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• TrMAD2014  + (4^th Regional Translational Research in Mitochondria, Aging, and Disease Symposium, Pittsburgh, PA, US. [http://www.upci.upmc.edu/trmad/ TrMAD2014])
• 4th Global Chinese Symposium & The 8th Symposium for Cross-straits on Free Radical Biology and Medicine 2018 Macao CN  + (4th Global Chinese Symposium & The 8th Symposium for Cross-straits, Hong Kong and Macao on Free Radical Biology and Medicine, Macao, China, 2018)
• 4th edition Metabolism & Cancer 2021 Virtual  + (4th edition Metabolism & Cancer, Virtu … 4th edition Metabolism & Cancer, Virtual, 2021 </br></br></br>== Program ==</br>:::: [https://www.metabolism-cancer.com/program/ here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://www.metabolism-cancer.com/under-construction/ here]</br></br>== Registration ==</br>:::: [https://www.metabolism-cancer.com/registration/ Registration and more information]</br></br>== Oroboros at MetaboCancer 2021==</br>:::: [[Gnaiger Erich]]: Oroboros Instruments innovations - NextGen-O2k and Bioenergetics Communications, ''May 28th at 11:25''</br></br>=== Booth ===</br>:::: The Oroboros team is looking forward to welcome you at our Oroboros booth which will be available at this conference.</br></br></br>== Support ==</br>[[File:Template NextGen-O2k.jpg|right|350px|link=NextGen-O2k]]</br></br>[[Category:NextGen-O2k]]</br>:::: Supported by project NextGen-O2k which has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 859770.</br><br/></br><br/></br><br/></br><br/> agreement No. 859770. <br/> <br/> <br/> <br/>)
• MacPherson 2016 Am J Physiol Cell Physiol  + (5'-AMP-activated protein kinase (AMPK) is … 5'-AMP-activated protein kinase (AMPK) is activated as a consequence of lipolysis and has been shown to play a role in regulation of adipose tissue mitochondrial content. Conversely, the inhibition of lipolysis has been reported to potentiate the induction of protein kinase A (PKA)-targeted genes involved in the regulation of oxidative metabolism. The purpose of the current study was to address these apparent discrepancies and to more fully examine the relationship between lipolysis, AMPK, and the β-adrenergic-mediated regulation of gene expression. In 3T3-L1 adipocytes, the adipose tissue triglyceride lipase (ATGL) inhibitor ATGListatin attenuated the Thr(172) phosphorylation of AMPK by a β3-adrenergic agonist (CL 316,243) independent of changes in PKA signaling. Similarly, CL 316,243-induced increases in the Thr(172) phosphorylation of AMPK were reduced in adipose tissue from whole body ATGL-deficient mice. Despite reductions in the activation of AMPK, the induction of PKA-targeted genes was intact or, in some cases, increased. Similarly, markers of mitochondrial content and respiration were increased in adipose tissue from ATGL knockout mice independent of changes in the Thr(172) phosphorylation of AMPK. Taken together, our data provide evidence that AMPK is not required for the regulation of adipose tissue oxidative capacity in conditions of reduced fatty acid release.</br></br>Copyright © 2016 the American Physiological Society.© 2016 the American Physiological Society.)
• Stride 2012 Front Physiol  + (5'-adenosine monophosphate-activated prote … 5'-adenosine monophosphate-activated protein kinase (AMPK) is considered central in regulation of energy status and substrate utilization within cells. In heart failure the energetic state is compromised and substrate metabolism is altered. We hypothesized that this could be linked to changes in AMPK activity and we therefore investigated mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytes from young and old mice expressing a dominant negative AMPKα2 (AMPKα2-KD) construct and their wildtype (WT) littermates. We found a 35-45% (P < 0.05) lower mitochondrial capacity for oxidizing MCFA in AMPKα2-KD of both age-groups, compared to WT. This coincided with marked decreases in protein expression (19/29%, P < 0.05) and activity (14/21%, P < 0.05) of 3-hydroxyacyl-CoA-dehydrogenase (HAD), in young and old AMPKα2-KD mice, respectively, compared to WT. Maximal LCFA oxidation capacity was similar in AMPKα2-KD and WT mice independently of age implying that LCFA-transport into the mitochondria was unaffected by loss of AMPK activity or progressing age. Expression of regulatory proteins of glycolysis and glycogen breakdown showed equivocal effects of age and genotype. These results illustrate that AMPK is necessary for normal mitochondrial function in the heart and that decreased AMPK activity may lead to an altered energetic state as a consequence of reduced capacity to oxidize MCFA. We did not identify any clear aging effects on mitochondrial function. any clear aging effects on mitochondrial function.)
