https://wiki.oroboros.at/index.php?title=Special:NewPages&feed=atom&hideredirs=1&limit=50&offset=&namespace=0&username=&tagfilter=&size-mode=max&size=0Bioblast - New pages [en]2024-03-28T12:10:28ZFrom BioblastMediaWiki 1.36.1https://wiki.oroboros.at/index.php/Insect_SciInsect Sci2024-03-27T14:18:19Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://onlinelibrary.wiley.com/journal/17447917 Insect Science] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://onlinelibrary.wiley.com/journal/17447917 Insect Science]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Hunter-Manseau_2024_Insect_SciHunter-Manseau 2024 Insect Sci2024-03-27T13:37:07Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Hunter-Manseau F, Cormier SB, Strang R, Pichaud N (2024) Fasting as a precursor to high-fat diet enhances mitochondrial resilience in ''Drosophila melanogaster''. Insect Sci [Epub ahead of print]. https://doi.org/10.1111/1744-7917.13355<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38514255 PMID: 38514255 Open Access]<br />
|authors=Hunter-Manseau Florence, Cormier Simon B, Strang Rebekah, Pichaud Nicolas<br />
|year=2024<br />
|journal=Insect Sci<br />
|abstract=Changes in diet type and nutrient availability can impose significant environmental stress on organisms, potentially compromising physiological functions and reproductive success. In nature, dramatic fluctuations in dietary resources are often observed and adjustments to restore cellular homeostasis are crucial to survive this type of stress. In this study, we exposed male ''Drosophila melanogaster'' to two modulated dietary treatments: one without a fasting period before exposure to a high-fat diet and the other with a 24-h fasting period. We then investigated mitochondrial metabolism and molecular responses to these treatments. Exposure to a high-fat diet without a preceding fasting period resulted in disrupted mitochondrial respiration, notably at the level of complex I. On the other hand, a short fasting period before the high-fat diet maintained mitochondrial respiration. Generally, transcript abundance of genes associated with mitophagy, heat-shock proteins, mitochondrial biogenesis, and nutrient sensing pathways increased either slightly or significantly following a fasting period and remained stable when flies were subsequently put on a high-fat diet, whereas a drastic decrease of almost all transcript abundances was observed for all these pathways when flies were exposed directly to a high-fat diet. Moreover, mitochondrial enzymatic activities showed less variation after the fasting period than the treatment without a fasting period. Overall, our study sheds light on the mechanistic protective effects of fasting prior to a high-fat diet and highlights the metabolic flexibility of ''Drosophila'' mitochondria in response to abrupt dietary changes and have implication for adaptation of species to their changing environment.<br />
|keywords=Dietary modulation, Fasting, High‐fat diet, Metabolic flexibility, Mitochondrial metabolism, Stress response<br />
|editor=[[Plangger M]]<br />
|mipnetlab=CA Moncton Hebert-Chatelain E, CA Moncton Pichaud N<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|organism=Drosophila<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Koumanov_FrancoiseKoumanov Francoise2024-03-25T11:39:06Z<p>Plangger Mario: </p>
<hr />
<div>{{Person<br />
|lastname=Koumanov<br />
|firstname=Francoise<br />
|title=PhD<br />
|institution=Department for Health, University of Bath<br />
|address=1 West, University of Bath, Claverton Down<br />
|area code=BA2 7AY<br />
|city=Bath<br />
|country=United Kingdom<br />
|mailaddress=F.Koumanov@bath.ac.uk<br />
}}<br />
{{Labelingperson}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Feero_2024_JAMAFeero 2024 JAMA2024-03-25T09:04:38Z<p>Gnaiger Erich: Created page with "{{Publication |title=Feero WG, Steiner RD, Slavotinek A, Faial T, Bamshad MJ, Austin J, Korf BR, Flanagin A, Bibbins-Domingo K (2024) Guidance on use of race, ethnicity, and g..."</p>
<hr />
<div>{{Publication<br />
|title=Feero WG, Steiner RD, Slavotinek A, Faial T, Bamshad MJ, Austin J, Korf BR, Flanagin A, Bibbins-Domingo K (2024) Guidance on use of race, ethnicity, and geographic origin as proxies for genetic ancestry groups in biomedical publications. JAMA https://doi.org/10.1001/jama.2024.3737.<br />
