opening of the mitochondr … '''Background'''—Opening of the mitochondrial permeability transition pore (mPTP) is a crucial event in lethal reperfusion injury. Phosphorylation (inhibition) of glycogen synthase kinase-3β (GSK3β) has been involved in cardioprotection. We investigated whether phosphorylated GSK3β may protect the heart via the inhibition of mPTP opening during postconditioning.'''Methods and Results'''—Wild-type and transgenic GSK3β-S9A mice (the cardiac GSK3β activity of which cannot be inactivated) underwent 60 minutes of ischemia and 24 hours of reperfusion. At reperfusion, wild-type and GSK3β-S9A mice received no intervention (control), postconditioning (3 cycles of 1 minute ischemia and 1 minute of reperfusion), the mPTP inhibitor cyclosporine A (CsA; 10 mg/kg IV), or the GSK3β inhibitor SB216763 (SB21; 70 µg/kg IV). Infarct size was assessed by triphenyltetrazolium chloride staining. The resistance of the mPTP to opening after Ca2+ loading was assessed by spectrofluorometry on mitochondria isolated from the area at risk. In wild-type mice, infarct size was significantly reduced by postconditioning, CsA, and SB21, averaging 39±2%, 35±5%, and 37±4%, respectively, versus 58±5% of the area at risk in control mice (P<0.05). In GSK3β-S9A mice, only CsA, but not postconditioning or SB21, reduced infarct size. Postconditioning, CsA, and SB21 all improved the resistance of the mPTP in wild-type mice, but only CsA did so in GSK3β-S9A mice.'''Conclusion'''—These results suggest that S9-phosphorylation of GSK3β is required for postconditioning and likely acts by inhibiting the opening of the mitochondrial permeability transition pore.pening of the mitochondrial permeability transition pore.)
Leadsham 2010 BMC Cell Biol + ('''Background:''' Appropriate control of m … '''Background:''' Appropriate control of mitochondrial function, morphology and biogenesis are crucial determinants of the general health of eukaryotic cells. It is therefore imperative that we understand the mechanisms that coordinatemitochondrial function with environmental signaling systems. The regulation of yeast mitochondrial function in response to nutritional change can be modulated by PKA activity. Unregulated PKA activity can lead to the production of mitochondria that are prone to the production of ROS, and an apoptotic form of cell death.'''Results:''' We present evidence that mitochondria are sensitive to the level of cAMP/PKA signaling and can respond by modulating levels of respiratory activity or committing to self execution. The inappropriate activation of one ofthe yeast PKA catalytic subunits, Tpk3p, is sufficient to commit cells to an apoptotic death through transcriptional changes that promote the production of dysfunctional, ROS producing mitochondria. Our data implies that cAMP/PKA regulation of mitochondrial function that promotes apoptosis engages the function of multiple transcription factors, including HAP4, SOK2 and SCO1.'''Conclusions:''' We propose that in yeast, as is the case in mammalian cells, mitochondrial function and biogenesis are controlled in response to environmental change by the concerted regulation of multiple transcription factors. The visualization of cAMP/TPK3 induced cell death within yeast colonies supports a model that PKA regulation plays a physiological role in coordinating respiratory function and cell death with nutritional status in budding yeast. with nutritional status in budding yeast.)
Kalbacova 2003 Cytometry + ('''Background:''' Determination of mitocho … '''Background:''' Determination of mitochondrial membrane potential ((m) is widely used to characterize cellular metabolism, viability, and apoptosis. Changes of ΔΨm induced by inhibitors of oxidative phosphorylation characterizerespective contributions of mitochondria and glycolysis to adenosine triphosphate (ATP) synthesis.'''Methods:''' ΔΨm in BSC-40 and HeLa G cell lines was determined by flow cytometry and spectrofluorometry. Its changes induced by specific mitochondrial inhibitors were evaluated using 3,3 ΔΨ-dihexyloxacarbocyanine iodide(DiOC6(3)), tetramethylrhodamine ethyl ester, and Mito-Tracker Red. Mitochondrial function was further characterized by oxygen consumption.'''Results:''' Inhibition of respiration by antimycin A or uncouplingof mitochondria by FCCP decreased ΔΨm in both cell lines. Inhibition of ATP production by oligomycin or atractyloside induced a moderate decrease of ΔΨmin HeLa G cells and an increase of ΔΨm in BSC-40 cells. Statistically significant differences in ΔΨm between the two cell lines were found with both flow cytometry and spectrofluorometry. Respirometry showed higher basaland FCCP-stimulated respiration in BSC-40 cells.'''Conclusion:''' Changes of ΔΨm and oxygen consumption showed that BSC-40 cells are more sensitive than HeLa G cells to inhibitors of mitochondrial function, suggesting that BSC-40 cells are more dependent than HeLa G cells onaerobic ATP production. Determination of ΔΨm changes by flow cytometry exhibited greater sensitivity than the ones by spectrofluorometry.ivity than the ones by spectrofluorometry.)
Hecker 2014 JPEN + ('''Background:''' Sepsis is a severe infla … '''Background:''' Sepsis is a severe inflammatory disorder with a high mortality in intensive care units mostly due to multiorgan failure. Mitochondrial dysfunction is regarded as a key factor involved in the pathogenesis of septic disorders, leading to a decline in energy supply. The aim of the present study was to evaluate whether application of short-chain fatty acids (SCFAs) and medium-chain fatty acids (MCFAs) could improve mitochondrial function and thus might serve as a potential energy source under inflammatory conditions. '''Materials and Methods:''' As an experimental approach, starved human endothelial cells and monocytes were incubated with hexanoic acid, heptanoic acid, octanoic acid, or glucose and subsequently subjected to high-resolution respirometry to assess mitochondrial function under baseline conditions. In a second set of experiments, cells were pretreated with tumor necrosis factor-α to mimic inflammation and sepsis. Results: We demonstrated that addition of SCFAs and MCFAs increases mitochondrial respiratory capacity at baseline and inflammatory conditions in both cell types. None of the fatty acids induced changes in mitochondrial DNA content or the generation of proinflammatory cytokines, indicating a beneficial safety profile. '''Conclusion:''' We deduce that SCFAs and MCFAs are suitable and safe sources of energy under inflammatory conditions with the capability to partly restore mitochondrial respiration. partly restore mitochondrial respiration.)
Basal respiration + ('''Basal respiration''' is well defined in physiology. Terminology in mitochondrial physiology gains quality by reference to established concepts.)
Bioblast 2022 + ('''Bioblast 2022: Inaugural Conference of ''Bioenergetics Communications''''')
Wiethuechter MiP2010 + ('''Bioblast''' was launched as a glossary … '''Bioblast''' was launched as a glossary and index for high-resolution respirometry (Oroboros Instruments: OroboPedia) and Mitochondrial Physiology (MitoPedia), to find topics quickly, as a dynamic tool for summarizing definitions of terms, symbols and abbreviations. However, it´s potential benefits as an innovative, self-developing database make the '''Bioblast Wiki''' much more than a service by Oroboros.i''' much more than a service by Oroboros.)
Bioenergetics Vienna + ('''Bioenergetics Vienna''', 1st Bioenergetics DE-CH-AT Meeting)
BMS2016 Lausanne CH + ('''Brain bioenergetics – From behavior to pathology, Lausanne, CH''')
EU-METAHEART Kick-off meeting Brussels BE + ('''COST CA22169 METAHEART Kick-off meeting MC1, Brussels, Belguim, 2023-10-18''')
MiP2019/MitoEAGLE Belgrade RS + ('''COST MitoEAGLE WG and MC Meeting, 2019, Belgrade, Serbia.''')
Brown 2018 McCarrison Society + ('''Call for research - We all need oxygen … '''Call for research - We all need oxygen – “The oceans are gasping for air”''' 1, 2, 3“Human dominion over planet Earth is driving profound changes that may culminate in extinction.” 4 Whilst there is wider research into the oceanic impact of climate change including warming and acidification,5, 6 and on oxygen content of oceans, there is very little research into the specific impact of acidification and related carbon dioxide changes on marine photosynthetic oxygen production.This is an important field of research as it also involves consideration of the consequent effects of excess atmospheric carbon dioxide, including warming, on oceanic and atmospheric oxygen, oxygen exchange between them and possibilities of tipping points whereby photosynthetic marine organisms may rapidly die off, potentially leading to severe existential consequences for aerobic life forms.We bemoan the loss of polar bears and rare alpine plants along with changes to weather and food, but as societies and individuals we are reluctant to severely moderate the day-to-day fossil fuel energy consumption that underlies 21st century life. When faced by the choice of polar bears vs cars, heating, laptops and phones, the polar bears lose!Ocean acidification is a more empirically evidenced phenomenon than climate change, however, it is also less prominent in the public psyche even though it springs from the same increased atmospheric carbon dioxide levels. Were research to be commissioned, though, that provides clear evidence of risk to oceanic oxygen production and therefore atmospheric oxygen levels, the conclusions could be far-reaching, including identifying a potential tipping point that may result in human extinction.This stark prospect would, arguably, be easier to convey to, and fix in the wider public consciousness than the more diffuse issues around climate change. Humans are reminded with every breath they take that oxygen is essential to their health function and, ultimately, their survival and existence as a species.7 The importance of the prospect of oxygen depletion for future generations would be easily understood by all, and so promote greater public engagement and cohesive demand for a global response to try and find viable energy alternatives to fossil fuels.iable energy alternatives to fossil fuels.)
Chemical biology approaches to assessing and modulating mitochondria 2016 Buckinghamshire UK + ('''Chemical biology approaches to assessing and modulating mitochondria, Buckinghamshire, UK''')
Gnaiger 2007 MitoPathways + ('''Contents''' * Introduction [http://www. … '''Contents'''* Introduction [http://www.oroboros.at/fileadmin/user_upload/Reprints/O-MiPNet-Publ/MitoPathways2_Introduction.pdf pdf]* MitoPathways to Complex I: [[MiPNet11.04]]* MitoPathways to Complex II: [[MiPNet11.09]]* MitoPathways to Complexes I&II: [[MiPNet12.12]]* MitoPathways compilation: [[MiPNet12.13]] * MitoPathways - respiratory states: [[MiPNet12.15]]* Cell respiration and phosphorylation control: [[MiPNet08.09]] * HRR and phosphorylation control: [[MiPNet10.04]]* FCRs in isolated mitochondria: [[MiPNet12.11]]* O2k manual titrations: [[MiPNet09.12]]* O2k-paradigm: [[MiPNet09.01]]* [[Gnaiger 2012 MitoPathways References|References]]* The Oroboros - Feeding on negative entropy [http://www.oroboros.at/fileadmin/user_upload/Reprints/O-MiPNet-Publ/MitoPathways2_Introduction.pdf pdf]Reprints/O-MiPNet-Publ/MitoPathways2_Introduction.pdf pdf])
Raboel 2010 J Clin Endocrinol Metab + ('''Context''': Previous studies on leg ske … '''Context''': Previous studies on leg skeletal musculature have demonstrated mitochondrial dysfunction associated with type 2 diabetes mellitus (T2DM), but it is not known whether mitochondrial dysfunction is present in the upper extremities.'''Objective''': The aim of the study was to compare mitochondrial respiration and markers of mitochondrial content in skeletal muscle of arm and leg in patients with T2DM and obese control subjects.'''Patients''': Ten patients with T2DM (age, 52.3 ± 2.7 yr; body mass index, 30.1 ± 1.2 kg/m2) (mean ± SE) were studied after a 2-wk washout period of oral antihyperglycemic agents. Ten control subjects (age, 54.3 ± 2.8 yr; body mass index, 30.4 ± 1.2 kg/m2) with normal fasting and 2-h oral glucosetolerance test blood glucose levels were also included. Main Outcome Measure:Wemeasured mitochondrial respiration in saponin-treated skinned musclefibers from biopsies of m. deltoideus and m. vastus lateralis using high-resolution respirometry.'''Results''': In the arm, mitochondrial respiration and citrate synthase activity did not differ between groups, but mitochondrial respiration per milligram of muscle was significantly higher in the leg muscle of the control subjects compared to T2DM. Fiber type compositions in arm and leg muscleswere not different between the T2DM and control group, and maximum rate of O2 consumption did not differ between the groups.'''Conclusion''': The results demonstrate that reduced mitochondrial function in T2DM is only present in the leg musculature. This novel finding suggests that mitochondrial dysfunction is not a primary defect affecting all skeletal muscle but could be related to a decreased response to locomotor muscle use in T2DM. (J Clin Endocrinol Metab 95: 857–863, 2010)J Clin Endocrinol Metab 95: 857–863, 2010))
MiPNet14.08 IOC52 + ('''Demo O2k-Course at MiPsummer 2009.''' Baton Rouge, USA; 2009 June 21.)
MiPNet14.04 IOC51 + ('''Demo O2k-Course at MiPsummer 2009.''' Baton Rouge, USA; 2009 June 21.)