• Hanley 2005 J Physiol  + (5-Hydroxydecanoate (5-HD) blocks pharmacol … 5-Hydroxydecanoate (5-HD) blocks pharmacological and ischaemic preconditioning, and has been postulated to be a specific inhibitor of mitochondrial ATP-sensitive K+ (KATP) channels. However, recent work has shown that 5-HD is activated to 5-hydroxydecanoyl-CoA (5-HD-CoA), which is a substrate for the first step of β-oxidation. We have now analysed the complete β-oxidation of 5-HD-CoA using specially synthesised (and purified) substrates and enzymes, as well as isolated rat liver and heart mitochondria, and compared it with the metabolism of the physiological substrate decanoyl-CoA. At the second step of β-oxidation, catalysed by enoyl-CoA hydratase, enzyme kinetics were similar using either decenoyl-CoA or 5-hydroxydecenoyl-CoA as substrate. The last two steps were investigated using l-3-hydroxyacyl-CoA dehydrogenase (HAD) coupled to 3-ketoacyl-CoA thiolase. ''V''max for the metabolite of 5-HD (3,5-dihydroxydecanoyl-CoA) was fivefold slower than for the corresponding metabolite of decanoate (l-3-hydroxydecanoyl-CoA). The slower kinetics were not due to accumulation of d-3-hydroxyoctanoyl-CoA since this enantiomer did not inhibit HAD. Molecular modelling of HAD complexed with 3,5-dihydroxydecanoyl-CoA suggested that the 5-hydroxyl group could decrease HAD turnover rate by interacting with critical side chains. Consistent with the kinetic data, 5-hydroxydecanoyl-CoA alone acted as a weak substrate in isolated mitochondria, whereas addition of 100 μm 5-HD-CoA inhibited the metabolism of decanoyl-CoA or lauryl-carnitine. In conclusion, 5-HD is activated, transported into mitochondria and metabolised via β-oxidation, albeit with rate-limiting kinetics at the penultimate step. This creates a bottleneck for β-oxidation of fatty acids. The complex metabolic effects of 5-HD invalidate the use of 5-HD as a blocker of mitochondrial KATP channels in studies of preconditioning.TP channels in studies of preconditioning.)
• Mitchell 2011 Biochim Biophys Acta  + (50 years ago Peter Mitchell proposed the c … 50 years ago Peter Mitchell proposed the chemiosmotic hypothesis for which he was awarded the Nobel Prize for Chemistry in 1978. His comprehensive review on chemiosmotic coupling known as the first “Grey Book”, has been reprinted here with permission, to offer an electronic record and easy access to this important contribution to the biochemical literature. This remarkable account of Peter Mitchell's ideas originally published in 1966 is a landmark and must-read publication for any scientist in the field of bioenergetics. As far as was possible, the wording and format of the original publication have been retained. Some changes were required for consistency with BBA formats though these do not affect scientific meaning. A scanned version of the original publication is also provided as a downloadable file in Supplementary Information. See also Editorial in this issue by Peter R. Rich. Original title: CHEMIOSMOTIC COUPLING IN OXIDATIVE AND PHOTOSYNTHETIC PHOSPHORYLATION, by Peter Mitchell, Glynn Research Laboratories, Bodmin, Cornwall, England.h Laboratories, Bodmin, Cornwall, England.)