|info=[https://jamanetwork.com/journals/jama/fullarticle/2816403 Open Access]<br />
|authors=Feero WG, Steiner RD, Slavotinek A, Faial T, Bamshad MJ, Austin J, Korf BR, Flanagin A, Bibbins-Domingo K<br />
|year=2024<br />
|journal=JAMA<br />
|abstract=In March 2023, the National Academies of Sciences, Engineering, and Medicine (NASEM) released a consensus study report titled Using Population Descriptors in Genetics and Genomics Research.1 Sponsored by the US National Institutes of Health, the report is more than a discussion of the use of terminology; the authors of the NASEM report suggest a tectonic shift away from current models that use race, ethnicity, and geographic origin as proxies for genetic ancestry groups (ie, a set of individuals who share more similar genetic ancestries) in genetic and genomic science. The recommendations are rooted in evidence that genetic variation in individuals falls, in general, on a continuum of variation not captured well by existing population descriptors and that the ongoing use of such descriptors as analytical variables jeopardizes the scientific validity of research.2 Furthermore, the authors of the NASEM report point out that current scientific practices can sometimes perpetuate harmful typological thinking about individuals, including racism.<br />
|editor=Gnaiger E<br />
}}<br />
{{Labeling<br />
|additional=BEC<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Communication_-_mitochondria_and_the_patientCommunication - mitochondria and the patient2024-03-24T19:08:33Z<p>Gnaiger Erich: </p>
<hr />
<div>{{MitoPedia<br />
|description=Mitochondria and the patient: communication between patients, medical professionals, scientists, and the public<br />
}}<br />
<br />
{{MitoPedia topics<br />
|mitopedia topic=MitoGlobal Organizations<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/World_Health_Organization_2010_IPECPWorld Health Organization 2010 IPECP2024-03-24T18:57:47Z<p>Gnaiger Erich: Created page with "{{Publication |title=World Health Organization (2010) Framework for Action on Interprofessional Education & Collaborative Practice (IPECP). World Health Organization, Geneva...."</p>
<hr />
<div>{{Publication<br />
|title=World Health Organization (2010) Framework for Action on Interprofessional Education & Collaborative Practice (IPECP). World Health Organization, Geneva. http://www.who.int/hrh/nursing_midwifery/en/<br />
|info=[https://interprofessional.global/wp-content/uploads/2018/11/WHO-2010-WHO-framework-for-action-on-interprofessional-education-collaborative-practice.pdf Open Access]<br />
|authors=World Health Organization<br />
|year=2010<br />
|journal=World Health Organization Geneva<br />
|abstract=At a time when the world is facing a shortage of health workers, policy-makers are looking for innovative strategies that can help them develop policy and programmes to bolster the global health workforce. The ''Framework for Action on Interprofessional Education and Collaborative Practice'' highlights the current status of interprofessional collaboration around the world, identifies the mechanisms that shape successful collaborative teamwork and outlines a series of action items that policy-makers can apply within their local health system (Figure 1). The goal of the Framework is to provide strategies and ideas that will help health policy-makers implement the elements of interprofessional education and collaborative practice that will be most beneficial in their own jurisdiction.<br />
<br />
* The World Health Organization (WHO) and its partners recognize interprofessional collaboration in education and practice as an innovative strategy that will play an important role in mitigating the global health workforce crisis.<br />
<br />
* Interprofessional education occurs when students from two or more professions learn about, from and with each other to enable effective collaboration and improve health outcomes.<br />
<br />
* Interprofessional education is a necessary step in preparing a “collaborative practice-ready” health workforce that is better prepared to respond to local health needs.<br />
<br />
* A collaborative practice-ready health worker is someone who has learned how to work in an interprofessional team and is competent to do so.<br />
<br />