Gnaiger 2014 Preface MiP2014 + ('''Do you ever dream about an equation?'' … '''Do you ever dream about an equation?''The Mitchell’s dream series by [[Odra Noel]] is a dream on equations and shows a dream on the equation that penetrates all of biology since Peter D Mitchell started publishing on the protonmotive force equation [1]. Can we imagine how many dreaming was required until the chemiosmotic hypothesis emerged on energy coupling by the protonmotive force of oxidative phosphorylation in the bioblasts, which comprise the mitochondria, chloroplasts, bacteria and archaea? Seeing Odra Noel’s pictures on Mitchell’s dream provides insights into the equations of biophysics and biochemistry: these equations do not just belong to our books. They do belong to our cells, our [[bioblasts]], to the living world. It is the mitochondria that help us to understand these equations, since the equations are in the mitochondria, they are the visible parts of the mitochondria and open insights into function beyond the visible form – this is mitochondrial physiology.e form – this is mitochondrial physiology.)
MiPNet17.03 Shredder vs Fibers + ('''Doerrier C, Draxl A, Wiethuechter A, Ei … '''Doerrier C, Draxl A, Wiethuechter A, Eigentler A, Gnaiger E (2015) Mitochondrial respiration in permeabilized fibers versus homogenate from fish liver and heart. An application study with the PBI-Shredder. Mitochondr Physiol Network 17.03(04):1-9.''' In the present study we compared mitochondrial function of permeabilized fibers and homogenate of heart muscle of mice. In addition, respiration of trout heart homogenate preparations were compared with permeabilized fibers, and the PBI-Shredder was successfully tested with preparation of trout liver.:» Product: [[Oroboros O2k]], [[OROBOROS O2k-Catalogue | O2k-Catalogue]][OROBOROS O2k-Catalogue | O2k-Catalogue]])
MiPNet08.09 CellRespiration + ('''Doerrier C, Gnaiger E (2003-2016) High- … '''Doerrier C, Gnaiger E (2003-2016) High-resolution respirometry and coupling-control protocol with living cells: ROUTINE, LEAK, ET-pathway, ROX. Mitochondr Physiol Network 08.09(11):1-8.'''An experiment on respiration of [[living cells]] is reported from an O2k-Workshop on high-resolution respirometry. Leukemia cells were incubated at a density of 1 million cells/ml in 2 ml culture medium in two O2k-Chambers operated in parallel. Cellular ROUTINE respiration, ''J''R, resulted in volume-specific oxygen consumption of 20 pmol·s-1·ml-1. Oxygen concentration changed by merely 6.4 and 6.5 µM in the two O2k-Chambers over a period of 5 min (<1% air saturation per minute). Inhibition by oligomycin (''JL''), and rotenone (residual oxygen consumption, ''J''ROX; after uncoupling) reduced respiration to 5 and 1 pmol·s-1·ml-1, while inducing the noncoupled state by the uncoupler FCCP revealed the capacity of the Electron transfer-pathway (ET-pathway) at ''JE'' of 50 pmol·s-1·ml-1. The ROUTINE control ratio, ''R/E'', was 0.4 (uncoupling control ratio, UCR=''E/R''=2.5), and the LEAK control ratio, ''L/E'', was 0.1 (''E/L''=12.0). This indicates tight coupling of OXPHOS, and a large ET-pathway excess capacity over ROUTINE respiration. The net ROUTINE control ratio, net''R''=(''R-L'')/''E'' was 0.30, indicating that 30% of ET-pathway capacity was activated for ATP production.Automatic correction for instrumental background amounted to 13% for ROUTINE respiration, but to >50% and 180% for ''JL'' and ''J''ROX, respectively, illustrating the importance of real-time correction. The experiment illustrates the sensitivity and resproducibility of high-resolution respirometry with the OROBOROS O2k. Calibrations and routine corrections provide the basis of the high accuracy required for mitochondrial respiratory physiology. Real-time analyses were performed, combining high-resolution with instant diagnostic information. In this update graphs are presented illustrating some features of DatLab.:» Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]]os O2k-Catalogue | O2k-Catalogue]])
MiPNet28.13 IOC164 Innsbruck AT + ('''EBEC2024 Satellite Oroboros O2k-Workshop: Mito&Chlora High-Resolution Respirometry and PhotoBiology'''. Innsbruck, Austria (2024 Sep 02-04). )
ESCI 2017 Genoa IT + ('''ESCI meeting, Genoa, IT''')
Electron-transfer-pathway state + ('''ET-pathway states''' are defined in [[mitochondrial preparations]] complementary to [[coupling-control state]]s in mitochondrial physiology.)
Wolter 2016 J Thromb Haemost + ('''Essentials:''' The role of protein C (P … '''Essentials:''' The role of protein C (PC) activation in experimental autoimmune encephalitis (EAE) is unknown. PC activation is required for mitochondrial function in the central nervous system. Impaired PC activation aggravates EAE, which can be compensated for by soluble thrombomodulin. Protection of myelin by activated PC or solulin is partially independent of immune-modulation.'''SUMMARY:''' Studies with human samples and in rodents established a function of coagulation proteases in neuro-inflammatory demyelinating diseases (e.g. in multiple sclerosis [MS] and experimental autoimmune encephalitis [EAE]). Surprisingly, approaches to increase activated protein C (aPC) plasma levels as well as antibody-mediated inhibition of PC/aPC ameliorated EAE in mice. Hence, the role of aPC generation in demyelinating diseases and potential mechanisms involved remain controversial. Furthermore, it is not known whether loss of aPC has pathological consequences at baseline (e.g. in the absence of disease). To explore the role of thrombomodulin (TM)-dependent aPC generation at baseline and in immunological and non-immunological demyelinating disease models. Myelination and reactive oxygen species (ROS) generation were evaluated in mice with genetically reduced TM-mediated protein C activation (TMPro/Pro) and in wild-type (WT) mice under control conditions or following induction of EAE. Non-immunological demyelination was analyzed in the cuprizone-diet model. Impaired TM-dependent aPC generation already disturbs myelination and mitochondrial function at baseline. This basal phenotype is linked with increased mitochondrial ROS and aggravates EAE. Reducing mitochondrial ROS (p66Shc deficiency), restoring aPC plasma levels or injecting soluble TM (solulin) ameliorates EAE in TMPro/Pro mice. Soluble TM additionally conveyed protection in WT-EAE mice. Furthermore, soluble TM dampened demyelination in the cuprizone-diet model, demonstrating that its myelin-protective effect is partially independent of an immune-driven process. These results uncover a novel physiological function of TM-dependent aPC generation within the CNS. Loss of TM-dependent aPC generation causes a neurological defect in healthy mice and aggravates EAE, which can be therapeutically corrected.© 2016 International Society on Thrombosis and Haemostasis.ically corrected. © 2016 International Society on Thrombosis and Haemostasis.)
Expert/inn/en-Workshop Medizintechnik Innsbruck AT + ('''Expert/inn/en-Workshop Medizintechnik, … '''Expert/inn/en-Workshop Medizintechnik, Innsbruck, AT.'''== Time and Location ==13:00 until 17:00 at Standortagentur Tirol, Ing.-Etzelstr. 17, Innsbruck == General information (German) ==Wie vielen bereits bekannt ist, hat sich die Standortagentur Tirol dazu entschlossen – gemeinsam mit IMP – das Projekt „Tirol 2025“ zu starten, um strategische Handlungsfelder für Tirol in ausgewählten Branchen zu definieren. Und in der Zwischenzeit hat sich diesbezüglich viel getan.'''WAS BISHER GESCHAH...'''In den letzten Monaten wurden Gespräche mit hochkarätigen internationalen Expertinnen und Experten aus Wirtschaft, Wissenschaft und Kultur geführt sowie zahlreiche Zukunftsthemen rund um die Tätigkeitsfelder der Standortagentur untersucht. Aus dem generierten Wissen konnten daraufhin konkrete Zukunftshypothesen entwickelt werden, die von knapp 450 Befragten bezüglich Eintrittswahrscheinlichkeit sowie Art der Auswirkung auf Tirol und seinen Branchen bewertet wurden. Darauf aufbauend konnten aus weiteren 40 Interviews mit Tiroler Branchenexpert/innen zukünftige Kernthemen für die Branchencluster der Standortagentur identifiziert werden. '''DER NÄCHSTE SCHRITT...'''Im nächsten Schritt geht es nun darum, gemeinsam mit 8 bis 12 Experten pro Themencluster Lösungsansätze zu den zentralen Zukunftsherausforderungen für Unternehmen, für die Standortagentur sowie für die Politik zu entwickeln und zu diskutieren. Im Bereich Medizintechnik werden folgende Fragestellungen behandelt:* Wie könnten neue Geschäftsmodelle helfen die Erfolgsgeschichte der Tiroler Medizintechnikunternehmen auszubauen? * Was sind spannende, digitale Lösungsansätze um die Wettbewerbsfähigkeit Tiroler Medizintechnikunternehmen erhöhen zu können? * Wie können Tiroler Medizintechnikunternehmen durch eine branchenübergreifende Vernetzung (IT, Gesundheit,..) innovative Angebote entwickeln? * Wie müsste eine wirksame Förderpolitik für Tiroler Medizintechnikunternehmen aussehen? * Welche Vermarktungsansätze könnten Tiroler Medizintechnikunternehmen im Wettbewerb massiv weiterhelfen? * Welche Ansätze helfen Tiroler Medizintechnikunternehmen deren Effektivität und Effizienz in der Entwicklung und Herstellung zu steigern? * Welche Ansätze könnten (kleineren) Tiroler Medizintechnikunternehmen helfen, mit der Flut an neuen Regularien umzugehen? Ihr Mitwirken in diesem Prozess ist uns ein zentrales Anliegen, da es nur mithilfe von hochkarätigem Expertenwissen gelingen kann, effektive strategische Schritte in die Zukunft zu setzen.egische Schritte in die Zukunft zu setzen.)
