Search by property

This page provides a simple browsing interface for finding entities described by a property and a named value. Other available search interfaces include the page property search, and the ask query builder.

List of results

• Jezek 2011 AbstractMitoComLectures  + ('''MitoCom Lecture''' '''2011-Nov-10, 8:1 … '''MitoCom Lecture'''</br></br>'''2011-Nov-10, 8:15 - 09:45'''. Medical University Innsbruck, Anichstr. 25, Chirurgie (8-U1-517) Seminarraum 2</br></br>Speaker: '''[[Jezek P|Prof. Dr. Petr Jezek, Prague]]'''</br></br>Host: [[Gnaiger E|Erich Gnaiger, DSL, MitoCom Tyrol]]</br></br></br>'''Abstract''': Three-dimensional (3D) super-resolution microscopy, using a biplane detection scheme, termed biplane photo-activated localization microscopy (Biplane FPALM), enables imaging of volumes as thick as whole cells and reveals otherwise unaccessible details of cellular organization [1]. Hence, we attempted to visualize mitochondrial reticulum via the matrix space loaded with mitochondria-addressed Eos, while transfecting cells by lentiviral expression. Our 3D images of single Eos molecules in the matrix space have proven the continuous character of mitochondrial reticulum tubules, i.e., an existence of a highly interconnected major mitochondrial reticulum in insulinoma Ins1E and oxidative-phosphorylation-dependent glutaminolytic hepatoma HepG2 cells [2] (Figure).</br></br>Also, using Eos-conjugate of mitochondrial transcription factor-A (TFAM), we have imaged nucleoids of mitochondrial DNA (mtDNA) in which TFAM represents a major assessor protein. Using PA-CFP2-TFAM and mitochondria-addressed Eos, the first 3D two color super-resolution images were obtained for mitochondrial reticulum together with the distribution of mt nucleoids in it. In intact cells we have found mt nucleoids of a narrow size distribution. The Biplane FPALM technique has proven to be robust and reliable for imaging of mitochondrion and related substructures.</br></br>Supported by grants P302/10/0346 (GACR); ME09029 (Czech Ministry of Education); IAA500110701, and M200110902 (Academy of Sciences).) and 1R01GM091791-02 (NIH). Disclosure statement: J.B. declares significant financial interest in Vutara, Inc.</br></br>[1] Juette MF, Gould TJ, Lessard MD, Mlodzianoski MJ, Nagpure BS, Bennett BT, Hess ST, Bewersdorf J (2008) 3D sub-100 nm resolution by biplane fluorescence photoactivation localization microscopy. Nat. Methods 5: 527-529.</br></br>[2] Mlodzianoski MJ, Schreiner JM, Callahan SP, Smolková K, Dlasková A, Šantorová J, Ježek P, Bewersdorf J (2011) Sample drift correction in 3D fluorescence photoactivation localization microscopy. Opt. Express. 19: 15009-15019.microscopy. Opt. Express. 19: 15009-15019.)
• MitoFit Open Seminar 2017-10-23  + ('''MitoFit Open Seminar on respiration, cryopreservation and viability test in human blood cells'''. Innsbruck, AT)
• UMDF2016 Seattle WA US  + ('''Mitochondrial Medicine 2016, Seattle, W … '''Mitochondrial Medicine 2016, Seattle, WA, USA.''' </br></br>The [[United Mitochondrial Disease Foundation]] Symposium has been recognized by many researchers, scientists, and families as THE symposium for mitochondrial disease in the world. 10 years ago, the UMDF had only a handful of exhibitors and less than 200 scientific attendees. We now have more exhibitors than space at times and close to 600 attendees … representing almost every state in the United States and more than 15 different countries from around the world.different countries from around the world.)
• UMDF2017 Washington DC US  + ('''Mitochondrial Medicine 2017, Washington DC, USA.''')
• MiPNet14.09 MiP-Collection  + ('''Mitochondrial Physiology (MiP) ''contin … '''Mitochondrial Physiology (MiP) ''continues a tradition of rigorous mitochondrial bioenergetics'' '''([http://www.mitophysiology.org quoting the International MiPsociety]). The company [[Oroboros Instruments]] Corp. values this tradition as a basis of our continuous instrumental development, which is part of our concept of Corporate Social Responsibility. In this spirit and with emphasis on our Educational Responsibility, we initiated and support the ''[[MiP-Collection]]''.[[MiP-Collection]]''.)