• ESCI 2021 Virtual  + (55^th ESCI meeting, Virtual, 2021)
• ESCI 2022 Bari IT  + (56^th ESCI meeting, Bari, Italy, 2022)
• ESCI 2023 Prague CZ  + (57^th ESCI meeting, Prague, Czech Republic, 2023)
• Targeting Mitochondria World Congress 2014  + (5^th Targeting Mitochondria World Congress - [http://www.targeting-mitochondria.com/ Targeting Mitochondria], Berlin DE)
• 5th Academic Symposium of Metabolic Biology Branch of Chinese Biophysical Society 2022 Zunyi CN  + (5th Academic Symposium of Metabolic Biology Branch of Chinese Biophysical Society, Zunyi, China, 2022)
• 5th International Conference of Mitochondrial Medicine  + (5th International Mitochondrial Medicine Conference Mitochondrial, Online, 2021)
• NHLBI Mitochondrial Biology Symposium 2019 Bethesda US  + (5th NHLBI Mitochondrial Biology Symposium, … 5th NHLBI Mitochondrial Biology Symposium, Bethesda, Maryland, USA, 2019 </br></br></br>== General information == </br>::::On September 26-27, 2019, experts from around the world will gather on the NIH Campus in Bethesda, Maryland to review advances in our understanding of how mitochondrial structure, function, and interactions within the cell contribute to diseases and aging; and to highlight recent progress made with animal models and therapeutic interventions.</br></br>== Venue == </br>:::: William H. Natcher Conference Center – Building 45</br>:::: National Institutes of Health</br>:::: 45 Center Drive</br>:::: Bethesda, MD 20814</br>:::: [https://2019mbs.com/meeting-venue/ How to get there]</br></br>== Organizer ==</br>:::: [https://2019mbs.com/organizers/ Information available here]</br></br>== Programme ==</br>:::: [https://2019mbs.com/agenda/ Agenda]</br></br>== Speakers == </br>:::: List of speakers can be found [https://2019mbs.com/featured-speakers/ here]</br></br>== Registration ==</br></br>:::: [https://www.eventbrite.com/e/the-2019-nhlbi-mitochondrial-biology-symposium-registration-54765893261 Registration and more information]</br></br>:::: The abstracts submission deadline is Friday, June 28, 2019, at 11:59PM EST. </br>:::: All submissions must be made through the abstract submission portal. </br>:::: Abstracts should be no longer than 500 words and include four clearly identifiable components: Background, Methods, Results, and Conclusion. </br>:::: Abstracts will be reviewed by the Organizing Committee. Acceptance will be based on the quality of the abstract and availability of space. Four high-quality abstracts will be selected for oral presentation.ts will be selected for oral presentation.)
• 5th edition Metabolism & Cancer 2023 Nice FR  + (5th edition Metabolism & Cancer, Nice, … 5th edition Metabolism & Cancer, Nice, France, 2023 </br></br>== Venue ==</br>:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 How to get there]</br></br>== Program ==</br>:::: Program available [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]</br></br>== Registration ==</br>:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 Registration and more information]utm_campaign=2023-01-04%20METABO%202023%201 Registration and more information])
• BPS19 2019 Baltimore US  + (63rd Annual Meeting of the Biophysical Soc … 63rd Annual Meeting of the Biophysical Society, Baltimore, Maryland USA, 2019 </br></br></br></br>== General information==</br>:::: The Biophysical Society meeting is the only major scientific meeting in the United States that routinely includes bioenergetics and mitochondrial topics. The Bioenergetics, Mitochondria, and Metabolism Subgroup has its two symposia on the first day of the meeting, March 2nd, and these two symposia have a distinguished group of speakers who are leaders in the field of bioenergetics. </br></br>== Venue == </br>:::: Baltimore Convention Center</br>:::: 1 W. Pratt Street</br>:::: Baltimore, Maryland 21201</br>::::[https://www.biophysics.org/2019meeting/hotel-travel Hotel and Travel]</br></br>== Programme ==</br>:::: [https://www.biophysics.org/2019meeting/program here]</br></br></br>== Registration ==</br>:::: [https://www.biophysics.org/2019meeting/registration Registration and more information]tration Registration and more information])
• AMI 2023 Jhansi IN  + (64^th Annual International Conference of the Associate of Microbiologists of India, Jhansi, India, 2023)
• BPS2023 San Diego US  + (67th Annual Meeting of the Biophysical Society, San Diego, California, USA, 2023)
• ISOTT 2017 Halle/Saale DE  + (6^th 45th Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT), Halle/Saale, Germany.)