FASEB 2017 West Palm Beach FL US + ('''FASEB, West Palm Beach, FL, US''')
FAT4BRAIN 1st Online ESR Workshop + ('''FAT4BRAIN 1st Online ESR Workshop, 2020''')
FAT4BRAIN 2nd Online ESR Workshop + ('''FAT4BRAIN 2nd Online ESR Workshop, 2021''')
FAT4BRAIN 3rd Online ESR Workshop + ('''FAT4BRAIN 3rd Online ESR Workshop, 2022''')
FAT4BRAIN 4th Online ESR Workshop + ('''FAT4BRAIN 4th Online ESR Workshop, 2022''')
MiPNet26.05 FAT4BRAIN Advanced O2k-Workshop IOC149 Virtual + ('''FAT4BRAIN Advanced Virtual O2k-Workshop IOC149 on Amplex UltraRed, Virtual Event, 2021''')
MiPNet26.09 FAT4BRAIN Advanced O2k-Workshop IOC150 Virtual + ('''FAT4BRAIN Advanced Virtual O2k-Workshop IOC150 on TMRM and Calcium Green, Virtual Event, 2021''')
FAT4BRAIN ESR Workshop + ('''FAT4BRAIN ESR Workshop, 2023''')
FAT4BRAIN Final review meeting Virtual + ('''FAT4BRAIN Final rview meeting, Virtual, 2023''')
FAT4BRAIN Kick-off meeting Riga LV + ('''FAT4BRAIN Kick-off meeting, Riga, Latvia, 2019''')
FAT4BRAIN Midterm Review meeting Virtual + ('''FAT4BRAIN Midterm Review meeting, Virtual, 2021''')
MiPNet28.04 FAT4BRAIN IOC159 Riga LV + ('''FAT4BRAIN O2k-Workshop IOC159 on HRR for the assessment of mitochondrial bioenergetics.''' Riga, LV, 2023)
MiPNet27.09 FAT4BRAIN O2k-Workshop Schroecken AT + ('''FAT4BRAIN O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2022 October 03-08). )
FAT4BRAIN Online Workshop: Brain energy metabolism in emotion and cognition + ('''FAT4BRAIN Online Workshop: Brain energy metabolism in emotion and cognition, 2021''')
FAT4BRAIN Online Workshop: Central regulatory mechanisms of energy metabolism + ('''FAT4BRAIN Online Workshop: Central regulatory mechanisms of energy metabolism, 2021''')
FAT4BRAIN School IOC147 Virtual Event + ('''FAT4BRAIN School IOC147 on mt-functionality assessment in CNS-related applications, Virtual Event, 2020''')
FAT4BRAIN Symposium Jena DE + ('''FAT4BRAIN Symposium - Long COVID and acetylcarnitines: From preclinical models to clinical applications and translation potential, Jena, Germany, 2022''')
FAT4BRAIN 2023 Riga LV + ('''FAT4BRAIN Symposium - Novel drug target and pathway identification, Riga, Latvia, 2023''')
MiPNet26.01 FAT4BRAIN O2k-Workshop IOC148 Virtual Event + ('''FAT4BRAIN Virtual O2k-Workshop IOC148 on HRR for the assessment of mitochondrial bioenergetics, Virtual Event, 2021''')
FAT4BRAIN Workshop IOC151 Innsbruck AT + ('''FAT4BRAIN Workshop IOC 151 on mitochondrial function in CNS-related applications: from pre-clinical to clinical studies, Innsbruck AT, 2022''')
IOC33 + ('''FEBS Advanced course - Frontiers in Molecular Biochemistry of Mitochondria.''' Warsaw, Poland; 2006 June 09. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[OROBOROS O2k-Catalogue | O2k-Catalogue]])
MiPNet14.13 Medium-MiR06 + ('''Fasching M, Fontana-Ayoub M, Gnaiger E … '''Fasching M, Fontana-Ayoub M, Gnaiger E (2018) Mitochondrial respiration medium - MiR06. Mitochondr Physiol Network 14.13(06):1-4.''' <div style="padding:0px;border: 1px solid #aaaaaa;margin-bottom:0px;margin-right:10px"><div style="font-size:100%;font-weight:bold;padding:0.2em;padding-right: 0.4em;padding-left: 0.4em;background-color:#eeeeee;border-bottom:1px solid #aaaaaa;text-align:left;">[[Image:O2k-support system.jpg|right|150px|link=http://wiki.oroboros.at/index.php/O2k-technical_support_and_open_innovation|O2k-technical support and open innovation]]: <big>Open the '''pdf document''' above.</big></div><div style="background-color:#ffffff;padding-top:0.2em;padding-right: 0.4em;padding-bottom: 0.2em;padding-left: 0.4em;">::::» Current O2k-series: '''[https://www.oroboros.at/index.php/product-category/products/o2k-packages/ NextGen-O2k Series XB and O2k Series J]'''::::» Current software versions DatLab 8.0: [[MitoPedia: DatLab]]::::* ''Further details:'' '''» [[MitoPedia: O2k-Open Support]]'''</div></div>Mitochondrial respiration medium MiR06 was developed for oxygraph incubations of mitochondrial preparations. MiR06 = MiR05 plus catalase. MiR06Cr = MiR06+creatine.:» Product: [[MiR05-Kit]]R05-Kit]])
MiPNet03.02 Chemicals-Media + ('''Fontana-Ayoub M, Fasching M, Gnaiger E … '''Fontana-Ayoub M, Fasching M, Gnaiger E (2016) Selected media and chemicals for respirometry with mitochondrial preparations. Mitochondr Physiol Network 03.02(18):1-10.'''Different media for tissue preparation and respiration are used in investigations of mitochondrial function. Initial decisions on the composition of media and chemicals are decisive for long-term studies and crucial for comparability of results. As a guideline, we summarize an update of our experience with media and chemicals for high-resolution respirometry with isolated mitochondria, permeabilized cells, muscle fibres and tissue homogenates. Whereas optimization is necessary for specific experimental protocols, standardization will improve the comparability of results obtained in different laboratories. Efforts towards standardization are important for the advancement of mitochondrial physiology.:» Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet19.01B POS-Service + ('''Gnaiger E (2014) Service of the polarog … '''Gnaiger E (2014) Service of the polarographic oxygen sensor OroboPOS. Mitochondr Physiol Network 19.01(B01):19-24.''' '''This is an old version, which applies up to O2k-Series F and to DatLab 5.''': ''New version:'' '''[[MiPNet19.18B POS-service|»MiPNet19.18B POS-service]]'''[[MiPNet19.18B POS-service|»MiPNet19.18B POS-service]]''')
MiPNet08.12 IOC22 + ('''Gnaiger E, Doeller JE, Kraus D, Shiva S … '''Gnaiger E, Doeller JE, Kraus D, Shiva S, Brookes PS, Darley-Usmar VM (2011) NO effect on mitochondrial oxygen kinetics at low oxygen. O2k workshop Report. Mitochondr Physiol Network 08.12(07).''' »[http://www.bioblast.at/index.php/File:MiPNet08.12_NO-O2kWorkshop.pdf Versions]A single pilot experiment was carried out during an O2k workshop on high-resolution respirometry (IOC22). Respiration of isolated rat liver mitochondria was inhibited by addition of NO, which increased the sensitivity to oxygen >25-fold when compared to the half-saturation oxygen pressure, p50, in the absence of NO. Oxygen kinetics followed a monophasic hyperbolic function up to 2.2 kPa with NO (p50=0.93 kPa), compared to the standard oxygen range to 1.1 kPa without NO (p50=0.035 kPa).[[Image:MiPNet08.12.jpg|400px|centre|thumb|Figure 1. Oxygen dependence of mt-respiration and competitive inhibition by NO. The full line shows oxygen kinetics at state 3 with pyruvate and malate in the absence of NO, measured in the physiological oxygen range (from Gnaiger et al. 1998a). Dotted lines show inhibition of respiration by the indicated NO concentrations, where measurements were performed with low-resoltion respirometry and are restricted to the high oxygen range (from Koivisto et al. 1977). Extrapolations into the physiological oxygen range (shaded region) suggest sigmoidal oxygen kinetics, which requires testing by direct measurements at low oxygen (modified after Gnaiger, Kuznetsov 2002).]][[Aguirre_2010_Biochim_Biophys_Acta| Reference: Biochim Biophys Acta 1797: 557-565 (2010)]]:» Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]]Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet02.05 DatLab2 O2Kinetics + ('''Gnaiger E, Lassnig B (1997) DatLab 2. Analysis of oxygen kinetics. Mitochondr Physiol Network 02.05.''' :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue]])
MiPNet02.07 Datlab2 Manual + ('''Gnaiger E, Reck M (1997) DatLab 2 Analysis. High resolution of data in the lab. Mitochondr Physiol Network 02.07: 1-72.''' :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue ]])
MiPNet04.05 Titration-Injection + ('''Gnaiger E, Rieger G (1999) From step ti … '''Gnaiger E, Rieger G (1999) From step titration to ramp injection: Uncoupling by FCCP with TIP. Mitochondr Physiol Network 04.05.''':» Product: [[O2k-Catalogue: TIP2k|TIP2k]], [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]]Fully supported by the O2k-Core and control of the TIP2k by the software DatLab: The TIP2k can be programmed for multiple titrations and continuous injections. As an alternative to traditional step titration, the TIP offers the new option of ramp injection, providing maximum resolution of the concentration dependence of oxygen flux. This is illustrated by the recording of cellular respiratory flux as a function of a continuous increase of uncoupler (FCCP) concentration.''Titration:''Programmable, automatic titration regimes, with titration volumes of 0.05 to 250 µl, variable titration intervals and duration of titration pulses.''Injection:''Steady-state injection: Operation at quasi steady-states by continuous injection of substrates at limiting rates of consumption, providing new flexibility in experimental design by combining the technical advantages of closed and open systems. Programmable injection flows: 0.01 to 25 µl.s-1.Ramp injection (MiPNet04.05, see above): Ramp increase of effector concentrations by "continuous titration".DatLab software for feedback control by the the TIP2k: for steady-state respirometry at selected oxygen levels and pH-stat applications.ed oxygen levels and pH-stat applications.)
Viola 2016 JACC: Basic to Translational Science + ('''Highlights''' Heterozygous mice (αMHC& … '''Highlights'''Heterozygous mice (αMHC403/+) expressing the human hypertrophic cardiomyopathy (HCM) disease causing mutation ''Arg403Gln'' exhibit cardinal features of HCM.This study investigated the role of L-type Ca2+ channel (ICa-L) in regulating mitochondrial function in ''Arg403Gln'' (αMHC403/+) mice.Activation of ICa-L in αMHC403/+ mice caused a significantly greater increase in mitochondrial membrane potential and metabolic activity when compared to wild-type mice.Increases in mitochondrial membrane potential and metabolic activity were attenuated with ICa-L antagonists and when F-actin or β-tubulin were depolymerized.ICa-L antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity.'''Summary'''Heterozygous mice (αMHC403/+) expressing the human disease-causing mutation ''Arg403Gln'' exhibit cardinal features of hypertrophic cardiomyopathy (HCM) including hypertrophy, myocyte disarray, and increased myocardial fibrosis. Treatment of αMHC403/+ mice with the L-type calcium channel (ICa-L) antagonist diltiazem has been shown to decrease left ventricular anterior wall thickness, cardiac myocyte hypertrophy, disarray, and fibrosis. However, the role of the ICa-L in the development of HCM is not known. In addition to maintaining cardiac excitation and contraction in myocytes, the ICa-L also regulates mitochondrial function through transmission of movement of ICa-L via cytoskeletal proteins to mitochondrial voltage-dependent anion channel. Here, the authors investigated the role of ICa-L in regulating mitochondrial function in αMHC403/+ mice. Whole-cell patch clamp studies showed that ICa-L current inactivation kinetics were significantly increased in αMHC403/+ cardiac myocytes, but that current density and channel expression were similar to wild-type cardiac myocytes. Activation of ICa-L caused a significantly greater increase in mitochondrial membrane potential and metabolic activity in αMHC403/+. These increases were attenuated with ICa-L antagonists and following F-actin or β-tubulin depolymerization. The authors observed increased levels of fibroblast growth factor-21 in αMHC403/+ mice, and altered mitochondrial DNA copy number consistent with altered mitochondrial activity and the development of cardiomyopathy. These studies suggest that the ''Arg403Gln'' mutation leads to altered functional communication between ICa-L and mitochondria that is associated with increased metabolic activity, which may contribute to the development of cardiomyopathy. ICa-L antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity.to altered functional communication between ICa-L and mitochondria that is associated with increased metabolic activity, which may contribute to the development of cardiomyopathy. ICa-L antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity.)
Gnaiger 2013 MiP2013-Opening + ('''How mitochondria work''' 10 years afte … '''How mitochondria work'''10 years after setting the foundations of the [[Mitochondrial Physiology Society]] (MiP2003, Schröcken, Austria) our search continues as to what mitochondrial physiology is. Mitochondrial physiology is the study of “''how mitochondria work''”. Animal physiology is the study of “''how animals work''” - says the title of a textbook by Knut Schmidt-Nielsen. Comparative physiology derives its fascination from the diversity of form and function. Organismic variation is studied in diverse environments and in extremes of physiological performance, with explosive activities and high power output in short bursts or endurance over prolonged periods of time with high efficiency. Diversity is nature’s treasure and the subject of comparative physiology. The famous August Krogh principle – Krogh received the Nobel Prize in 1920 - is frequently cited [1,2]: “''For a large number of problems there will be some animal of choice or a few such animals on which it can be most conveniently studied.''” This principle was first formulated in 1975 by another Nobel laureate who received the Prize in 1953 for the metabolic cycle that carries his name, Sir Hans Krebs [3,4]. This direct link between one of the most famous mitochondrial biochemists and the August Krogh principle that “''epitomized the very essence of comparative physiology''” [2] immediately raises the question: Why was comparative mitochondrial physiology not established some 30 to 40 years ago?y not established some 30 to 40 years ago?)
DORA and Bioenergetics Communications + ('''Implementing DORA principles by publishing in Bioenergetics Communications - beyond counting papers''' - presentation by Erich Gnaiger, BEC Editor-in-chief)
Corlin 2020 JAMA Cardiol + ('''Importance''': The American Heart Assoc … '''Importance''': The American Heart Association ideal cardiovascular health (CVH) score is associated with the risk of cardiovascular disease (CVD) and mortality. However, it is unclear whether the number of years spent in ideal CVH is associated with morbidity or with mortality.'''Objective:''' To evaluate whether living longer with a higher CVH score in midlife is associated with lower risk of hypertension, diabetes, chronic kidney disease, CVD and its subtypes (coronary heart disease, stroke, congestive heart failure, and peripheral artery disease), or all-cause mortality in later life.'''Design, Setting, and Participants''': This prospective cohort study used data from 1445 participants from 1991 to 2015 who participated in the community-based Framingham Heart Study Offspring investigation conducted in Massachusetts. The CVH scores of participants were assessed at examination cycles 5, 6, and 7 (1991-1995; 1995-1998; and 1998-2001, respectively). Individuals were excluded from analyses of the association between duration of CVH score and outcomes if they had the outcome of interest at the seventh examination. The median follow-up was approximately 16 years. Data were analyzed from April 2018 to October 2019. The CVH score categories were poor for scores 0 to 7, intermediate for scores 8 to 11, and ideal for scores 12 to 14. A composite score was derived based on smoking status, diet, physical activity, resting blood pressure levels, body mass index, fasting blood glucose levels, and total serum cholesterol levels.'''Main Outcomes and Measures''': Number of events and number at risk for each main outcome, including incident hypertension, diabetes, chronic kidney disease, CVD, and all-cause mortality, after the seventh examination.'''Results''': Of 1445 eligible participants, the mean (SD) age was 60 (9) years, and 751 (52 %) were women. Number of events/number at risk for each main outcome after the seventh examination were 348/795 for incident hypertension, 104/1304 for diabetes, 198/918 for chronic kidney disease, 210/1285 for CVD, and 300/1445 for all-cause mortality. At the seventh examination, participants mostly had poor (568 [39 %]) or intermediate (782 [54 %]) CVH scores. For each antecedent (before examination cycle 7) 5-year duration that participants had intermediate or ideal CVH, they were less likely to develop adverse outcomes (hazards ratios of 0.67 [95 % CI, 0.56-0.80] for incident hypertension, 0.73 [95 % CI, 0.57-0.93] for diabetes, 0.75 [95 % CI, 0.63-0.89] for chronic kidney disease, 0.73 [95 % CI, 0.63-0.85] for CVD, and 0.86 [95 % CI, 0.76-0.97] for all-cause mortality) relative to living the same amount of time in poor CVH (referent group). No effect modification was observed by age or by sex.'''Conclusions and Relevance''': These results suggest that more time spent in better CVH in midlife may have salutary cardiometabolic benefits and may be associated with lower mortality later in life.ciated with lower mortality later in life.)