* Collaborative practice happens when multiple health workers from different professional backgrounds work together with patients, families, carers and communities to deliver the highest quality of care. It allows health workers to engage any individual whose skills can help achieve local health goals.<br />
<br />
* After almost 50 years of enquiry, the World Health Organization and its partners acknowledge that there is sufficient evidence to indicate that effective interprofessional education enables effective collaborative practice.<br />
<br />
* Collaborative practice strengthens health systems and improves health outcomes.<br />
<br />
* Integrated health and education policies can promote effective interprofessional education and collaborative practice.<br />
<br />
* A range of mechanisms shape effective interprofessional education and collaborative practice. These include: <br />
:- supportive management practices <br />
:- identifying and supporting champions <br />
:- the resolve to change the culture and attitudes of health workers<br />
:- a willingness to update, renew and revise existing curricula <br />
:- appropriate legislation that eliminates barriers to collaborative practice.<br />
<br />
* Mechanisms that shape interprofessional education and collaborative practice are not the same in all health systems. Health policy-makers should utilize the mechanisms that are most applicable and appropriate to their own local or regional context.<br />
<br />
* Health leaders who choose to contextualize, commit and champion interprofessional education and collaborative practice position their health system to facilitate achievement of the health-related Millennium Development Goals (MDGs).<br />
<br />
* The ''Framework for Action on Interprofessional Education and Collaborative Practice'' provides policy-makers with ideas on how to implement interprofessional education and collaborative practice within their current context.<br />
<br><br />
<br />
|editor=Gnaiger E<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/World_Health_Organization_2001_ICFWorld Health Organization 2001 ICF2024-03-24T16:15:36Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=World Health Organization (2001) International classification of functioning, disability and health (ICF). World Health Organization, Geneva. https://iris.who.int/bitstream/handle/10665/42407/9241545429.pdf?sequence=1<br />
|info=[https://iris.who.int/bitstream/handle/10665/42407/9241545429.pdf?sequence=1 Open Access]<br />
|authors=World Health Organization<br />
|year=2001<br />
|journal=World Health Organization Geneva<br />
|abstract=This volume contains the ''International Classification of Functioning, Disability and Health'', known as ICF. The overall aim of the ICF classification is to provide a unified and standard language and framework for the description of health and health-related states. It defines components of health and some health-related components of well-being (such as education and labour). The domains contained in ICF can, therefore, be seen as ''health domains'' and ''health-related domains''. These domains are described from the perspective of the body, the individual and society in two basic lists: (1) Body Functions and Structures; and (2) Activities and Participation.<sup>2</sup> As a classification, ICF systematically groups different domains<sup>3</sup> for a person in a given health condition (e.g. what a person with a disease or disorder does do or can do). Functioning is an umbrella term encompassing all body functions, activities and participation; similarly, disability serves as an umbrella term for impairments, activity limitations or participation restrictions. ICF also lists environmental factors that interact with all these constructs. In this way, it enables the user to record useful profiles of individuals’ functioning, disability and health in various domains.<br />
<br />
<sup>2</sup> These terms, which replace the formerly used terms “impairment”, “disability” and “handicap”, extend the scope of the classification to allow positive experiences to be described. The new terms are further defined in this Introduction and are detailed within the classification. It should be noted that these terms are used with specific meanings that may differ from their everyday usage.<br />
<br />