• 6th Annual Conference of Chinese Society for Neurobiological Control of Metabolism 2024 Quanzhou CN  + (6^th Annual Conference of Chinese Society for Neurobiological Control of Metabolism, Quanzhou, China, 2024)
• SMRM2017 New Delhi IN  + (6^th Annual Conference of the Society for Mitochondrial Research and Medicine, New Delhi, India.)
• MiPschool Copenhagen DK 2013  + (6^th MiP''summer school'' on Mitochondrial Physiology, 2013 August 26-30, Copenhagen, Denmark.)
• 6th Biannual Meeting on Mitochondria Apoptosis & Cancer 2019 Prague CZ  + (6th Biannual Meeting on Mitochondria Apoptosis & Cancer, Prague, Czech Republic, 2019)
• 6th EU-Cardioprotection Meeting 2021 Riga LV  + (6th EU-Cardioprotection WG Meeting CA16625 on mito and metabolism as targets for cardioprotection., Virtual Event, 2021)
• 6th International Conference on Tumor Microenvironment and Cellular Stress 2019 Crete GR  + (6th International Conference on Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging and Therapeutic Targets, Chania, Crete, Greece, 2019)

• 6th Research Day Innsbruck AT  + (6th Research Day, Innsbruck, Austria, 2023)

• 77th Annual Meeting of the JCA 2018 Osaka JP  + (77th Annual Meeting of the Japanese Cancer Association at the Osaka International Convention Center and RIHGA, Osaka, Japan, 2018)
• The 77th Japanese Society of Physical Fitness and Sports Medicine 2022 Tochigi JP  + (77th Japanese Society of Physical Fitness and Sports Medicine, Tochigi, 2022)
• ISOTT 2018 Seoul KR  + (7^th 46th Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT). Seoul, South Korea, 2018)
• ISAP 2021 Virtual  + (7th Conference of the International Society for Applied Phycology - ISAP2021, Tsukuba, Japan, 2021)
• 7th European Phycological Congress 2019 Zagreb HR  + (7th European Phycological Congress, Zagreb, Croatia, 2019)
• 7th Molecular Mechanisms of Axon Degeneration Meeting Loch Lomond GB  + (7th Molecular Mechanisms of Axon Degeneration Meeting, Loch Lomond, Scotland, Great Britain, 2019)
• 7th World Congress on Targeting Microbiota 2019 Krakow PL  + (7th World Congress on Targeting Microbiota … 7th World Congress on Targeting Microbiota, Krakow, Poland, 2019 </br></br></br></br>== Venue == </br>:::: Park Inn by Radisson Krakow Hotel</br>:::: Ul. Monte Cassino 2 PL</br>:::: 30337 - Krakow - Poland</br>:::: [https://www.microbiota-site.com/venue.html More information]</br></br>== Organizer ==</br>:::: [https://www.microbiota-site.com/committee.html Information available here]</br></br>== Programme ==</br>:::: [https://www.microbiota-site.com/images/2019/PDF/Targeting_Microbiota_2019_Agenda_-_V7.pdf Agenda]</br></br>== Speakers == </br>:::: List of speakers can be found [https://www.microbiota-site.com/microbiota-2019-speakers.html here]</br></br>== Registration ==</br></br>:::: [https://www.microbiota-site.com/registrations.html Registration and more information]ns.html Registration and more information])
• MiPschool London 2015  + (8^th MiP''school'' on Mitochondrial Physiology, 2015 Apr 20-24, London, UK.)
• SMRM2020 Virtual  + (8th Annual Meeting of the Society for Mitochondria Research and Medicine-India , Virtual.)