• Gnaiger 2011 Abstract-MonteVerita  + ('''Mitochondrial capacity''': [[OXPHOS]] … '''Mitochondrial capacity''': [[OXPHOS]] capacity is evaluated in isolated mitochondria (mt) and permeabilized cells with physiological substrate cocktails to reconstitute tricarboxylic acid cycle function. As a consequence, convergent electron flow from Complexes CI+II of the electron transfer-pathway ([[ET-pathway]]) to the [[Q-junction]] exerts an additive effect on flux [1].</br></br>'''Oxygen kinetics of mt-respiration''': The apparent ''K''_m,O2 or ''c''₅₀ [µM] (''p''₅₀ [kPa]) of mt-respiration increases linearly with respiratory capacity controlled by metabolic state, from 0.2 to 1.6 µM determined by [[high-resolution respirometry]]. O₂ gradients are significant only in large cells including cardiomyocytes. The apparent ''p''₅₀ increases 100-fold in permeabilized muscle fibers due to diffusion gradients [2].</br></br>'''mt-function at ''V''_O2max''': Aerobic capacity of the human leg muscle exceeds maximum O₂ uptake of isolated mitochondria [3] and v. lateralis during ''V''_O2max [4]. Therefore, oxygen supply limits aerobic performance, proportional to the apparent mt-excess capacity [5]. mt-respiration is more sensitive to average ''p''_O2 in heterogenous tissues than under homogenous conditions in vitro. Tissue heterogeneity increases the kinetic dependence of flux on average intracellular ''p''_O2. High mt-density reinforces the steepness of oxygen gradients and oxygen heterogeneity in the tissue, contributing to the O₂ limitation in athletic vs sedentary individuals at ''V''_O2max [6]. This provides a functional rationale for the observation that hypoxia does not specifically trigger mt-biogenesis [7].</br></br>Contribution to K-Regio ''[[MitoCom_O2k-Fluorometer|MitoCom Tyrol]]''.</br></br>[1] [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger 2009]]; [[Lemieux_2011_Int J Biochem Cell Biol|Lemieux et al 2011 Int J Biochem Cell Biol]] </br></br>[2] [[Gnaiger_2003_Adv Exp Med Biol|Gnaiger 2003]]; [[Scandurra_2010_Adv Exp Med Biol|Scandurra, Gnaiger 2010 Adv Exp Med Biol]]. </br></br>[3] Rasmussen et al 2001 AJP.</br></br>[4] [[Boushel_2011_Mitochondrion|Boushel et al 2011 Mitochondrion]].</br></br>[5] [[Gnaiger_1998_J_Exp_Biol|Gnaiger et al 1998 JEB]].</br></br>[6] Richardson et al; Haseler et al JAP.</br></br>[7] [[Pesta_2011_AJP|Pesta et al 2011 AJP]]; [[Jacobs_2011_J_Appl_Physiol|Jacobs et al 2011 JAP]].Jacobs_2011_J_Appl_Physiol|Jacobs et al 2011 JAP]].)
• MitoEAGLE preprint 2017-09-21  + ('''Note''': Subscript ‘§’ indicates throug … '''Note''': Subscript ‘§’ indicates throughout the text those parts, where ''potential differences'' provide a mathematically correct but physicochemically incomplete description and should be replaced by ''stoichiometric potential differences'' ([[Gnaiger 1993 Pure Appl Chem |Gnaiger 1993b]]). A unified concept on vectorial motive transformations and scalar chemical reactions will be derived elsewhere (Gnaiger, in prep.). Appreciation of the fundamental distinction between ''differences of potential'' versus ''differences of stoichiometric potential'' may be considered a key to critically evaluate the arguments presented in Section 3 on the protonmotive force. Since this discussion appears to be presently beyond the scope of a MitoEAGLE position statement, Section 3 is removed from the next version and [[Gnaiger 2019 MitoFit Preprint Arch |'''final manuscript''']]. This section should become a topic of discussion within [[WG1 MitoEAGLE protocols, terminology, documentation |Working Group 1]] of the MitoEAGLE consortium, following a primary peer-reviewed publication of the concept of stoichiometric potential differences.t of stoichiometric potential differences.)