<sup>3</sup> A domain is a practical and meaningful set of related physiological functions, anatomical structures, actions, tasks, or areas of life.<br />
|editor=Gnaiger E<br />
}}<br />
== ICF ==<br />
<br />
:::* Towards a common language for functioning, disability and health ICF (2002) WHO/EIP/GPE/CAS/01.3 - [https://cdn.who.int/media/docs/default-source/classification/icf/icfbeginnersguide.pdf Open Access]<br />
<br />
:::: ICF: "It is the conceptual basis for the definition, measurement and policy formulations for health and disability. It is a universal classification of disability and health for use in health and health-related sectors."<br />
<br />
:::: "ICF is named as it is because of its stress is on health and functioning, rather than on disability. Previously, disability began where health ended; once you were disabled, you where in a separate category. We want to get away from this kind of thinking. We want to make ICF a tool for measuring functioning in society, no matter what the reason for one's impairments. So it becomes a much more versatile tool with a much broader area of use than a traditional classification of health and disability. .. This is a radical shift. From emphasizing people's disabilities, we now focus on their level of health."</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/The_National_Academies_Press,_Washington,_DCThe National Academies Press, Washington, DC2024-03-24T08:37:14Z<p>Gnaiger Erich: Gnaiger Erich moved page The National Academies Press, Washington, DC to National Academies Press</p>
<hr />
<div>{{Journal<br />
|Title=[https://nap.nationalacademies.org/ National Academies Press]<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/National_Academies_of_Sciences,_Engineering,_and_Medicine_2024_Body_composition_and_obesityNational Academies of Sciences, Engineering, and Medicine 2024 Body composition and obesity2024-03-24T08:32:37Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=National Academies of Sciences, Engineering, and Medicine (2024) Exploring the science on measures of body composition, body fat distribution, and obesity. National Academies Press, Washington, DC https://doi.org/10.17226/27461.<br />
|info=[https://nap.nationalacademies.org/catalog/27461/exploring-the-science-on-measures-of-body-composition-body-fat-distribution-and-obesity?utm_source=NASEM+News+and+Publications&utm_campaign=ef8dee7bac-Final_Book_2024_03_22_27461&utm_medium=email&utm_term=0_-ef8dee7bac-%5BLIST_EMAIL_ID%5D&goal=0_96101de015-ef8dee7bac-104786469&mc_cid=ef8dee7bac&mc_eid=50f76db947 National Academies Press, Open Access]<br />
|authors=National Academies of Sciences, Engineering, and Medicine<br />
|year=2024<br />
|journal=National Academies Press<br />
|abstract=The National Academies Roundtable on Obesity Solutions hosted a public workshop series in April and June 2023 that explored the current science on measures of body composition and body fat distribution. Discussions focused on the strengths and limitations, and clinical and anthropological perspectives of body mass index (BMI) as a measure of adiposity and health. Presentations also shed light on the connection between misinformation and bias and stigma, as well as challenged current communication strategies to improve messaging about obesity.<br />
|editor=Gnaiger E<br />
}}<br />
----<br />
{{BME_navigation_line}}<br />
__TOC__<br />
<br />
== From BMI to BME ==<br />
''Work in progress'' by [[Gnaiger E]] 2020-02-10 linked to a preprint in preparation on [[body mass excess |'''BME''']] and [[:Category:BME and mitObesity |'''mitObesity''']].<br />
<br />
{{Template:Publications: BME and body fat}}<br />
{{Template:Publications: BME and height}}<br />
<br />
{{MitoPedia: BME and mitObesity}}<br />
<br />
{{Labeling<br />
|area=Exercise physiology;nutrition;life style<br />
|diseases=Obesity<br />
|organism=Human<br />
|tissues=Fat<br />
|additional=BMI, BME, Fat<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Club17_Innsbruck_ATClub17 Innsbruck AT2024-03-21T11:07:01Z<p>Tindle Lisa: </p>
<hr />
<div>{{MitoGlobal header page name}}<br />
<br />
{{Publication<br />
|title=[[File:Tirol sat lining RGB.png|right|200px|link=https://www.standort-tirol.at/|Standortagentur Tirol]]'''Innsbruck AT''', 2024 Mar 21. Club17 <br />