• 8th SMRM and Mitochondria-Metabolism Network Meeting 2020 Pune IN  + (8th SMRM and Mitochondria-Metabolism Netwo … 8th SMRM and Mitochondria-Metabolism Network Meeting, Pune, India, 2020 </br></br></br>== General information == </br>:::: Flyer available for [https://www.mitoeagle.org/images/b/b2/8th_SMRM_and_Mitochondria-Metabolism_Network_Meeting_Poster.pdf download]</br></br>== Venue == </br>:::: Indian Institute of Science Education and Research (ISER Pune)</br>:::: Dr. Homi Bhabha Road</br>:::: Pashan, Pune 411 008</br>:::: INDIA</br>::::[http://www.iiserpune.ac.in/facilities/guesthouse-cum-convention-centre Hotel and Travel]</br></br>== Programme ==</br>:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=12&confId=7288 here]</br></br>== Speakers == </br>:::: List of speakers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=0&confId=7288 here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=9&confId=7288 here]</br></br>== Registration ==</br>:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=6&confId=7288 Registration and more information]ageId=6&confId=7288 Registration and more information])
• TriMAD Sysposium 2018 Pennsylvania US  + (8th Translational Research in Mitochondria … 8th Translational Research in Mitochondria, Aging, and Disease (TRiMAD) Symposium, Pennsylvania, United States, 2018 </br></br></br></br>== General information ==</br>:::: TRiMAD is a collaborative venture between The Pennsylvania State University, University of Pittsburgh Medical Center, The Children’s Hospital of Philadelphia (CHoP) Research Institute, and The University of Pennsylvania Perelman School of Medicine ([https://www.huck.psu.edu/node/15830 Website])</br></br>== Venue == </br>:::: The Pennsylvania State University</br>:::: 100 Huck Life Sciences Building</br>:::: University Park, Pennsylvania 16802</br>:::: [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/directions-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx directions]</br></br>== Organizers ==</br>:::: Kateryna Makova, PhD - Penn State, University Park</br>:::: Donna Korzick, PhD - Penn State, University Park</br></br>[[File:Image001.jpg|right|550px]]</br>== Programme ==</br>:::: Please find the programme [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/agenda-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx here]</br></br></br>== Registration ==</br>:::: [https://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/registration-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx?fqp=true Register here]</br> </br>== Lecturers and tutors ==</br></br>:::: The list of speakers can be found [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/custom-18-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx here]6730cf0fe2c47a1b79f1a3b9ab0b364.aspx here])
• SBC 2023 Goa IN  + (92^nd Annual Meet of The Society of Biological Chemists, Goa, India, 2023)
• Annual Meeting of the DPG 2016 Luebeck DE  + (95^th Annual Meeting of the DPG, [http://www.dpg2016.de/ DPG 2016], Luebeck, DE)
• ASMRM 2012 Bejing CN  + (9^th Conference of t … 9^th Conference of the Asian Society of Mitochondrial Research and Medicine and 5^th Conference of Chinese Society of Mitochondrial Research and Medicine (Chinese-Mit), [http://asmrm2012.csp.escience.cn/dct/page/65540 ASMRM 2012], Bejing CN://asmrm2012.csp.escience.cn/dct/page/65540 ASMRM 2012], Bejing CN)
• DNA Forensics 2014  + (9^th International Y-chromosome workshop & 6^th International EMPOP meeting, Brussels, Belgium; DNA Forensics 2014)
• MiPschool Greenville 2015  + (9^th MiP''school'' f … 9^th MiP''school'' for cellular bioenergetics and mitochondrial physiology students, 2015 Aug 10-14, Greenville, US.</br></br>» [http://www.ecu.edu/cs-admin/news/mip.cfm '''Global conference highlights mitochondria expertise at ECU'''], by Kathryn Kennedy ECU News Services.tise at ECU'''], by Kathryn Kennedy ECU News Services.)
• SMRM2023 Hyderabad IN  + (9th Annual Conference of the SMRM, Hyderabad, India.)