MiPNet16.02 IOC64 + ('''International Course on High-Resolution … '''International Course on High-Resolution Respirometry - Satellite to 1st SMRM.''' Hyderabad, India; 2011 December 08:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
Regueira 2008 Crit Care Med + ('''Introduction''' Low blood pressure, in … '''Introduction'''Low blood pressure, inadequate tissue oxygen delivery and mitochondrial dysfunction have all been implicated in the development of sepsis-induced organ failure. This study evaluated the effect on liver mitochondrial function of using norepinephrine to increase blood pressure in experimental sepsis.'''Methods'''Thirteen anaesthetized pigs received endotoxin (Escherichia coli lipopolysaccharide B0111:B4; 0.4 μg/kg per hour) and were subsequently randomly assigned to norepinephrine treatment or placebo for 10 hours. Norepinephrine dose was adjusted at 2-hour intervals to achieve 15 mmHg increases in mean arterial blood pressure up to 95 mmHg. Systemic (thermodilution) and hepatosplanchnic (ultrasound Doppler) blood flow were measured at each step. At the end of the experiment, hepatic mitochondrial oxygen consumption (high-resolution respirometry) and citrate synthase activity (spectrophotometry) were assessed.'''Results'''Mean arterial pressure (mmHg) increased only in norepinephrine-treated animals (from 73 [median; range 69 to 81] to 63 [60 to 68] in controls [''P'' = 0.09] and from 83 [69 to 93] to 96 [86 to 108] in norepinephrine-treated animals [''P'' = 0.019]). Cardiac index and systemic oxygen delivery (''D''O2) increased in both groups, but significantly more in the norepinephrine group (''P'' < 0.03 for both). Cardiac index (ml/min per·kg) increased from 99 (range: 72 to 112) to 117 (110 to 232) in controls (''P'' = 0.002), and from 107 (84 to 132) to 161 (147 to 340) in norepinephrine-treated animals (''P'' = 0.001). ''D''O2 (ml/min per·kg) increased from 13 (range: 11 to 15) to 16 (15 to 24) in controls (''P'' = 0.028), and from 16 (12 to 19) to 29 (25 to 52) in norepinephrine-treated animals (''P'' = 0.018). Systemic oxygen consumption (systemic VO2) increased in both groups (''P'' < 0.05), whereas hepatosplanchnic flows, ''D''O2 and ''V''O2 remained stable. The hepatic lactate extraction ratio decreased in both groups (''P'' = 0.05). Liver mitochondria Complex I-dependent and II-dependent respiratory control ratios were increased in the norepinephrine group (Complex I: 3.5 [range: 2.1 to 5.7] in controls versus 5.8 [4.8 to 6.4] in norepinephrine-treated animals [''P'' = 0.015]; Complex II: 3.1 [2.3 to 3.8] in controls versus 3.7 [3.3 to 4.6] in norepinephrine-treated animals [''P'' = 0.09]). No differences were observed in citrate synthase activity.'''Conclusion'''Norepinephrine treatment during endotoxaemia does not increase hepatosplanchnic flow, oxygen delivery or consumption, and does not improve the hepatic lactate extraction ratio. However, norepinephrine increases the liver mitochondria Complex I-dependent and II-dependent respiratory control ratios. This effect was probably mediated by a direct effect of norepinephrine on liver cells. direct effect of norepinephrine on liver cells.)
Marelsson 2011 Abstract IOC61 + ('''Introduction''' Mitochondrial disorders … '''Introduction'''Mitochondrial disorders are extremely heterogeneous and can involve single tissue, such as the optic nerve to widespread pathologies including muscle disorders, peripheral neuropathies, encephalopathy, cardiomyopathies or complex multisystem disorders. The age at onset ranges from neonatal to adult life. Mitochondrial dysfunction is a relatively common disorder but the clinical and genetic variability makes it difficult to diagnose. Our primary hypothesis is that disturbance in mitochondrial respiratory chain can be diagnosed with blood test and skin biopsy, by combining structural (Blue native page) and functional information, with high-resolution respirometry of the respiratory chain in blood cells. This rapid diagnostic method can be used to diagnose the flora of undiagnosed and unknown encephalopathy in children today. '''Methods'''Our aim is to 1. Establish reference material for mitochondrial normal function in children through high resolution respirometry by diagnosing thrombocytes and fibroblasts. We also want to establish reference material for structural information with Blue Native PAGE (BNP) in fibroblasts. 2. We want to use these methods in children with known mitochondrial disease to confirm that our methods are usefull.3. We want to compare our methods to known methods today for diagnoses of mitochondrial disease (muscle biopsy).4. We want to see the benefits of treatment by comparing results through BNP and respirometry before and after treatment. 5. We want to use these methods for diagnosis of unknown encephalopathy in children.'''Results'''We have started collecting reference material from children from 0-17 years old. We collect blood and skin biopsy from healthy children that are having a small operation at the University Hospital in Lund. Our aim is to collect reference material from 60 children in different age groups. We also collect blood and skin biopsy from 30 newborn babies from the umbilical cord.We have also done respirometry on children that have both suspected mitochondrial disease and children with known mitochondrial disease. The results are promising. We have also taken skin biopsy from these children but we do not know the outcome yet. We have also started using our methods to look at children with autism and other encephalopathy. '''Conclusion'''Mitochondrial dysfunction has been difficult to diagnose. Our methods give us the opportunity to diagnose mitochondrial dysfunction in unknown encephalopathy in children by a more rapid and simple way than before.y a more rapid and simple way than before.)
Sjoevall 2010 Crit Care + ('''Introduction''' Mitochondrial dysfuncti … '''Introduction'''Mitochondrial dysfunction has been suggested as a contributing factor to the pathogenesis of sepsis-induced multiple organ failure. Also, restoration of mitochondrial function, known as mitochondrial biogenesis, has been implicated as a key factor for the recovery of organ function in patients with sepsis. Here we investigated temporal changes in platelet mitochondrial respiratory function in patients with sepsis during the first week after disease onset.'''Methods'''Platelets were isolated from blood samples taken from 18 patients with severe sepsis or septic shock within 48 hours of their admission to the intensive care unit. Subsequent samples were taken on day 3 to 4 and day 6 to 7. Eighteen healthy blood donors served as controls. Platelet mitochondrial function was analyzed by high-resolution respirometry. Endogenous respiration of viable, intact platelets suspended in their own plasma or PBS glucose was determined. Further, in order to investigate the role of different dehydrogenases and respiratory complexes as well as to evaluate maximal respiratory activity of the mitochondria, platelets were permeabilized and stimulated with complex-specific substrates and inhibitors.'''Results'''Platelets suspended in their own septic plasma exhibited increased basal non-phosphorylating respiration (state 4) compared to controls and to platelets suspended in PBS glucose. In parallel, there was a substantial increase in respiratory capacity of the Electron transfer-pathway from day 1 to 2 to day 6 to 7 as well as compared to controls in both intact and permeabilized platelets oxidizing Complex I and/or II-linked substrates. No inhibition of respiratory complexes was detected in septic patients compared to controls. Non-survivors, at 90 days, had a more elevated respiratory capacity at day 6 to 7 as compared to survivors. Cytochrome c increased over the time interval studied but no change in mitochondrial DNA was detected.'''Conclusions'''The results indicate the presence of a soluble plasma factor in the initial stage of sepsis inducing uncoupling of platelet mitochondria without inhibition of the Electron transfer-pathway. The mitochondrial uncoupling was paralleled by a gradual and substantial increase in respiratory capacity. This may reflect a compensatory response to severe sepsis or septic shock, that was most pronounced in non-survivors, likely correlating to the severity of the septic insult.ting to the severity of the septic insult.)
Hroudova 2012 European Psychiatry + ('''Introduction''': Alzheimer's disease (A … '''Introduction''': Alzheimer's disease (AD) is the most frequent neurodegenerative disease, characterized by progressive decline in variety of higher brain functions - memory, orientation, and thinking. According to increasing evidences, mitochondrial insufficiencies contribute to pathology of AD; changes were described in AD brains, blood cells and human fibroblasts.'''Objectives''': On molecular level, oxygen and glucose metabolism is altered and energy metabolism is impaired.Mitochondrial abnormalities and alterations in mitochondrial enzymes, especially Complex I and cytochrome ''c'' oxidase, were observed. However, the cause and important aspects of AD mechanism have not yet been sufficiently clarified.'''Aims''': The aim of our study was to find whether kinetics of oxygen consumption is modified in AD patients. Further, we afford to suggest parameters that could be suitable as AD markers.'''Methods''': AD patients and healthy control group were included in the study. Respiratory rate of mitochondria, as measure of total activity of the system of oxidative phosphorylation (OXPHOS), was measured in mitochondria using oxygraph with Clark-type electrodes. High-resolution respirometry was performed in intact as well as in permeabilized platelets.'''Results''': Our results indicate significantly lower respiratory rate in intact platelets as well as lower respiratory capacity of Electron transfer-pathway in patients with AD compared to controls.'''Conclusions''': We propose that decrease in oxygen consumption may participate in pathophysiology of AD, and respiratory rate in platelets could be AD marker.tory rate in platelets could be AD marker.)
Groeger 2010 Crit Care + ('''Introduction:''' Hydrogen sulfide (H< … '''Introduction:''' Hydrogen sulfide (H2S) is a potent inhibitor of cytochrome c oxidase (COX) and, thus, of mitochondrial respiration [1]. Since H2S was reported to induce a suspended animation-like status characterized by reduced energy expenditure and hypothermia [2], we sought to determine the effect of hypothermia on mitochondrial respiratory capacity and H2S-related COX inhibition. We further studied the influence of variations in pH on both variables.'''Methods:''' All measurements were conducted in digitonin-permeabilised cultured peritoneal macrophages using high-resolution respirometry [3] (Oxygraph-2 k, Oroboros, Austria). Maximum mitochondrial respiration (1 to 2 Mio cells/ml respiration medium) was achieved in the uncoupled state by adding pyruvate, malate, glutamate and succinate as respiratory substrates. Then, in one of the two chambers of the oxygraph, mitochondrial respiration was inhibited stepwise by incremental concentrations of the H2S donor Na2S (1 to 64 μM). In the parallel chamber, the identical inhibitor titration sequence was preceded by the inhibition of the respiratory chain by rotenone and antimycin A followed by the selective stimulation of CIV after addition of ascorbate and TMPD. COX excess capacity (% of ET-pathway) was calculated based on the ratio of inhibition of mitochondrial respiration with full operating respiratory chain versus the CIV-stimulated condition. This experimental sequence was repeated at 37 °C and 25 °C with a medium pH of 7.1 and then at 37°C with a pH of 6.8 and 7.7.'''Results:''' CIV excess capacity (median (quartiles)) was significantly higher at 25 °C than at 37 °C (134 (113; 140) vs 61 (47; 79)), most likely due to the almost halved mitochondrial respiratory capacity at hypothermia (50 (37; 63) vs 95 (81; 103) pmol O2/s × Mio cells). Changing the medium pH from 6.8 to 7.7 significantly increased the COX excess capacity (91 (79; 103) vs 71 (64; 82) pmol O2/s × Mio cells), which again was related to the significantly lower mitochondrial respiratory capacity with more acidic conditions (80 (70; 89) vs 94 (85; 98)).'''Conclusions:''' Our results suggest that COX excess capacity is temperature as well as pH dependent in peritoneal macrophages. This effect may protect cells from H2S toxicity at low temperatures and high pH values. in peritoneal macrophages. This effect may protect cells from H2S toxicity at low temperatures and high pH values.)