|info= [https://www.standort-tirol.at/26-club17--21maerz2024 Event website]<br />
|authors= Standortagentur Tirol<br />
|year=2024-03-21<br />
|journal=MitoGlobal<br />
|abstract= Club17, Innsbruck, Austria, 2024<br />
}}<br />
<br />
== Venue ==<br />
:::: Standortagentur Tirol<br />
:::: Ing.-Etzel-Straße 17/ 2.OG<br />
:::: 6020 Innsbruck <br />
:::: Austria <br />
<br />
== Organizers ==<br />
:::: Standortagentur Tirol<br />
:::: Vera Schrattmaier<br />
<br />
== Program ==<br />
:::: Please see the [https://www.standort-tirol.at/26-club17--21maerz2024 event website].<br />
<br />
<br />
== Oroboros at Club17 ==<br />
:::: [[Laner Verena| Verena Laner]]: Functional Mitochondrial Diagnostics, ''Mar 21, 17:00'', presentation held in German<br />
:::: The project [[Functional Mitochondrial Diagnostics]] is a collaboration between VASCage and Oroboros Instruments with the aim of establishing in-vitro mitochondrial diagnostic standards. You can learn more exciting information about this topic during the presentation.<br />
<br />
<br />
:::: German: Funktionale Mitochondriendiagnostik<br />
:::: Das Projekt [[Functional Mitochondrial Diagnostics| Funktionale Mitochondriendiagnostik]] ist eine Zusammenarbeit zwischen VASCage und Oroboros Instruments mit dem Ziel, in vitro mitochondriale diagnostische Standards zu etablieren. Weitere spannende Informationen zu diesem Thema erhalten Sie während dem Vortrag.<br />
<br />
<br />
{{Labeling<br />
|instruments=<br />
|additional=2024, MitoGlobal, ORO, Mitochondrial Diagnostics events<br />
}}<br />
<br />
<br />
[[Image:MitoGlobal.jpg|right|80px|link=http://www.bioblast.at/index.php/MitoGlobal|MitoGlobal]] <br />
Listed under [[MitoGlobal Events]].</div>Gnaiger Chttps://wiki.oroboros.at/index.php/Wefers_2019_J_Emergency_Critical_Care_MedWefers 2019 J Emergency Critical Care Med2024-03-16T09:30:17Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Wefers BM, Arbous M, Raat N, Mik E (2019) Mind the mitochondria! J Emergency Critical Care Med 3. https://jeccm.amegroups.org/article/view/5352<br />
|info=[https://jeccm.amegroups.org/article/view/5352 Open Access]<br />
|authors=Wefers BM, Arbous M, Raat N, Mik E<br />
|year=2019<br />
|journal=J Emergency Critical Care Med<br />
|abstract=Safeguarding an adequate oxygen transport to organs and tissues is a prime goal in the care for critically ill patients. Over the last two decades it has become clear that in certain pathophysiological circumstances macrocirculatory derailment is followed, or accompanied, by microcirculatory dysfunction. Resuscitation strategies to restore and optimize blood flow to organs are based on the idea that restoring oxygen supply will re-establish aerobic metabolism and lead to “healthy parenchymal cells”. However, mitochondrial damage and subsequent dysfunction, or cellular adaptation to hypoxia, might attenuate or even counterbalance the positive effects of resuscitation on the cellular level. In this short review we will address mitochondrial function and adaptation, causes of mitochondrial dysfunction, the concept of cytopathic hypoxia, (loss of) hemodynamic coherence and ways to assess aspects of mitochondrial function in patients. Mitochondria are the primary consumers of oxygen and the ultimate destination of approximately 98% of oxygen reaching our tissue cells. Most of the oxygen is used for energy production by oxidative phosphorylation, but a small amount is used for generating reactive oxygen species and heat generation. While adenosine triphosphate (ATP) production is the best-known function of mitochondria, they also play key roles in calcium homeostasis and cell-death mechanisms. Oxidative phosphorylation has a very high affinity for oxygen and functions well at very low oxygen levels. However, cellular respiration does adapt to changes in oxygen availability at physiological levels, a mechanism known as “oxygen conformance”. Oxygen conformance, mitochondrial damage by certain hits (e.g., toxins and medication), mitochondrial dysfunction and autonomic metabolic reprogramming are factors that could contribute to what is known as “cytopathic hypoxia”. This concept describes insufficient oxygen metabolism in cells despite sufficient oxygen delivery in sepsis. Altered cellular oxygen utilization and thus reduced oxygen demand could in itself cause decreased microcirculatory