• 9th ÖGMBT Annual Meeting & 8th Life Science Meeting 2017 Innsbruck AT  + (9th ÖGMBT Annual Meeting & 8th Life Science Meeting, Innsbruck, Austria)
• Crispim 2019 MitoFit Preprint Arch EA  + ( ::: <small> Version 2 ('''v2''') '' … </br>::: <small> Version 2 ('''v2''') '''2019-06-27''' [https://www.mitofit.org/images/6/68/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.v2.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007.v2]; v1 2019-06-17 [https://wiki.oroboros.at/images/8/81/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007]</br>::: <small>Version 1 (v1) [https://wiki.oroboros.at/images/8/81/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007]</br></br></br>== Although atovaquone is one of the newest antimalarial compounds discovered, resistant parasites have already been reported1. Atovaquone mechanism of action is established to be the competition with ubiquinol (UQH2) for the bc1 union at mitochondrial cytochrome bc1 complex and preventing the parasite from maintaining an oxidized ubiquinone (UQ) pool, essential for the DHODH activity and consequently for the pyrimidine's biosynthesis. In this sense, possible inhibitors of the ubiquinone biosynthesis pathway would be candidates by stimulating the effects of atovaquone. 4-nitrobenzoate (4-NB) is a well-known inhibitor of 4HPT (4-hydroxybenzoate polyprenyltransferase), the first enzyme of UQ biosynthesis. 4-NB also showed an important effect on reducing the UQs pool in P. falciparum. Herein is presenting the effect of atovaquone and 4-NB on parasitic respiration UQ biosynthesis. The purpose of this study was to better understand the atovaquone mechanism of action in a molecular scale, drug target potential of UQ biosynthesis. Oxygen consumption assays revealed 4-NB potentiates atovaquone mitochondrial effects and showed itself the ability to decrease the respiration rate. ==</br>- ''Extended abstract''</br>crease the respiration rate. == - ''Extended abstract'' )
• Gnaiger 2019 MitoFit Preprints Editorial  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2019-04-24''' [http://www.mitofit.org/images/d/d3/Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf doi:10.26124/mitofit:190002.v2]</small></br>::: <small>Version 1 (v1) 2019-04-01 [http://www.mitofit.org/images/archive/d/d3/20190424180311%21Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf doi:10.26124/mitofit:190002] - [http://www.mitofit.org/index.php/File:Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf#Links_to_all_versions »Link to all versions«]</small></br></br>A manuscript in preparation for publication on ‘Mitochondrial states and rates’ is the first preprint posted on ''[[MitoFit Preprints]]'' (Gnaiger ''et al'' 2019). It actually triggered the initiation of a preprint server for mitochondrial physiology and bioenergetics. This editorial presents the story behind starting ''MitoFit Preprints'', to develop a vision of science communication beyond traditional journal and preprint publication. This is an open invitation to scientists of mitochondrial physiology and bioenergetics to join the preprint community by submitting manuscripts as preprints. We face the ''reproducibility crisis'' in the battle to separate doubtful data from relevant information. This is linked to the ''inflation crisis'' emanating from an exponential increase of scientific articles published per day. Unsustainable exponential growth leads to the ''value-impact crisis'' in the struggle to forge scientific innovation into knowledge and community benefits.</br> forge scientific innovation into knowledge and community benefits. )
• Gnaiger 2020 MitoFit x  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2021-09-06''' [https://www.mitofit.org/images/4/4a/Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf doi:10.26124/mitofit:200004.v2]</small></br>::: <small>Version 1 ('''v1''') 2020-08-11 [https://wiki.oroboros.at/images/archive/4/4a/20210906072525%21Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf doi:10.26124/mitofit:200004] — [https://www.mitofit.org/index.php/File:Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf »Link to all versions«]</small></br></br>“The International System of Units, the SI, has been used around the world as the preferred system of units, the basic language for science, technology, industry and trade since it was established in 1960.” This statement heralds the 9th edition of the SI released on 2019-May-20. An new approach was introduced by defining the SI base units ― and thus the abstract SI units in general ― by their relation to fixed numerical values of fundamental constants of nature. Previous definitions of abstract units relied on a reference to concrete individual things realized as material artefacts, such as the International Prototype of the Kilogram (IPK). The (general) abstract unit ‘kilogram’ had to be calibrated in balance against an (individual) ‘entetic’ unit defining “1 kg” as a reference for the unit of mass and the mole [mol] as the unit of amount. Now the SI defines the mole as the fixed number of entities given by the Avogadro constant ''N''_A. The elementary charge ''e'' is a fixed number of charges per proton. Amount and charge are thus in a fixed relation to the count of elementary entities ''U''_''X'' [x]. Count, amount, and charge are isomorphic elementary quantities. Amount and charge are linked to the count ''N''_''X'' = ''N''∙''U''_''X'' with elementary unit x by fixed conversion constants ''N''_A^-1 [mol∙x⁻¹] and ''e'' [C∙x⁻¹], respectively. The SI does not use the elementary unit x. This causes a number of formal inconsistencies as discussed in the present communication on Euclid’s unit, which is ''U''_''X'', and Euclid’s number, which is a count ''N''_''X''.</br>sistencies as discussed in the present communication on Euclid’s unit, which is ''U''_''X'', and Euclid’s number, which is a count ''N''_''X''. )
• Baglivo 2022 MitoFit-QC  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2022-05-09''' [https://wiki.oroboros.at/images/c/c8/Baglivo_2022_MitoFit-QC.pdf doi:10.26124/mitofit:2022-0018.v2]</small></br>::: <small>Version 1 (v1) 2022-05-05 [https://wiki.oroboros.at/images/archive/c/c8/20220506062726%21Baglivo_2022_MitoFit-QC.pdf doi:10.26124/mitofit:2022-0018.v1] - [https://wiki.oroboros.at/index.php/File:Baglivo_2022_MitoFit-QC.pdf »Link to all versions«]</small></br></br>[[File:Baglivo 2022 MitoFit QC graphical-abstract.png|right|300px|Graphical abstract]]</br></br>[[Baglivo 2022 Abstract Bioblast]]: Evaluation of instrumental reproducibility is a primary component of quality control to quantify the precision and limit of detection of analytical procedures. A pre-analytical instrumental standard operating procedure (SOP) is implemented in high-resolution respirometry consisting of: (''1'') a daily SOP-POS for air calibration of the polarographic oxygen sensor (POS) in terms of oxygen concentration ''c''_O₂ [µM]. This is part of the ''sensor test'' to evaluate POS performance; (''2'') a monthly SOP-BG starting with the SOP-POS followed by the ''chamber test'' quantifying the instrumental O₂ background. The chamber test focuses on the slope d''c''_O₂/d''t'' [pmol∙s⁻¹∙mL⁻¹] to determine O₂ consumption by the POS and O₂ backdiffusion into the chamber as a function of ''c''_O₂ in the absence of sample. Finally, zero O₂ calibration completes the sensor test. </br></br>We applied this SOP in a 3-year study using 48 Oroboros O2k chambers. Stability of air and zero O₂ calibration signals was monitored throughout intervals of up to 8 months without sensor service. Maximum drift over 1 to 3 days was 0.06 pmol∙s⁻¹∙mL⁻¹, without persistence over time since drift was <0.004 pmol∙s⁻¹∙mL⁻¹ for time intervals of one month, corresponding to a drift per day of 0.2 % of the signal at air saturation. Instrumental O₂ background -d''c''_O₂/d''t'' was stable within ±1 pmol∙s⁻¹∙mL⁻¹ when measured at monthly intervals. These results confirm the instrumental limit of detection of volume-specific O₂ flux at ±1 pmol∙s⁻¹∙mL⁻¹. The instrumental SOP applied in the present study contributes to the generally applicable internal quality control management ensuring the unique reproducibility in high-resolution respirometry.</br> These results confirm the instrumental limit of detection of volume-specific O₂ flux at ±1 pmol∙s⁻¹∙mL⁻¹. The instrumental SOP applied in the present study contributes to the generally applicable internal quality control management ensuring the unique reproducibility in high-resolution respirometry. )
• Gainutdinov 2022 MitoFit  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2022-08-16''' [https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0015.v2]</small></br>::: <small>Version 1 (v1) 2022-04-21 [https://wiki.oroboros.at/images/archive/5/5a/20220816100352%21Gainutdinov_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0015]- [https://wiki.oroboros.at/index.php/File:Gainutdinov_2022_MitoFit.pdf »Link to all versions«]</small></br></br>Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis are believed to be the disturbance of calcium homeostasis in the cell and dysfunction of mitochondria. Both factors mutually influence each other. As a result, chronic mitochondrial energy stress impairs fine cellular signaling and transport processes, leading to degeneration of motor neurons. In the current study we comparatively evaluated the cytosolic Ca²⁺ in healthy and ALS fibroblasts. We found that the mitochondrial calcium capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differs between two subtypes and from that in healthy individuals. The changes of [Ca²⁺]cyt dynamics in ALS fibroblasts could be almost completely rescued by treatment with antioxidants (Trolox and CoQ10). These data confirm an important role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS.</br>portant role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS. )