Fischer 2021 MitoFit Fe liver + ('''Journal publication 2021-11-16 in [[Fischer 2021 Antioxidants |»Antioxidants«]]'' … '''Journal publication 2021-11-16 in [[Fischer 2021 Antioxidants |»Antioxidants«]]'''</big>[[File:Fischer_2021_MitoFit_Fe_liver - graphical abstract.png|right|500px|Graphical abstract]] Iron is an essential co-factor for many cellular metabolic processes, and mitochondria are main sites of utilization. Iron accumulation promotes production of reactive oxygen species (ROS) via the catalytic activity of iron species. Herein, we investigated the consequences of dietary and genetic iron overload on mitochondrial function. C57/BL6N wildtype and ''Hfe-/-'' mice, the latter a genetic hemochromatosis model, received either normal diet (ND) or high iron diet (HI) for two weeks. Liver mitochondrial respiration was measured using high-resolution respirometry along with analysis of expression of specific proteins and ROS production. HI promoted tissue iron accumulation and slightly affected mitochondrial function in wildtype mice. Hepatic mitochondrial function was impaired in ''Hfe-/-'' mice on ND and HI. Compared to wildtype mice, ''Hfe-/-'' mice on ND showed increased mitochondrial respiratory capacity. ''Hfe-/-'' mice on HI showed very high liver iron levels, decreased mitochondrial respiratory capacity and increased ROS production associated with reduced mitochondrial aconitase activity. Although ''Hfe-/-'' resulted in increased mitochondrial iron loading, the concentration of metabolically reactive cytoplasmic iron and mitochondrial density remained unchanged. Our data shows multiple effects of dietary and genetic iron loading on mitochondrial function and linked metabolic pathways, providing an explanation for fatigue in iron-overloaded hemochromatosis patients and suggests iron reduction therapy for improvement of mitochondrial function. chromatosis patients and suggests iron reduction therapy for improvement of mitochondrial function. )
Zdrazilova 2021 MitoFit ace-sce + ('''Journal publication 2022-03-03 in [[Zdrazilova 2022 PLOS ONE |»'''PLOS ONE 17:e0264496'''«]]'' … '''Journal publication 2022-03-03 in [[Zdrazilova 2022 PLOS ONE |»'''PLOS ONE 17:e0264496'''«]]'''Version 1 ('''v1''') '''2021-09-21''' [https://www.mitofit.org/images/1/15/Zdrazilova_2021_MitoFit_ace-sce.pdf doi:10.26124/mitofit:2021-0007]Measurement of oxygen consumption of cultured cells is widely used for diagnosis of mitochondrial diseases, drug testing, biotechnology and toxicology. Fibroblasts are cultured in monolayers but physiological measurements are carried out in suspended or attached cells. We address the question whether respiration differs in attached and suspended cells using multiwell respirometry (Agilent Seahorse XF24) and high-resolution respirometry (Oroboros O2k), respectively. Respiration of human dermal fibroblasts measured in culture medium was baseline-corrected for residual oxygen consumption and expressed as oxygen flow per cell.No differences were observed in ROUTINE respiration of living cells and LEAK respiration obtained after inhibition of ATP synthase by oligomycin. Multiple steps of uncoupler titrations in the O2k allowed for evaluation of maximum electron transfer capacity, which was higher than respiration obtained in the XF24 due to a limitation to two uncoupler titrations.Quantitative evaluation of respiration measured in different platforms revealed that short-term suspension of fibroblasts did not affect respiratory activity and coupling control. Consistent results obtained with different platforms provide a test for reproducibility and allow for building an extended respirometric database. extended respirometric database. )
Fischer 2022 MitoFit Fe + ('''Journal publication 2022-03-21 in [[Fischer 2022 Metabolites |»Metabolites«]]'' … '''Journal publication 2022-03-21 in [[Fischer 2022 Metabolites |»Metabolites«]]'''</big>Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue. ng in the blood cells and liver tissue. )
Viola 2016 J Physiol + ('''KEY POINTS:''' Genetic mutations in car … '''KEY POINTS:'''Genetic mutations in cardiac troponin I (cTnI) are associated with development of hypertrophic cardiomyopathy characterised by myocyte remodeling, disorganisation of cytoskeletal proteins and altered energy metabolism. The L-type Ca2+ channel is the main route for calcium influx and critical to cardiac excitation and contraction. The channel also regulates mitochondrial function in the heart by a functional communication between the channel and mitochondria via the cytoskeletal network. We find that L-type Ca2+ channel kinetics are altered in cTnI-G203S cardiac myocytes, and that activation of the channel causes a significantly greater increase in mitochondrial membrane potential and metabolic activity in cTnI-G203S cardiac myocytes. These responses occur as a result of impaired communication between the L-type Ca2+ channel and cytoskeletal protein F-actin, involving decreased movement of actin-myosin, and block of mitochondrial VDAC, resulting in a 'hypermetabolic' mitochondrial state. We propose that L-type Ca2+ channel antagonists such as diltiazem may be effective in reducing the cardiomyopathy by normalising mitochondrial metabolic activity.'''ABSTRACT:'''Genetic mutations in cardiac troponin I (cTnI) account for 5% of families with hypertrophic cardiomyopathy (HCM). HCM is associated with disorganisation of cytoskeletal proteins and altered energy metabolism. The L-type Ca2+ channel (ICa-L ) plays an important role in regulating mitochondrial function. This involves a functional communication between ICa-L and mitochondria via the cytoskeletal network. We investigate the role of ICa-L in regulating mitochondrial function in 25-30-week old cardiomyopathic mice expressing human disease causing mutation Gly203Ser in cTnI (cTnI-G203S). The inactivation rate of ICa-L is significantly faster in cTnI-G203S myocytes (cTnI-G203S: τ1 = 40.68 ± 3.22, n = 10 versus wt: τ1 = 59.05 ± 6.40, n = 6, P < 0.05). Activation of ICa-L caused a greater increase in mitochondrial membrane potential (Ψm , 29.19 ± 1.85%, n = 15 versus wt: 18.84 ± 2.01%, n = 10, P < 0.05) and metabolic activity (24.40 ± 6.46%, n = 8 versus wt: 9.98 ± 1.57%, n = 9, P < 0.05). The responses occurred due to impaired communication between ICa-L and F-actin, involving lack of dynamic movement of actin-myosin, and block of mitochondrial VDAC. Similar responses were observed in pre-cardiomyopathic mice. ICa-L antagonists nisoldipine and diltiazem decreased Ψm to basal levels. We conclude that the Gly203Ser mutation leads to impaired functional communication between ICa-L and mitochondria resulting in a 'hypermetabolic' state. This may contribute to development of cTnI-G203S cardiomyopathy because the response is present in young pre-cardiomyopathic mice. ICa-L antagonists may be effective in reducing the cardiomyopathy by altering mitochondrial function. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.e is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.)
Klinische MitochondrienMedizin und Umweltmedizin 2015 + ('''Klinische MitochondrienMedizin und Umwe … '''Klinische MitochondrienMedizin und Umweltmedizin 2015, Internationales Wissenschaftsforum der Universität, Heidelberg, DE.'''Im März 2015 startet in Heidelberg bereits vierte Auflage eines erfolgreichen Curriculums Klinische MitochondrienMedizin und Umweltmedizin. Die Veranstaltung ist als ärztliche Fortbildung mit Ärztekammer-, Zahnärzte- und Apothekerkammer-Anerkennung und als Wahlpflichtmodul des KWKM-Masterstudiengangs an der Europa-Universität Viadrina konzipiert. An sechs intensiven Wochenenden (freitags und samstags) werden in Vorträgen und Übungen:* Grundlagen der Mitochondrien-Medizin,* aktuelle Forschungsergebnisse,* Diagnosemethoden und* Therapieverfahren der mitochondrialen Medizinu.a. in Verbindung mit der Umweltmedizin, Umwelt-Zahnmedizin, Frauenheilkunde und Psychotherapie erläutert. Ergänzend zu dem theoretischen Teil werden Hospitanten-Tage im Centrum für Integrative Medizin in Speyer angeboten, welches auf dem Gebiet der Mitochondrien-Medizin spezialisiert ist.r Mitochondrien-Medizin spezialisiert ist.)
Klinische MitochondrienMedizin und Umweltmedizin 2016 Heidelberg DE + ('''Klinische MitochondrienMedizin und Umwe … '''Klinische MitochondrienMedizin und Umweltmedizin 2016, Internationales Wissenschaftsforum der Universität, Heidelberg, DE.''' [[Media:MitochondrialMedicine_2016.pdf| »Flyer]] Im März 2016 startet in Heidelberg bereits fünfte Auflage eines erfolgreichen Curriculums '''Klinische MitochondrienMedizin und Umweltmedizin'''. Die Veranstaltung ist als ärztliche Fortbildung mit Ärztekammer-, Zahnärzte- und Apothekerkammer-Anerkennung und als Wahlpflichtmodul des KWKM-'''Masterstudiengangs an der Europa-Universität Viadrina''' konzipiert. An sechs intensiven Wochenenden (freitags und samstags) werden in Vorträgen und Übungen:* Grundlagen der Mitochondrien-Medizin* Aktuelle Forschungsergebnisse* Diagnosemethoden* Therapieverfahren der mitochondrialen Medizinu.a. in Verbindung mit der Umweltmedizin, Umwelt-Zahnmedizin, Frauenheilkunde undPsychotherapie erläutert. Ergänzend zu dem theoretischen Teil werden Hospitanten-Tage im BioMedical Center in Speyer angeboten, welches auf dem Gebiet der Mitochondrien-Medizin spezialisiert ist. Mehr Informationen finden Sie hier: http://www.mito-medizin.de/fortbildung/ '''Termine 2016:''' :* Kurs A: 04. - 05.03:* Kurs B: 15. - 16.04:* Kurs C: 20. - 21.05:* Kurs D: 17. - 18.06:* Kurs E: 09. - 10.09:* Kurs F: 11. - 12.11Kurs E: 09. - 10.09 :* Kurs F: 11. - 12.11)
MiPNet08.15 Complex-I + ('''Kuznetsov AV, Gnaiger E. Laboratory pro … '''Kuznetsov AV, Gnaiger E. Laboratory protocol: Complex I (NADH:Ubiquinone Oxidoreductase, EC 1.6.5.3). Mitochondrial membrane enzyme. Mitochondr Physiol Network 08.15.'''Complex I (CI) is the segment of the electron transport system (integral enzyme of the inner mitochondrial membrane) responsible for electron transfer from NADH to ubiquinone. CI is sensitive to different pathologies, particularly to oxidative stress, which is involved in ischemia-reperfusion injury, anoxia/ reoxygenation, aging, etc (Kuznetsov et al 2004; Rouslin & Millard 1981; Rouslin & Ranganathan, 1983; Rouslin, 1983). For the assessment of CI activity, among the ubiquinone isoprenologs, it is most convenient to use ubiquinone-1 (CoQ1) as electron acceptor, because of its relative water solubility. Importantly, CoQ1 yields one of the lowest rotenone insensitive rates and a high enzymatic rate. It is, therefore, the best electron acceptors for the CI assay.:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue]][[Oroboros O2k-Catalogue]])
MiPNet08.18 LactateDehydrogenase + ('''Kuznetsov AV, Gnaiger E. Laboratory pro … '''Kuznetsov AV, Gnaiger E. Laboratory protocol: Lactate dehydrogenase. Cytosolic marker enzyme. Mitochondr Physiol Network 08.18.''' Lactate dehydrogenase (EC 1.1.1.27) is an enzyme, which catalyzes the last step in glycolysis. LDH is a soluble enzyme and localized in the cytosol (cytoplasm). LDH, therefore, is used as a quantitative marker enzyme for the intact cell, its activity providing information on cellular glycolytic capacity (Renner et al, 2003). Measurement of LDH release (leakage) is an important and frequently applied test for cellular membrane permeabilization (rupture) and severe irreversible cell damage. LDH leakage normally correlates well with CK release and the trypan blue viability test.:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue]][[Oroboros O2k-Catalogue]])
MiPNet08.13 mt-Isolation-RLM + ('''Lassnig B, Gnaiger E. Laboratory protoc … '''Lassnig B, Gnaiger E. Laboratory protocol: Isolation of rat liver mitochondria. Mitochondr Physiol Network 08.13.''' <div style="padding:0px;border: 1px solid #aaaaaa;margin-bottom:0px;margin-right:10px"><div style="font-size:100%;font-weight:bold;padding:0.2em;padding-right: 0.4em;padding-left: 0.4em;background-color:#eeeeee;border-bottom:1px solid #aaaaaa;text-align:left;">[[Image:O2k-support system.jpg|right|150px|link=http://wiki.oroboros.at/index.php/O2k-technical_support_and_open_innovation|O2k-technical support and open innovation]]: <big>Open the '''pdf document''' above.</big></div><div style="background-color:#ffffff;padding-top:0.2em;padding-right: 0.4em;padding-bottom: 0.2em;padding-left: 0.4em;">::::» Current O2k-series: '''[https://www.oroboros.at/index.php/product-category/products/o2k-packages/ NextGen-O2k Series XB and O2k Series J]'''::::» Current software versions DatLab 8.0: [[MitoPedia: DatLab]]::::* ''Further details:'' '''» [[MitoPedia: O2k-Open Support]]'''</div></div>:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue]]roboros O2k-Catalogue]])
IOC10 + ('''Lectures on High-Resolution Respirometr … '''Lectures on High-Resolution Respirometry and Oroboros O2k Demonstration at BTK 1994.''' Innsbruck, Tyrol, Austria; 1994 September.:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
Long Night of Research 2016 Innsbruck AT + ('''Long Night of Research 2016: MitoFit – Training for the powerhouses of your blood- and muscle cells. Innsbruck, AT.''')