blood flow, making microcirculatory dysfunction in sepsis under some circumstances a possible epiphenomenon. Resuscitation and forced restoration of microcirculatory flow could lead to relative hyperoxia, and be counterproductive by increasing reactive oxygen production and intervening with protective adaptation mechanisms. The complex pathophysiology of a critically ill patient, especially in severe sepsis and septic shock, requires a multilevel approach. In understanding the interplay between macrocirculation, microcirculation, and parenchymal cells the mitochondria are key players that should not be overlooked. Progress is being made in technologies to assess aspects of mitochondrial function at the bedside, for example direct measurement of mitochondrial oxygen tension and oxygen consumption.<br />
|editor=Gnaiger E<br />
}}<br />
{{Labeling<br />
|area=mt-Medicine<br />
|diseases=Sepsis<br />
|injuries=Hypoxia<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/San-Millan_2023_Antioxidants_(Basel)San-Millan 2023 Antioxidants (Basel)2024-03-16T09:00:13Z<p>Gnaiger Erich: Created page with "{{Publication |title=San-Millán I (2023) The key role of mitochondrial function in health and disease. Antioxidants (Basel) 12:782. https://doi.org/10.3390/antiox12040782 |in..."</p>
<hr />
<div>{{Publication<br />
|title=San-Millán I (2023) The key role of mitochondrial function in health and disease. Antioxidants (Basel) 12:782. https://doi.org/10.3390/antiox12040782<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/37107158/ PMID: 37107158 Open Access]<br />
|authors=San-Millan I<br />
|year=2023<br />
|journal=Antioxidants (Basel)<br />
|abstract=The role of mitochondrial function in health and disease has become increasingly recognized, particularly in the last two decades. Mitochondrial dysfunction as well as disruptions of cellular bioenergetics have been shown to be ubiquitous in some of the most prevalent diseases in our society, such as type 2 diabetes, cardiovascular disease, metabolic syndrome, cancer, and Alzheimer's disease. However, the etiology and pathogenesis of mitochondrial dysfunction in multiple diseases have yet to be elucidated, making it one of the most significant medical challenges in our history. However, the rapid advances in our knowledge of cellular metabolism coupled with the novel understanding at the molecular and genetic levels show tremendous promise to one day elucidate the mysteries of this ancient organelle in order to treat it therapeutically when needed. Mitochondrial DNA mutations, infections, aging, and a lack of physical activity have been identified to be major players in mitochondrial dysfunction in multiple diseases. This review examines the complexities of mitochondrial function, whose ancient incorporation into eukaryotic cells for energy purposes was key for the survival and creation of new species. Among these complexities, the tightly intertwined bioenergetics derived from the combustion of alimentary substrates and oxygen are necessary for cellular homeostasis, including the production of reactive oxygen species. This review discusses different etiological mechanisms by which mitochondria could become dysregulated, determining the fate of multiple tissues and organs and being a protagonist in the pathogenesis of many non-communicable diseases. Finally, physical activity is a canonical evolutionary characteristic of humans that remains embedded in our genes. The normalization of a lack of physical activity in our modern society has led to the perception that exercise is an "intervention". However, physical activity remains the modus vivendi engrained in our genes and being sedentary has been the real intervention and collateral effect of modern societies. It is well known that a lack of physical activity leads to mitochondrial dysfunction and, hence, it probably becomes a major etiological factor of many non-communicable diseases affecting modern societies. Since physical activity remains the only stimulus we know that can improve and maintain mitochondrial function, a significant emphasis on exercise promotion should be imperative in order to prevent multiple diseases. Finally, in populations with chronic diseases where mitochondrial dysfunction is involved, an individualized exercise prescription should be crucial for the "metabolic rehabilitation" of many patients. From lessons learned from elite athletes (the perfect human machines), it is possible to translate and apply multiple concepts to the betterment of populations with chronic diseases.<br />
