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A list of all pages that have property "Has abstract" with value "'''FAT4BRAIN Advanced Virtual O2k-Workshop IOC150 on TMRM and Calcium Gr". Since there have been only a few results, also nearby values are displayed.

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  • 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</br></br></br>“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.</br></br>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.</br>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!</br></br>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.</br>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'''</br>* Introduction [http://www.oroboros.at/fileadmin/user_upload/Reprints/O-MiPNet-Publ/MitoPathways2_Introduction.pdf pdf]</br>* MitoPathways to Complex I: [[MiPNet11.04]]</br>* MitoPathways to Complex II: [[MiPNet11.09]]</br>* MitoPathways to Complexes I<small>&</small>II: [[MiPNet12.12]]</br>* MitoPathways compilation: [[MiPNet12.13]] </br>* MitoPathways - respiratory states: [[MiPNet12.15]]</br>* Cell respiration and phosphorylation control: [[MiPNet08.09]] </br>* HRR and phosphorylation control: [[MiPNet10.04]]</br>* FCRs in isolated mitochondria: [[MiPNet12.11]]</br>* O2k manual titrations: [[MiPNet09.12]]</br>* O2k-paradigm: [[MiPNet09.01]]</br>* [[Gnaiger 2012 MitoPathways References|References]]</br>* 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.</br></br>'''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.</br></br>'''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 glucose</br>tolerance test blood glucose levels were also included. Main Outcome Measure:Wemeasured mitochondrial respiration in saponin-treated skinned muscle</br>fibers from biopsies of m. deltoideus and m. vastus lateralis using high-resolution respirometry.</br></br>'''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 muscles</br>were not different between the T2DM and control group, and maximum rate of O2 consumption did not differ between the groups.</br></br>'''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?''</br></br>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.''' </br></br>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.</br>:» 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.'''</br></br>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''<sub>R</sub>, resulted in volume-specific oxygen consumption of 20 pmol·s<sup>-1</sup>·ml<sup>-1</sup>. 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 (''J<sub>L</sub>''), and rotenone (residual oxygen consumption, ''J''<sub>ROX</sub>; after uncoupling) reduced respiration to 5 and 1 pmol·s<sup>-1</sup>·ml<sup>-1</sup>, while inducing the noncoupled state by the uncoupler FCCP revealed the capacity of the Electron transfer-pathway (ET-pathway) at ''J<sub>E</sub>'' of 50 pmol·s<sup>-1</sup>·ml<sup>-1</sup>. 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.</br></br>Automatic correction for instrumental background amounted to 13% for ROUTINE respiration, but to >50% and 180% for ''J<sub>L</sub>'' and ''J''<sub>ROX</sub>, 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.</br>:» 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).<br>)
  • 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.</br></br>'''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). </br></br>To explore the role of thrombomodulin (TM)-dependent aPC generation at baseline and in immunological and non-immunological demyelinating disease models. </br></br>Myelination and reactive oxygen species (ROS) generation were evaluated in mice with genetically reduced TM-mediated protein C activation (TM<sup>Pro/Pro</sup>) and in wild-type (WT) mice under control conditions or following induction of EAE. Non-immunological demyelination was analyzed in the cuprizone-diet model. </br></br>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 (p66<sup>Shc</sup> deficiency), restoring aPC plasma levels or injecting soluble TM (solulin) ameliorates EAE in TM<sup>Pro/Pro</sup> 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. </br></br>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.</br></br>© 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.'''</br></br></br>== Time and Location ==</br></br>13:00 until 17:00 at Standortagentur Tirol, Ing.-Etzelstr. 17, Innsbruck</br> </br></br>== General information (German) ==</br></br>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.</br></br>'''WAS BISHER GESCHAH...'''</br></br>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. </br></br>'''DER NÄCHSTE SCHRITT...'''</br></br>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. </br>Im Bereich Medizintechnik werden folgende Fragestellungen behandelt:</br>* Wie könnten neue Geschäftsmodelle helfen die Erfolgsgeschichte der Tiroler Medizintechnikunternehmen auszubauen? </br>* Was sind spannende, digitale Lösungsansätze um die Wettbewerbsfähigkeit Tiroler Medizintechnikunternehmen erhöhen zu können? </br>* Wie können Tiroler Medizintechnikunternehmen durch eine branchenübergreifende Vernetzung (IT, Gesundheit,..) innovative Angebote entwickeln? </br>* Wie müsste eine wirksame Förderpolitik für Tiroler Medizintechnikunternehmen aussehen? </br>* Welche Vermarktungsansätze könnten Tiroler Medizintechnikunternehmen im Wettbewerb massiv weiterhelfen? </br>* Welche Ansätze helfen Tiroler Medizintechnikunternehmen deren Effektivität und Effizienz in der Entwicklung und Herstellung zu steigern? </br>* Welche Ansätze könnten (kleineren) Tiroler Medizintechnikunternehmen helfen, mit der Flut an neuen Regularien umzugehen? </br> </br>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 Advanced Virtual O2k-Workshop IOC150 on TMRM and Calcium Gr)