Long Night of Research 2018 Innsbruck AT + ('''Long Night of Research 2018: The diagnostic bioenergetic report – a milestone on the way to mitochondrial fitness and physical well-being. Innsbruck, AT.''')
Long Night of Research 2020 Virtual Event + ('''Long Night of Research 2020: The diagnostic bioenergetic report – a milestone on the way to mitochondrial fitness and physical well-being. Virtual Event.''')
ESCI 2016 Paris FR + ('''Meeting of the European Society for Clinical Investigation, Paris, FR''')
IOC05 + ('''Metabolic Energetics in Ecological, Cellular and Biomedical Research.''' Aberystwyth Wales United Kingdom; 1993 March 01-03. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiP2023 Obergurgl AT + ('''MiP2023, Obergurgl, Austria, 2023.''')
MiPschool Obergurgl 2023 + ('''MiPschool, Obergurgl, Austria, 2023: Mitochondrial structure and function, respiratory supercomplexes, and respiratory control''')
Jezek 2011 AbstractMitoComLectures + ('''MitoCom Lecture''' '''2011-Nov-10, 8:1 … '''MitoCom Lecture''''''2011-Nov-10, 8:15 - 09:45'''. Medical University Innsbruck, Anichstr. 25, Chirurgie (8-U1-517) Seminarraum 2Speaker: '''[[Jezek P|Prof. Dr. Petr Jezek, Prague]]'''Host: [[Gnaiger E|Erich Gnaiger, DSL, MitoCom Tyrol]]'''Abstract''': Three-dimensional (3D) super-resolution microscopy, using a biplane detection scheme, termed biplane photo-activated localization microscopy (Biplane FPALM), enables imaging of volumes as thick as whole cells and reveals otherwise unaccessible details of cellular organization [1]. Hence, we attempted to visualize mitochondrial reticulum via the matrix space loaded with mitochondria-addressed Eos, while transfecting cells by lentiviral expression. Our 3D images of single Eos molecules in the matrix space have proven the continuous character of mitochondrial reticulum tubules, i.e., an existence of a highly interconnected major mitochondrial reticulum in insulinoma Ins1E and oxidative-phosphorylation-dependent glutaminolytic hepatoma HepG2 cells [2] (Figure).Also, using Eos-conjugate of mitochondrial transcription factor-A (TFAM), we have imaged nucleoids of mitochondrial DNA (mtDNA) in which TFAM represents a major assessor protein. Using PA-CFP2-TFAM and mitochondria-addressed Eos, the first 3D two color super-resolution images were obtained for mitochondrial reticulum together with the distribution of mt nucleoids in it. In intact cells we have found mt nucleoids of a narrow size distribution. The Biplane FPALM technique has proven to be robust and reliable for imaging of mitochondrion and related substructures.Supported by grants P302/10/0346 (GACR); ME09029 (Czech Ministry of Education); IAA500110701, and M200110902 (Academy of Sciences).) and 1R01GM091791-02 (NIH). Disclosure statement: J.B. declares significant financial interest in Vutara, Inc.[1] Juette MF, Gould TJ, Lessard MD, Mlodzianoski MJ, Nagpure BS, Bennett BT, Hess ST, Bewersdorf J (2008) 3D sub-100 nm resolution by biplane fluorescence photoactivation localization microscopy. Nat. Methods 5: 527-529.[2] Mlodzianoski MJ, Schreiner JM, Callahan SP, Smolková K, Dlasková A, Šantorová J, Ježek P, Bewersdorf J (2011) Sample drift correction in 3D fluorescence photoactivation localization microscopy. Opt. Express. 19: 15009-15019.microscopy. Opt. Express. 19: 15009-15019.)
MitoFit Open Seminar 2017-10-23 + ('''MitoFit Open Seminar on respiration, cryopreservation and viability test in human blood cells'''. Innsbruck, AT)
UMDF2016 Seattle WA US + ('''Mitochondrial Medicine 2016, Seattle, W … '''Mitochondrial Medicine 2016, Seattle, WA, USA.''' The [[United Mitochondrial Disease Foundation]] Symposium has been recognized by many researchers, scientists, and families as THE symposium for mitochondrial disease in the world. 10 years ago, the UMDF had only a handful of exhibitors and less than 200 scientific attendees. We now have more exhibitors than space at times and close to 600 attendees … representing almost every state in the United States and more than 15 different countries from around the world.different countries from around the world.)
UMDF2017 Washington DC US + ('''Mitochondrial Medicine 2017, Washington DC, USA.''')
MiPNet14.09 MiP-Collection + ('''Mitochondrial Physiology (MiP) ''contin … '''Mitochondrial Physiology (MiP) ''continues a tradition of rigorous mitochondrial bioenergetics'' '''([http://www.mitophysiology.org quoting the International MiPsociety]). The company [[Oroboros Instruments]] Corp. values this tradition as a basis of our continuous instrumental development, which is part of our concept of Corporate Social Responsibility. In this spirit and with emphasis on our Educational Responsibility, we initiated and support the ''[[MiP-Collection]]''.[[MiP-Collection]]''.)
Gnaiger 2011 Abstract-MonteVerita + ('''Mitochondrial capacity''': [[OXPHOS]] … '''Mitochondrial capacity''': [[OXPHOS]] capacity is evaluated in isolated mitochondria (mt) and permeabilized cells with physiological substrate cocktails to reconstitute tricarboxylic acid cycle function. As a consequence, convergent electron flow from Complexes CI+II of the electron transfer-pathway ([[ET-pathway]]) to the [[Q-junction]] exerts an additive effect on flux [1].'''Oxygen kinetics of mt-respiration''': The apparent ''K''m,O2 or ''c''50 [µM] (''p''50 [kPa]) of mt-respiration increases linearly with respiratory capacity controlled by metabolic state, from 0.2 to 1.6 µM determined by [[high-resolution respirometry]]. O2 gradients are significant only in large cells including cardiomyocytes. The apparent ''p''50 increases 100-fold in permeabilized muscle fibers due to diffusion gradients [2].'''mt-function at ''V''O2max''': Aerobic capacity of the human leg muscle exceeds maximum O2 uptake of isolated mitochondria [3] and v. lateralis during ''V''O2max [4]. Therefore, oxygen supply limits aerobic performance, proportional to the apparent mt-excess capacity [5]. mt-respiration is more sensitive to average ''p''O2 in heterogenous tissues than under homogenous conditions in vitro. Tissue heterogeneity increases the kinetic dependence of flux on average intracellular ''p''O2. High mt-density reinforces the steepness of oxygen gradients and oxygen heterogeneity in the tissue, contributing to the O2 limitation in athletic vs sedentary individuals at ''V''O2max [6]. This provides a functional rationale for the observation that hypoxia does not specifically trigger mt-biogenesis [7].Contribution to K-Regio ''[[MitoCom_O2k-Fluorometer|MitoCom Tyrol]]''.[1] [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger 2009]]; [[Lemieux_2011_Int J Biochem Cell Biol|Lemieux et al 2011 Int J Biochem Cell Biol]] [2] [[Gnaiger_2003_Adv Exp Med Biol|Gnaiger 2003]]; [[Scandurra_2010_Adv Exp Med Biol|Scandurra, Gnaiger 2010 Adv Exp Med Biol]]. [3] Rasmussen et al 2001 AJP.[4] [[Boushel_2011_Mitochondrion|Boushel et al 2011 Mitochondrion]].[5] [[Gnaiger_1998_J_Exp_Biol|Gnaiger et al 1998 JEB]].[6] Richardson et al; Haseler et al JAP.[7] [[Pesta_2011_AJP|Pesta et al 2011 AJP]]; [[Jacobs_2011_J_Appl_Physiol|Jacobs et al 2011 JAP]].Jacobs_2011_J_Appl_Physiol|Jacobs et al 2011 JAP]].)
MitoEAGLE preprint 2017-09-21 + ('''Note''': Subscript ‘§’ indicates throug … '''Note''': Subscript ‘§’ indicates throughout the text those parts, where ''potential differences'' provide a mathematically correct but physicochemically incomplete description and should be replaced by ''stoichiometric potential differences'' ([[Gnaiger 1993 Pure Appl Chem |Gnaiger 1993b]]). A unified concept on vectorial motive transformations and scalar chemical reactions will be derived elsewhere (Gnaiger, in prep.). Appreciation of the fundamental distinction between ''differences of potential'' versus ''differences of stoichiometric potential'' may be considered a key to critically evaluate the arguments presented in Section 3 on the protonmotive force. Since this discussion appears to be presently beyond the scope of a MitoEAGLE position statement, Section 3 is removed from the next version and [[Gnaiger 2019 MitoFit Preprint Arch |'''final manuscript''']]. This section should become a topic of discussion within [[WG1 MitoEAGLE protocols, terminology, documentation |Working Group 1]] of the MitoEAGLE consortium, following a primary peer-reviewed publication of the concept of stoichiometric potential differences.t of stoichiometric potential differences.)
IOC42 + ('''O2k-International course on high-resolution respirometry.''' 2007 August 24, 9:00 a.m. to 3:00 p.m. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet14.03 IOC50 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria;2009 April 18 to 22. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet12.24 IOC44 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2007 December 12-16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet11.06 IOC36 + ('''O2k-International course on high-resolution respirometry and MiPNet workshop.''' Schroecken, Voralberg, Austria; 2006 December 13 to 17. :>> O2k-Workshop: [[Oroboros Events]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet09.11 IOC29 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2004 December 9-13. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet11.03 IOC35 Schroecken + ('''O2k-International course on high-resolution respirometry: O2k, TIP-2k and DatLab 4.''' Schroecken, Voralberg, Austria; 2006 August 18-22.)
MiPNet09.05 IOC28 + ('''O2k-International course on high-resolu … '''O2k-International course on high-resolution respirometry and MiPNet meeting.''' Schroecken, Voralberg, Austria; 2004 September 15-21.:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet13.04 IOC47 + ('''O2k-International course on high-resolution respirometry.''' Schroecken,Voralberg, Austria; 2008 July 12-16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
IOC43 Montevideo UY 2007 + ('''O2k-International course on high-resolution respirometry.''' 2007 September 1 and 6. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet11.02 IOC32 + ('''O2k-International course on high-resolu … '''O2k-International course on high-resolution respirometry: Oroboros O2k, TIP-2k and DatLab 4.''' Schroecken, Voralberg, Austria; 2006 April 21-25.:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet10.08 IOC31 + ('''O2k-International course on high-resolution respirometry and ROS/NO detection.''' Schroecken, Voralberg, Austria; 2005 September 13-16.)
MiPNet13.02 IOC46 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2008 April 04-08. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet14.15 IOC54 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2009 December 11 to 16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet14.11 IOC53 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg,Austria; 2009 July 30 to August 04. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet14.02 IOC49 + ('''O2k-International course on high-resolution respirometry.''' Gainsville, USA; 2009 February 23-25. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet10.02 IOC30 + ('''O2k-International course on high-resolution respirometry: Oxygraph-2k, TIP-2k and DatLab 4.''' Schroecken, Voralberg, Austria; 2005 April 08-10.)