|editor=Gnaiger E<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style, mt-Medicine<br />
|diseases=Aging;senescence, Cancer, Cardiovascular, Diabetes, Obesity<br />
|organism=Human<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Shi_2024_Clin_Sci_(Lond)Shi 2024 Clin Sci (Lond)2024-03-15T13:04:11Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Shi L, Yang J, Tao Z, Zheng L, Bui TF, Alonso RL, Yue F, Cheng Z (2024) Loss of FoxO1 activates an alternate mechanism of mitochondrial quality control for healthy adipose browning. Clin Sci (Lond) 138:371-85. https://doi.org/10.1042/cs20230973<br />
|info=[https://www.ncbi.nlm.nih.gov/pubmed/38469619 PMID: 38469619 Open Access]<br />
|authors=Shi Limin, Yang Jinying, Tao Zhipeng, Zheng Louise, Bui Tyler F, Alonso Ramon L, Yue Feng, Cheng Zhiyong<br />
|year=2024<br />
|journal=Clin Sci (Lond)<br />
|abstract=Browning of white adipose tissue is hallmarked by increased mitochondrial density and metabolic improvements. However, it remains largely unknown how mitochondrial turnover and quality control are regulated during adipose browning. In the present study, we found that mice lacking adipocyte FoxO1, a transcription factor that regulates autophagy, adopted an alternate mechanism of mitophagy to maintain mitochondrial turnover and quality control during adipose browning. Post-developmental deletion of adipocyte FoxO1 (adO1KO) suppressed Bnip3 but activated Fundc1/Drp1/OPA1 cascade, concurrent with up-regulation of Atg7 and CTSL. In addition, mitochondrial biogenesis was stimulated via the Pgc1α/Tfam pathway in adO1KO mice. These changes were associated with enhanced mitochondrial homeostasis and metabolic health (e.g., improved glucose tolerance and insulin sensitivity). By contrast, silencing Fundc1 or Pgc1α reversed the changes induced by silencing FoxO1, which impaired mitochondrial quality control and function. Ablation of Atg7 suppressed mitochondrial turnover and function, causing metabolic disorder (e.g., impaired glucose tolerance and insulin sensitivity), regardless of elevated markers of adipose browning. Consistently, suppression of autophagy via CTSL by high-fat diet was associated with a reversal of adO1KO-induced benefits. Our data reveal a unique role of FoxO1 in coordinating mitophagy receptors (Bnip3 and Fundc1) for a fine-tuned mitochondrial turnover and quality control, underscoring autophagic clearance of mitochondria as a prerequisite for healthy browning of adipose tissue.<br />
|keywords=FoxO1, Adipose browning, Metabolism, Mitochondrial quality control, Mitophagy<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/MiPNet28.13_IOC165_Innsbruck_ATMiPNet28.13 IOC165 Innsbruck AT2024-03-14T16:35:38Z<p>Cardoso Luiza: </p>
<hr />
<div>{{OROBOROS header page name}}<br />
{{Publication<br />
|title=[[Image:O2k-Workshops.png|right|80px|link=O2k-Workshops]]'''Innsbruck AT''', 2024 Sep 02-04. EBEC2024 Satellite Oroboros O2k-Workshop: Mito&Chlora High-Resolution Respirometry and PhotoBiology, '''IOC165'''.<br />
|authors=Oroboros<br />
|year=2024-09-02<br />
|journal=Mitochondr Physiol Network<br />
|abstract='''EBEC2024 Satellite Oroboros O2k-Workshop: Mito&Chlora High-Resolution Respirometry and PhotoBiology'''. Innsbruck, Austria (2024 Sep 02-04).<br><br />
|mipnetlab=AT_Innsbruck_Oroboros<br />
}}<br />
<br />
__TOC__<br />
== General information ==<br />
:::: This 2.5-day training course provides an introduction the [[Oroboros_O2k|Oroboros O2k and NextGen-O2k]] including the [[PB-Module|O2k-PB-Module]], [[NADH-Module|O2k-NADH-Module]], [[Q-Module|O2k-Q-Module]] and [[DatLab]] 8 and applications of the [[TIP2k-Module|TIP2k]]. Demo experiments illustrate the principle and show the unique advantages and limitations of simultaneous monitoring of oxygen concentration, mitochondrial respiration, NADH- and Q-redox states. An application of the [[O2k-NO Amp-Module]] to measure endogenous NO production will be presented. Many optimized [[SUIT protocols]] are available as DL-Protocols. The [[SUITbrowser]] helps you find the best SUIT protocol for your specific research questions. Furthermore, this workshop covers interpretation of data from SUIT protocols.<br />