• Alencar 2022 MitoFit  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2022-07-07''' [https://wiki.oroboros.at/images/5/54/Alencar_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0009.v2]</small></br>::: <small>Version 1 (v1) 2022-04-07 [https://wiki.oroboros.at/images/archive/5/54/20220707123437%21Alencar_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0009.v1] - [https://wiki.oroboros.at/index.php/File:Alencar_2022_MitoFit.pdf »Link to all versions«]</small></br></br>[[Oliveira 2022 Abstract Bioblast]]: The parasite ''Trypanosoma brucei'' is the causative agent of sleeping sickness and involves an insect vector and a mammalian host through its complex life-cycle. ''T. brucei'' mammalian bloodstream forms (BSF) exhibit unique metabolic features including: ''i)'' reduced expression and activity of mitochondrial enzymes; ''ii)'' respiration mediated by the glycerol phosphate shuttle (GPSh) and the ''Trypanosome'' alternative oxidase (TAO) that is intrinsically uncoupled from generation of mitochondrial membrane potential; ''iii)'' maintenance of mitochondrial membrane potential by ATP hydrolysis through the reversal of F1Fo ATP synthase activity; ''iv)'' strong reliance on glycolysis to meet their energy demands; ''v)'' high susceptibility to oxidants. Here, we critically review the main metabolic features of BSF and provide a hypothesis to explain the unusual metabolic network and its biological significance for this parasite form. We postulate that intrinsically uncoupled respiration provided by GPSh-TAO system would act as a preventive antioxidant defense by limiting mitochondrial superoxide production and complementing the NADPH-dependent scavenging antioxidant defenses to maintain parasite redox balance. Given the uncoupled nature of the GPSh-TAO system, BSF would avoid programmed cell death processes by maintaining mitochondrial membrane potential through the reversal of ATP synthase activity using the ATP generated by glycolysis. This unique “metabolic design” in BSF has no biological parallel outside of Trypanosomatids and highlights the enormous diversity of the parasite mitochondrial processes to adapt to distinct environments.</br>parasite mitochondrial processes to adapt to distinct environments. )
• Ganguly 2022 MitoFit  + ( ::: <small>Version 2 ('''v2''') ''' … </br>::: <small>Version 2 ('''v2''') '''2022-11-10''' [https://wiki.oroboros.at/images/6/64/Ganguly_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0013.v2]</small></br>::: <small>Version 1 (v1) 2022-04-19 [https://wiki.oroboros.at/images/archive/6/64/20221110103433%21Ganguly_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0013]- [https://wiki.oroboros.at/index.php/File:Ganguly_2022_MitoFit.pdf »Link to all versions«]</small></br>Ferroptosis has been identified as a type of regulated cell death triggered by a diverse set of agents with implications in various diseases like cancer and neurodegenerative diseases. Ferroptosis is iron-dependent and accompanied by an accumulation of reactive oxygen species (ROS) and lipid oxidation products, a depletion of reduced glutathione, mitochondrial morphological alterations and the rupture of cell membrane; the process is inhibited by specific antioxidants like ferrostatin-1 and liproxstatin-1 and by other general antioxidants like the iron-chelator deferoxamine, vitamin E and N-acetylcysteine. However, the mechanism of cell death in ferroptosis subsequent to the accumulation of ROS and lipid oxidation products is not clearly established. We show here that the classical mitochondrial Complex I inhibitor rotenone (0.5 µM) causes death of SH-SY5Y cells (a human neuroblastoma cell line) over a period of 48 h accompanied by mitochondrial membrane depolarization and intracellular ATP depletion. This is associated with an intracellular accumulation of ROS and the lipid oxidation product malondialdehyde or MDA and a decrease in reduced glutathione content. All these processes are inhibited very conspicuously by specific inhibitors of ferroptosis such as ferrostatin-1 and liproxstatin-1. However, the decrease in Complex I activity upon rotenone-treatment of SH-SY5Y cells is not significantly recovered by ferrostatin-1 and liproxstatin-1. When the rotenone-treated cells are analyzed morphologically by Hoechst 33258 and propidium iodide (PI) staining, a mixed picture is noticed with densely fluorescent and condensed nuclei indicating apoptotic death of cells (Hoechst 33258) and also significant numbers of necrotic cells with bright red nuclei (PI staining).</br>ant numbers of necrotic cells with bright red nuclei (PI staining). )