MiPNet12.14 IOC39 + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2007 April 13 to 17. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet12.19 IOC41 + ('''O2k-International course on high-resolution respirometry.''' 2007 July 18-22. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet15.02 IOC56 + ('''O2k-MultiSensor Workshop.''' Schroecken, Voralberg, Austria;2010 April 12 to 16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet10.05 O2-Concentration-Flux + ('''O2k-Protocol for Oxygen flux''' In a … '''O2k-Protocol for Oxygen flux''' In a closed oxygraph chamber, the oxygen concentration declines over time as a result of respiratory processes. The time derivative, therefore, is a negative number. Why is then the ‘rate of oxygen consumption’ not expressed as a negative value? Why is the term ‘oxygen flux’ used in this context of chemical reactions? The rationale is based on fundamental concepts of physical chemistry and non-equilibrium thermodynamics.[[Image:O2k-Protocols.jpg|right|150px|link=http://www.oroboros.at/?o2k-protocols|O2k-Protocols contents]][[Image:MiPNet10.05.jpg|centre|500px|thumb]]Respiratory oxygen flux: On-line display of oxygen concentration (blue) and oxygen flux (respiration, red). Endogenous respiration of endothelial cells leads to oxygen depletion, followed by reoxygenations (dotted arrows). Cell membrane permeabilization by digitonin causes a decline of respiration to the resting level (without adenylates in the medium, -ANP). ADP titration activates respiration about 2-fold above the endogenous level of oxygen consumption.Eye-fitted slopes of oxygen chart recorder traces belong to the past. With [[DatLab|DatLab]], trends are resolved. Accuracy is improved by standard numerical corrections. Graphs and protocols are stored and printed ready for publication.'''Reference'''[[Gnaiger_1993_Pure_Appl_Chem| Gnaiger E (1993) Nonequilibrium thermodynamics of energy transformations. Pure Appl Chem 65: 1983-2002.]]:>> O2k-Protocols:[[O2k-Protocols| Overall contents]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]]os O2k-Catalogue | O2k-Catalogue]])
MiPNet08.17 IOC26 + ('''O2k-Training course on high-resolution respirometry.''' Innsbruck, Tyrol, Austria; 2003 December 11-13. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet08.11 IOC24 + ('''O2k-Workshop and training course on high-resolution respirometry.''' Schroecken, Vorarlberg, Austria; 2003 September 09-12. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet17.10 IOC70 + ('''O2k-Workshop on High-Resolution Respirometry.''' Barcelona, Catalonia, Spain; 2012 May 29 to 30 :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet16.01 IOC61 + ('''O2k-Workshop on High-Resolution Respiro … '''O2k-Workshop on High-Resolution Respirometry - O2k-Basic and TPP-Basic.''' Schröcken, Vorarlberg, Austria; 2011 April 26 to May 1.[[File:O2k-TIP2k.jpg|right|200px|caption]]:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet17.14 IOC72 Schroecken AT + ('''O2k-Workshop on High-Resolution Respirometry: O2k-Basic.''' Schroecken, Vorarlberg, Austria 2012 December 05 to 10 :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet16.03 IOC65 + ('''O2k-Workshop on High-Resolution Respiro … '''O2k-Workshop on High-Resolution Respirometry: O2k-Basic and TPP-Basic.''' Schröcken, Vorarlberg, Austria; 2011 10 - 15 December :>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet15.10 IOC60 + ('''O2k-Workshop on High-Resolution Respiro … '''O2k-Workshop on High-Resolution Respirometry - Introductory and Advanced.'''Schroecken, Voralberg, Austria; 2010 December 11 to 16.The past O2k-Workshop on HRR ('''IOC60''') was a success based on long-term experience combined with continuous improvements and innovations. With introductory and advanced groups working in parallel, the needs of the participants could be met more specifically compared to introductory and advanced workshops organized separately. The next O2k-Workshop, therefore, will again offer parallel introductory and advanced workpackages.:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet15.01 IOC55 + ('''O2k-Workshop on high-resolution respirometry.''' Voralberg, Austria;2010 April 07 to 12.)
MiPNet07.05 IOC21 + ('''O2k-Workshop on high-resolution respirometry.''' Innsbruck, Tyrol, Austria; 2002 June 12-15. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet12.03 IOC37 + ('''O2k-Workshop on high-resolution respiro … '''O2k-Workshop on high-resolution respirometry and mitochondrial physiology.''' Seoul, Korea; 2007 February 4. Satellite to [[ASMRM]] 2007.:>> O2k-Workshop: [[Oroboros Events| Current dates]]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet06.09 IOC19 + ('''O2k-Workshop on high-resolution respirometry.''' Innsbruck, Tyrol, Austria; 2001 October 04-05. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet17.07 IOC67 + ('''O2k-Workshop on high-resolution respirometry.''' Sidney, Australia; 2012 April 02 to 04. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet17.08 IOC68 Schroecken AT + ('''O2k-Workshop on high-resolution respirometry: O2k-Basic and TPP-Basic.''' Schroecken, Voralberg,Austria; 2012 April 11 to 16. :» O2k-Workshop: [[OROBOROS_Events|Current dates]] :» Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet08.02 IOC23 + ('''O2k: Mitochondrial physiology (MiP) workshop on high-resolution respirometry.''' Schroecken AT, 27-31 March 2003. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
Hassoun 2008 Crit Care Med + ('''OBJECTIVE''': Growing evidence suggests … '''OBJECTIVE''': Growing evidence suggests that mitochondria function is impaired in sepsis. Here, we tested the hypothesis that lipopolysaccharide would induce mitochondrial Ca2+ overload and oxygen utilization abnormalities as consequences of sarcoplasmic reticulum Ca2+ handling derangements that are typically observed in sepsis. As lipopolysaccharide-induced sarcoplasmic reticulum dysfunction was mainly characterized by reduced sarcoplasmic reticulum Ca2+ uptake and Ca2+ leak, we tested whether dantrolene, a sarco(endo)plasmic reticulum calcium ATPase leak inhibitor, would prevent mitochondrial and cardiac contractile dysfunction.'''DESIGN''': Randomized controlled trial.'''SETTING''': Experimental laboratory.'''SUBJECTS''': Male Sprague Dawley rats.'''INTERVENTIONS''': Sepsis was induced by injection of endotoxin lipopolysaccharide (10 mg/kg/intravenously). Assessment of contractile function and Ca2+ handling was performed 4 hr after lipopolysaccharide. The relative contribution of the different Ca2+ transporters to relaxation in intact cardiomyocytes was studied during successive electrically evoked twitches and caffeine stimulation. Sarcoplasmic reticulum vesicles and mitochondria from ventricles of rats treated or not with lipopolysaccharide were prepared to evaluate Ca2+ uptake-release and oxygen fluxes, respectively. Effects of dantrolene (10 mg/kg) treatment in rats were evaluated in sarcoplasmic reticulum vesicles, mitochondria, and isolated hearts.'''MEASUREMENTS AND MAIN RESULTS''': Lipopolysaccharide challenge elicited cardiac contractile dysfunction that was accompanied by severe derangements in sarcoplasmic reticulum function, i.e., reduced Ca2+ uptake and increased sarcoplasmic reticulum Ca2+ leak. Functional sarcoplasmic reticulum changes were associated with modification in the status of phospholamban phosphorylation whereas SERCA was unchanged. Rises in mitochondrial Ca2+ content observed in lipopolysaccharide-treated rats coincided with derangements in mitochondrial oxygen efficacy, i.e., reduced respiratory control ratio. Administration of dantrolene in lipopolysaccharide-treated rats prevented mitochondrial Ca2+ overload and mitochondrial oxygen utilization abnormalities. Moreover, dantrolene treatment in lipopolysaccharide rats improved heart mitochondrial redox state and myocardial dysfunction.'''CONCLUSION:''' These experiments suggest that sarcoplasmic reticulum Ca2+ handling dysfunction is an early event during endotoxemia that could be responsible for, or contribute to, mitochondrial Ca2+ overload, metabolic failure, and cardiac dysfunction.tion is an early event during endotoxemia that could be responsible for, or contribute to, mitochondrial Ca2+ overload, metabolic failure, and cardiac dysfunction.)
Akude 2011 Diabetes + ('''OBJECTIVE:''' Impairments in mitochondr … '''OBJECTIVE:''' Impairments in mitochondrial function have been proposed to play a role in the etiology of diabetic sensory neuropathy. We tested the hypothesis that mitochondrial dysfunction in axons of sensory neurons in type 1 diabetes is due to abnormal activity of the respiratory chain and an altered mitochondrial proteome.'''RESEARCH DESIGN AND METHODS:''' Proteomic analysis using stable isotope labeling with amino acids in cell culture (SILAC) determined expression of proteins in mitochondria from dorsal root ganglia (DRG) of control, 22-week-old streptozotocin (STZ)-diabetic rats, and diabetic rats treated with insulin. Rates of oxygen consumption and complex activities in mitochondria from DRG were measured. Fluorescence imaging of axons of cultured sensory neurons determined the effect of diabetes on mitochondrial polarization status, oxidative stress, and mitochondrial matrix-specific reactive oxygen species (ROS).'''RESULTS:''' Proteins associated with mitochondrial dysfunction, oxidative phosphorylation, ubiquinone biosynthesis, and the citric acid cycle were downregulated in diabetic samples. For example, cytochrome c oxidase subunit IV (COX IV; a Complex IV protein) and NADH dehydrogenase Fe-S protein 3 (NDUFS3; a Complex I protein) were reduced by 29 and 36% (''P'' < 0.05), respectively, in diabetes and confirmed previous Western blot studies. Respiration and mitochondrial complex activity was significantly decreased by 15 to 32% compared with control. The axons of diabetic neurons exhibited oxidative stress and depolarized mitochondria, an aberrant adaption to oligomycin-induced mitochondrial membrane hyperpolarization, but reduced levels of intramitochondrial superoxide compared with control.'''CONCLUSIONS:''' Abnormal mitochondrial function correlated with a downregulation of mitochondrial proteins, with components of the respiratory chain targeted in lumbar DRG in diabetes. The reduced activity of the [[respiratory chain]] was associated with diminished superoxide generation within the mitochondrial matrix and did not contribute to oxidative stress in axons of diabetic neurons. Alternative pathways involving polyol pathway activity appear to contribute to raised ROS in axons of diabetic neurons under high glucose concentration.tic neurons under high glucose concentration.)
Japiassu 2011 Crit Care Med + ('''OBJECTIVE:''' Increasing evidence point … '''OBJECTIVE:''' Increasing evidence points to the role of mitochondrial dysfunction in the pathogenesis of sepsis. Previous data indicate that mitochondrial function is affected in monocytes from septic patients, but the underlying mechanisms and the impact of these changes on the patients' outcome are unknown. We aimed to determine the mechanisms involved in mitochondrial dysfunction in peripheral blood mononuclear cells from patients with septic shock.'''DESIGN:''' A cohort of patients with septic shock to study peripheral blood mononuclear cell mitochondrial respiration by high-resolution respirometry analyses and to compare with cells from control subjects.'''SETTING:''' Three intensive care units and an academic research laboratory.'''SUBJECTS:''' Twenty patients with septic shock and a control group composed of 18 postoperative patients without sepsis or shock.'''INTERVENTIONS:''' Ex vivo measurements of mitochondrial oxygen consumption were carried out in digitonin-permeabilized peripheral blood mononuclear cells from 20 patients with septic shock taken during the first 48 h after intensive care unit admission as well as in peripheral blood mononuclear cells from control subjects. Clinical parameters such as hospital outcome and sepsis severity were also analyzed and the relationship between these parameters and the oxygen consumption pattern was investigated.'''MEASUREMENTS AND MAIN RESULTS:''' We observed a significant reduction in the respiration specifically associated with adenosine-5'-triphosphate synthesis ([[State 3]]) compared with the control group (5.60 vs. 9.89 nmol O2/min/10(7) cells, respectively, ''P'' < .01). Reduction of State 3 respiration in patients with septic shock was seen with increased prevalence of organ failure (''r'' = -0.46, ''P'' = .005). Nonsurviving patients with septic shock presented significantly lower adenosine diphosphate-stimulated respiration when compared with the control group (4.56 vs. 10.27 nmol O2/min/10(7) cells, respectively; ''P'' = .004). Finally, the presence of the functional F1Fo adenosine-5'-triphosphate synthase complex (0.51 vs. 1.00 ng oligo/mL/10(6) cells, ''P'' = .02), but not the adenine nucleotide translocator, was significantly lower in patients with septic shock compared with control cells.'''CONCLUSION:''' Mitochondrial dysfunction is present in immune cells from patients with septic shock and is characterized as a reduced respiration associated to adenosine-5'-triphosphate synthesis. The molecular basis of this phenotype involve a reduction of F1Fo adenosine-5'-triphosphate synthase activity, which may contribute to the energetic failure found in sepsis.ute to the energetic failure found in sepsis.)