  • 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).<br>)
  • 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.'''</br><br/></br></br><div style="padding:0px;border: 1px solid #aaaaaa;margin-bottom:0px;margin-right:10px"></br><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;"></br>[[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]]</br>: <big>Open the '''pdf document''' above.</big></br></div></br><div style="background-color:#ffffff;padding-top:0.2em;padding-right: 0.4em;padding-bottom: 0.2em;padding-left: 0.4em;"></br>::::» Current O2k-series: '''[https://www.oroboros.at/index.php/product-category/products/o2k-packages/ NextGen-O2k Series XB and O2k Series J]'''</br>::::» Current software versions DatLab 8.0: [[MitoPedia: DatLab]]</br>::::* ''Further details:'' '''» [[MitoPedia: O2k-Open Support]]'''</br></div></br></div></br></br>Mitochondrial respiration medium MiR06 was developed for oxygraph incubations of mitochondrial preparations. MiR06 = MiR05 plus catalase. MiR06Cr = MiR06+creatine.</br></br>:» 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.'''</br>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.</br>:» 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.''' </br></br>'''This is an old version, which applies up to O2k-Series F and to DatLab 5.'''</br>: ''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]</br></br>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).</br></br>[[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).]]</br></br>[[Aguirre_2010_Biochim_Biophys_Acta| Reference: Biochim Biophys Acta 1797: 557-565 (2010)]]</br></br>:» 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.'''</br></br>:» Product: [[O2k-Catalogue: TIP2k|TIP2k]], [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]]</br></br>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.</br></br>''Titration:''</br>Programmable, automatic titration regimes, with titration volumes of 0.05 to 250 µl, variable titration intervals and duration of titration pulses.</br></br></br>''Injection:''</br>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.</br>Ramp injection (MiPNet04.05, see above): Ramp increase of effector concentrations by "continuous titration".</br>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'''</br></br>Heterozygous mice (αMHC<sup>403/+</sup>) expressing the human hypertrophic cardiomyopathy (HCM) disease causing mutation ''Arg403Gln'' exhibit cardinal features of HCM.</br>This study investigated the role of L-type Ca<sup>2+</sup> channel (I<sub>Ca-L</sub>) in regulating mitochondrial function in ''Arg403Gln'' (αMHC<sup>403/+</sup>) mice.</br>Activation of I<sub>Ca-L</sub> in αMHC<sup>403/+</sup> mice caused a significantly greater increase in mitochondrial membrane potential and metabolic activity when compared to wild-type mice.</br>Increases in mitochondrial membrane potential and metabolic activity were attenuated with I<sub>Ca-L</sub> antagonists and when F-actin or β-tubulin were depolymerized.</br>I<sub>Ca-L</sub> antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity.</br></br>'''Summary'''</br></br>Heterozygous mice (αMHC<sup>403/+</sup>) expressing the human disease-causing mutation ''Arg403Gln'' exhibit cardinal features of hypertrophic cardiomyopathy (HCM) including hypertrophy, myocyte disarray, and increased myocardial fibrosis. Treatment of αMHC<sup>403/+</sup> mice with the L-type calcium channel (I<sub>Ca-L</sub>) antagonist diltiazem has been shown to decrease left ventricular anterior wall thickness, cardiac myocyte hypertrophy, disarray, and fibrosis. However, the role of the I<sub>Ca-L</sub> in the development of HCM is not known. In addition to maintaining cardiac excitation and contraction in myocytes, the I<sub>Ca-L</sub> also regulates mitochondrial function through transmission of movement of I<sub>Ca-L</sub> via cytoskeletal proteins to mitochondrial voltage-dependent anion channel. Here, the authors investigated the role of I<sub>Ca-L</sub> in regulating mitochondrial function in αMHC<sup>403/+</sup> mice. Whole-cell patch clamp studies showed that I<sub>Ca-L</sub> current inactivation kinetics were significantly increased in αMHC<sup>403/+</sup> cardiac myocytes, but that current density and channel expression were similar to wild-type cardiac myocytes. Activation of I<sub>Ca-L</sub> caused a significantly greater increase in mitochondrial membrane potential and metabolic activity in αMHC<sup>403/+</sup>. These increases were attenuated with I<sub>Ca-L</sub> antagonists and following F-actin or β-tubulin depolymerization. The authors observed increased levels of fibroblast growth factor-21 in αMHC<sup>403/+</sup> 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 I<sub>Ca-L</sub> and mitochondria that is associated with increased metabolic activity, which may contribute to the development of cardiomyopathy. I<sub>Ca-L</sub> antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity.to altered functional communication between I<sub>Ca-L</sub> and mitochondria that is associated with increased metabolic activity, which may contribute to the development of cardiomyopathy. I<sub>Ca-L</sub> 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'''</br></br>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''”. </br></br>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.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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.)