• IOC42  + ('''O2k-International course on high-resolution respirometry.''' 2007 August 24, 9:00 a.m. to 3:00 p.m. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet14.03 IOC50  + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria;2009 April 18 to 22. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet12.24 IOC44  + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2007 December 12-16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet11.06 IOC36  + ('''O2k-International course on high-resolution respirometry and MiPNet workshop.''' Schroecken, Voralberg, Austria; 2006 December 13 to 17. :>> O2k-Workshop: [[Oroboros Events]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet09.11 IOC29  + ('''O2k-International course on high-resolution respirometry.''' Schroecken, Voralberg, Austria; 2004 December 9-13. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet11.03 IOC35 Schroecken  + ('''O2k-International course on high-resolution respirometry: O2k, TIP-2k and DatLab 4.''' Schroecken, Voralberg, Austria; 2006 August 18-22.)
• MiPNet09.05 IOC28  + ('''O2k-International course on high-resolu … '''O2k-International course on high-resolution respirometry and MiPNet meeting.''' Schroecken, Voralberg, Austria; 2004 September 15-21.</br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet13.04 IOC47  + ('''O2k-International course on high-resolution respirometry.''' Schroecken,Voralberg, Austria; 2008 July 12-16. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• IOC43 Montevideo UY 2007  + ('''O2k-International course on high-resolution respirometry.''' 2007 September 1 and 6. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet11.02 IOC32  + ('''O2k-International course on high-resolu … '''O2k-International course on high-resolution respirometry: Oroboros O2k, TIP-2k and DatLab 4.''' Schroecken, Voralberg, Austria; 2006 April 21-25.</br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> 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''' </br></br>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.</br>[[Image:O2k-Protocols.jpg|right|150px|link=http://www.oroboros.at/?o2k-protocols|O2k-Protocols contents]]</br>[[Image:MiPNet10.05.jpg|centre|500px|thumb]]</br></br>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.</br></br>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.</br></br></br>'''Reference'''</br></br>[[Gnaiger_1993_Pure_Appl_Chem| Gnaiger E (1993) Nonequilibrium thermodynamics of energy transformations. Pure Appl Chem 65: 1983-2002.]]</br></br></br></br>:>> O2k-Protocols:[[O2k-Protocols| Overall contents]]</br>:>> 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]]</br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> 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 </br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> 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.</br></br>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.</br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> 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.</br>:>> O2k-Workshop: [[Oroboros Events| Current dates]]</br>:>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]][[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet06.09 IOC19  + ('''O2k-Workshop on high-resolution respirometry.''' Innsbruck, Tyrol, Austria; 2001 October 04-05. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet17.07 IOC67  + ('''O2k-Workshop on high-resolution respirometry.''' Sidney, Australia; 2012 April 02 to 04. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet17.08 IOC68 Schroecken AT  + ('''O2k-Workshop on high-resolution respirometry: O2k-Basic and TPP-Basic.''' Schroecken, Voralberg,Austria; 2012 April 11 to 16. :» O2k-Workshop: [[OROBOROS_Events|Current dates]] :» Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• MiPNet08.02 IOC23  + ('''O2k: Mitochondrial physiology (MiP) workshop on high-resolution respirometry.''' Schroecken AT, 27-31 March 2003. :>> O2k-Workshop: [[Oroboros Events| Current dates]] :>> Product: [[Oroboros O2k]], [[Oroboros O2k-Catalogue | O2k-Catalogue]])
• Hassoun 2008 Crit Care Med  + ('''OBJECTIVE''': Growing evidence suggests … '''OBJECTIVE''': Growing evidence suggests that mitochondria function is impaired in sepsis. Here, we tested the hypothesis that lipopolysaccharide would induce mitochondrial Ca²⁺ overload and oxygen utilization abnormalities as consequences of sarcoplasmic reticulum Ca²⁺ handling derangements that are typically observed in sepsis. As lipopolysaccharide-induced sarcoplasmic reticulum dysfunction was mainly characterized by reduced sarcoplasmic reticulum Ca²⁺ uptake and Ca²⁺ leak, we tested whether dantrolene, a sarco(endo)plasmic reticulum calcium ATPase leak inhibitor, would prevent mitochondrial and cardiac contractile dysfunction.</br></br>'''DESIGN''': Randomized controlled trial.</br></br>'''SETTING''': Experimental laboratory.</br></br>'''SUBJECTS''': Male Sprague Dawley rats.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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).</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''SETTING:''' Three intensive care units and an academic research laboratory.</br></br>'''SUBJECTS:''' Twenty patients with septic shock and a control group composed of 18 postoperative patients without sepsis or shock.</br></br>'''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.</br></br>'''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.</br></br>'''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).</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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.</br></br>'''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''.</br></br>'''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]])