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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]])

('''Gnaiger E, Lassnig B (1997) DatLab 2. Analysis of oxygen kinetics. Mi)

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.''')