Rostambeigi 2011 Transplantation + ('''OBJECTIVE:''' To determine biological m … '''OBJECTIVE:''' To determine biological mechanisms involved in posttransplantation diabetes mellitus caused by the immunosuppressant tacrolimus (FK506).'''METHODS:''' INS-1 cells and isolated rat islets were incubated with vehicle or FK506 and harvested at 24-hr intervals. Cells were assessed for viability, apoptosis, proliferation, cell insulin secretion, and content. Gene expression studies by microarray analysis, quantitative polymerase chain reaction, and motifADE analysis of the microarray data identified potential FK506-mediated pathways and regulatory motifs. Mitochondrial functions, including cell respiration, mitochondrial content, and bioenergetics were assessed.'''RESULTS:''' Cell replication, viability, insulin secretion, oxygen consumption, and mitochondrial content were decreased (''P''<0.05) 1.2-, 1.27-, 1.77-, 1.32-, and 1.43-fold, respectively, after 48-hr FK506 treatment. Differences increased with time. FK506 (50 ng/mL) and cyclosporine A (800 ng/mL) had comparable effects. FK506 significantly decreased mitochondrial content and mitochondrial bioenergetics and showed a trend toward decreased oxygen consumption in isolated islets. Cell apoptosis and proliferation, mitochondrial DNA copy number, and ATP:ADP ratios were not significantly affected. Pathway analysis of microarray data showed FK506 modification of pathways involving ATP metabolism, membrane trafficking, and cytoskeleton remodeling. PGC1-α mRNA was down-regulated by FK506. MotifADE identified nuclear factor of activated T-cells, an important mediator of β-cell survival and function, as a potential factor mediating both up- and down-regulation of gene expression.'''CONCLUSIONS:''' At pharmacologically relevant concentrations, FK506 decreases insulin secretion and reduces mitochondrial density and function without changing apoptosis rates, suggesting that posttransplantation diabetes induced by FK506 may be mediated by its effects on mitochondrial function.ted by its effects on mitochondrial function.)
Chowdhury 2010 Diabetes + ('''Objective''': Impairments in mitochondr … '''Objective''': Impairments in mitochondrial physiology may play a role in diabetic sensory neuropathy. We tested the hypothesis that mitochondrial dysfunction in sensory neurons is due to abnormal mitochondrial respiratory function.'''Research design and methods''': Rates of oxygen consumption were measured in mitochondria from dorsal root ganglia (DRG) of 12- to- 22-week streptozotocin (STZ)-induced diabetic rats, diabetic rats treated with insulin, and age-matched controls. Activities and expression of components of mitochondrial complexes and reactive oxygen species (ROS) were analyzed.'''Results''': Rates of coupled respiration with pyruvate + malate (P + M) and with ascorbate + TMPD (Asc + TMPD) in DRG were unchanged after 12 weeks of diabetes. By 22 weeks of diabetes, respiration with P + M was significantly decreased by 31-44% and with Asc + TMPD by 29-39% compared with control. Attenuated mitochondrial respiratory activity of STZ-diabetic rats was significantly improved by insulin that did not correct other indices of diabetes. Activities of mitochondrial complexes I and IV and the Krebs cycle enzyme, citrate synthase, were decreased in mitochondria from DRG of 22-week STZ-diabetic rats compared with control. ROS levels in perikarya of DRG neurons were not altered by diabetes, but ROS generation from mitochondria treated with antimycin A was diminished compared with control. Reduced mitochondrial respiratory function was associated with downregulation of expression of mitochondrial proteins.'''Conclusions''': Mitochondrial dysfunction in sensory neurons from type 1 diabetic rats is associated with impaired rates of respiratory activity and occurs without a significant rise in perikaryal ROS.hout a significant rise in perikaryal ROS.)
Haendeler 2009 Arterioscler Thromb Vasc Biol + ('''Objective'''—The enzyme telomerase and … '''Objective'''—The enzyme telomerase and its catalytic subunit the telomerase reverse transcriptase (TERT) are important for maintenance of telomere length in the nucleus. Recent studies provided evidence for a mitochondrial localization of TERT. Therefore, we investigated the exact localization of TERT within the mitochondria and its function.'''Methods and Results'''—Here, we demonstrate that TERT is localized in the matrix of the mitochondria. TERT binds to mitochondrial DNA at the coding regions for ND1 and ND2. Binding of TERT to mitochondrial DNA protects against ethidium bromide–induced damage. TERT increases overall respiratory chain activity, which is most pronounced at Complex I and dependent on the reverse transcriptase activity of the enzyme. Moreover, mitochondrial reactive oxygen species are increased after genetic ablation of TERT by shRNA. Mitochondrially targeted TERT and not wild-type TERT revealed the most prominent protective effect on H2O2-induced apoptosis. Lung fibroblasts from 6-month-old TERT-/- mice (F2 generation) showed increased sensitivity toward UVB radiation and heart mitochondria exhibited significantly reduced respiratory chain activity already under basal conditions, demonstrating the protective function of TERT ''in vivo''.'''Conclusion'''—Mitochondrial TERT exerts a novel protective function by binding to mitochondrial DNA, increasing respiratory chain activity and protecting against oxidative stress–induced damage.iratory chain activity and protecting against oxidative stress–induced damage.)
Virtual OroDM02 + ('''Oroboros Distributor Meeting'''. Virtual.)
MiPNet26.07 Installation and startup support session + ('''Oroboros Installation and startup support session'''.)
MiPNet15.07 IOC59 + ('''Oroboros O2k-Workshop on High-Resolution Respirometry. Obergurgl, Tyrol, Austria; 2010 October 01 to 06. Satellite to [[MiP2010]].''' :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
MiPNet28.11 IOC163 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2024 June 17-22). )
MiPNet28.12 IOC167 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2024 Sep 30 - Oct 05). )
MiPNet24.02 IOC141 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria; 2019 September.)
MiPNet28.02 IOC162 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2023 October 02-07). )
MiPNet24.01 IOC139 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria; 2019.)
MiPNet28.01 IOC160 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2023 June 19-24). )
MiPNet27.04 IOC155 Schroecken AT + ('''Oroboros O2k-Workshop on high-resolutio … '''Oroboros O2k-Workshop on high-resolution respirometry'''. Schroecken, Austria (2022 October 03-08). Following the [[MiPNet27.05_Schroecken_BEC_tutorial-Living_Communications_pmP|BEC tutorial on mitochondrial membrane potential and protonmotive pressure]] (2022 Sep 30 - Oct 03).[[MiPNet27.05_Schroecken_BEC_tutorial-Living_Communications_pmP|BEC tutorial on mitochondrial membrane potential and protonmotive pressure]] (2022 Sep 30 - Oct 03).)
MiPNet25.02 IOC Schroecken AT + ('''Oroboros O2k-Workshop on high-resolution respirometry'''.)
MiPNet25.17 Virtual O2k-Workshop PhotoBiology + ('''Oroboros Virtual O2k-Workshop on high-resolution respirometry and PhotoBiology'''.)
MiPNet26.02 Virtual O2k-Workshop:Q-Module + ('''Oroboros Virtual O2k-Workshop on high-resolution respirometry and and measurement of the redox state of the Q-pool'''.)
MiPNet25.16 Virtual O2k-Workshop HRR + ('''Oroboros Virtual O2k-Workshops on high-resolution respirometry''' were offered during the COVID-19 lockdown and are discontinued.)
MiPNet14.14 PermeabilizedFiberPreparation + ('''Pesta D, Gnaiger E (2015) Preparation o … '''Pesta D, Gnaiger E (2015) Preparation of permeabilized muscle fibers for diagnosis of mitochondrial respiratory function. Mitochondr Physiol Network 14.14(02):1-5.''' Application of [[permeabilized muscle fibers]] and [[high-resolution respirometry]] offer a sensitive diagnostic test of mitochondrial dysfunction in small [[biopsy]] specimens of human muscle. By using these techniques in conjunction with multiple [[substrate-uncoupler-inhibitor titration]] (SUIT) protocols, respirometric studies of human and animal tissue biopsies improve our fundamental understanding of mitochondrial respiratory control and the pathophysiology of mitochondrial myopathies.[[Image:MiPNet14.14.jpg|right|200px|thumb]]:>> Product: [[O2k-Catalogue: O2k-MultiSensor]], [[O2k-Core]], [[Oroboros O2k-Catalogue]][[Oroboros O2k-Catalogue]])
Pasdois 2015 Fatty Acid Oxidation O2k-Network Discussion Forum + ('''Protocol''': Couple palmitoylcarnitine (10µM) + malate (1mM) on isolated mitochondria and permeabilized fibers. In such case the buffer is always supplemented with 2mg/ml of BSA.)
Ciapaite 2015 Fatty Acid Oxidation O2k-Network Discussion Forum + ('''Protocol''': I use either palmitoyl-L-carnitine plus malate (25 µM + 2.5 mM) or palmitoyl-CoA + L-carnitine + malate (25 µM + 2 mM + 2.5 mM) as substrates. Respiratory control index is usually around 5-6 for healthy controls.)
Robidoux 2015 Fatty Acid Oxidation O2k-Network Discussion Forum + ('''Protocol''': Palmitate, Stearate, Oleate and Linoleate in intact cells. We use various BSA-fatty acid combinations that result in free fatty acid levels that are in the 2 to 12 nM range.)
Chou 2015 Fatty Acid Oxidation O2k-Network Discussion Forum + ('''Protocol''': final concentration of dig … '''Protocol''': final concentration of digitonin in chamber is 10μg/mlcell number in chamber is 2 millions cell/ml, cell type PBMC, Malate (2mM), Palmitoyl-DLcarnitine-HCl (20μM), ADP (2.5mM), pyruvate (5mM), glutamate (10mM), succinate (10mM), rotenone (0.1μM), malonic acid(5mM), myxothiazol (0.5μM), antimycin A (2.5μM), TMPD (0.5mM), azide (100mM)cin A (2.5μM), TMPD (0.5mM), azide (100mM))
Lanza 2010 Curr Opin Clin Nutr Metab Care + ('''Purpose of review''': Mitochondrial con … '''Purpose of review''': Mitochondrial content and function vary across species, tissue types, and lifespan. Alterations in skeletal muscle mitochondrial function have been reported to occur in in aging and in many other pathological conditions. This review focuses on the state of the art ''in vivo'' and ''in vitro'' methodologies for assessment of muscle mitochondrial function.'''Recent findings''': Classic studies of isolated mitochondria have measured function from maximal respiratory capacity. These fundamental methods have recently been substantially improved and novel approaches to asses mitochondrial functions ''in vitro'' have been emerged. Noninvasivemethods based on magnetic resonance spectroscopy (MRS) and near-infraredspectroscopy (NIRS) permit ''in vivo'' assessment of mitochondrial function and are rapidly becoming more accessible to many investigators. Moreover, it is now possible to gather information on regulation of mitochondrial content by measuring the ''in vivo'' synthesis rate of individual mitochondrial proteins.'''Summary: High-resolution respirometry has emerged as a powerful tool for ''in vitro'' measurements of mitochondrial function in isolated mitochondria and permeabilized fibers.''' Direct measurements of ATP production are possible by bioluminescence. Mechanistic data provided by these methods is further complimented by ''in vivo'' assessment using MRS and NIRS and the translational rate of gene transcripts.he translational rate of gene transcripts.)
Votion 2010 Equine Vet J + ('''REASONS FOR PERFORMING STUDY:''' Limite … '''REASONS FOR PERFORMING STUDY:''' Limited information exists about the muscle mitochondrial respiratory function changes that occur in horses during an endurance season.'''OBJECTIVES:''' To determine effects of training and racing on muscle oxidative phosphorylation (OXPHOS) and electron transport system (ET-pathway) capacities in horses with high resolution respirometry (HRR).'''METHODS:''' Mitochondrial respiration was measured in microbiopsies taken from the triceps brachii (tb) and gluteus medius (gm) muscles in 8 endurance horses (7 purebred Arabians and 1 crossbred Arabian) before training (T0), after two 10 week training periods (T1, T2) and after 2 CEI** endurance races (R1, R2). Muscle OXPHOS capacity was determined using 2 titration protocols without (SUIT 1) or with pyruvate (SUIT 2) as substrate. Electrons enter at the level of Complex I, Complex II or both complexes simultaneously (Complexes I+II). Muscle ET capacity was obtained by uncoupling Complexes I+II sustained respiration.'''RESULTS:''' T1 improved OXPHOS and ET capacities in the tb as demonstrated by the significant increase of oxygen fluxes vs. T0 (Complex I: +67%; ET-pathway: +37%). Training improved only OXPHOS in the gm (Complex I: +34%). Among horses that completed the race, a significant decrease in OXPHOS (Complex I: ∼ -35%) and ET-pathway (-22%) capacities was found in the tb with SUIT 2 indicating a reduced aerobic glycolysis. Significant correlations between CK activities and changes in OXPHOS were found suggesting a relationship between exercise-induced muscle damage and depression of mitochondrial respiration.'''CONCLUSIONS:''' For the first time, OXPHOS and ET capacities in equine muscle at different steps of an endurance season have been determined by HRR. Significant alterations in mitochondrial respiratory function in response to endurance training and endurance racing have been observed although these changes appeared to be muscle group specific.nges appeared to be muscle group specific.)
MiPNet02.04 DatLab2 TimeConstant + ('''Reck M, Wyss M, Lassnig B, Gnaiger E (1 … '''Reck M, Wyss M, Lassnig B, Gnaiger E (1997) DatLab 2. High time resolution. Mitochondr Physiol Network 02.04:1-11.''' »[http://www.bioblast.at/index.php/File:MiPNet02.04_DatLab2_TimeConstant.pdf Versions]:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue ]][Oroboros O2k-Catalogue ]])