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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]])

('''O2k-Workshop on high-resolution respirometry.''' Innsbruck, Tyrol, Au)

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.)