<br />
== Venue ==<br />
::::» Oroboros O2k-Laboratory and ''MiPArt''<br />
::::: Schoepfstrasse 18, 6020 Innsbruck<br />
::::» Information on travel and venue: '''[[IOC Innsbruck]]'''<br />
<br />
<br />
== Registration ==<br />
:::: Registration will open soon.<br />
<br />
== Program ==<br />
:::: A new program is being created and will be uploaded when finalized. <br />
<br><br />
<br />
=== Tutors and lecturers ===<br />
<gallery mode=default perrow=6 widths="140px" heights="150px"><br />
File:Erich Gnaiger.jpg|'''[[Gnaiger E |Erich Gnaiger]]''', PhD, Oroboros Instruments - CEO, ''Innovation Alchemist''<br />
</gallery><br />
<br />
=== Participants ===<br />
<br />
{| class="wikitable"<br />
|-<br />
!<br />
!<br />
! Participant<br />
! Institution<br />
|-<br />
|1.<br />
|-<br />
|}<br />
<br />
<br />
<br />
<br />
<br />
<br />
== Contact ==<br />
:::: [mailto:instruments@oroboros.at| instruments@oroboros.at]<br />
<br />
:::: '''Oroboros Instruments'''<br />
:::: High-Resolution Respirometry <br />
:::: Schoepfstrasse 18<br />
:::: A-6020 Innsbruck, Austria<br />
:::: Tel: +43 677 647 929 17<br />
:::: Fax: +43 512 566796 20 <br />
<br />
:::: '''Mitochondria and Cell Research'''<br />
<br />
<br />
== IOC recommended reading ==<br />
::::» '''[[IOC recommended reading]]'''<br />
::::» '''[[MitoPedia: Respiratory states]]'''<br />
:::: [[Image:P.jpg|link=OXPHOS capacity|35px|OXPHOS]] [[Image:R.jpg|link=ROUTINE respiration|35px|ROUTINE]] [[Image:E.jpg|link=ET capacity|35px|ETS]] [[Image:L.jpg|link=LEAK respiration|35px|LEAK]] [[Image:ROX.jpg|link=Residual oxygen consumption|65px|ROX]]<br />
<br />
<br />
[[Image:MitoGlobal.jpg|right|80px|link=MitoGlobal|MitoGlobal]] <br />
O2k-Workshops are listed as [[MitoGlobal Events]].<br />
<br />
<br />
{{Labeling<br />
|additional=ORO, IOC, MitoFit, 2024, MitoGlobal, NextGen-O2k, Next, O2k-Network Award,<br />
}}<br />
<br />
[[Category:O2k-Workshops]]</div>Tindle Lisahttps://wiki.oroboros.at/index.php/RSC_Chem_BiolRSC Chem Biol2024-03-13T13:59:20Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://www.rsc.org/journals-books-databases/about-journals/rsc-chemical-biology/ RSC Chemical Biology] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://www.rsc.org/journals-books-databases/about-journals/rsc-chemical-biology/ RSC Chemical Biology]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Kleinwaechter_2022_RSC_Chem_BiolKleinwaechter 2022 RSC Chem Biol2024-03-13T13:58:36Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Kleinwaechter I, Mohr B, Joppe A, Hellmann N, Bereau T, Osiewacz HD, Schneider D (2022) CLiB - a novel cardiolipin-binder isolated via data-driven and ''in vitro'' screening. RSC Chem Biol 3:941-54. https://doi.org/10.1039/d2cb00125j<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/35866160 PMID: 35866160 Open Access]<br />
|authors=Kleinwaechter Isabel, Mohr Bernadette, Joppe Aljoscha, Hellmann Nadja, Bereau Tristan, Osiewacz Heinz D, Schneider Dirk<br />
|year=2022<br />
|journal=RSC Chem Biol<br />
|abstract=Cardiolipin, the mitochondria marker lipid, is crucially involved in stabilizing the inner mitochondrial membrane and is vital for the activity of mitochondrial proteins and protein complexes. Directly targeting cardiolipin by a chemical-biology approach and thereby altering the cellular concentration of "available" cardiolipin eventually allows to systematically study the dependence of cellular processes on cardiolipin availability. In the present study, physics-based coarse-grained free energy calculations allowed us to identify the physical and chemical properties indicative of cardiolipin selectivity and to apply these to screen a compound database for putative cardiolipin-binders. The membrane binding properties of the 22 most promising molecules identified in the ''in silico'' approach were screened ''in vitro'', using model membrane systems finally resulting in the identification of a single molecule, CLiB (CardioLipin-Binder). CLiB clearly affects respiration of cardiolipin-containing intact bacterial cells as well as of isolated mitochondria. Thus, the structure and function of mitochondrial membranes and membrane proteins might be (indirectly) targeted and controlled by CLiB for basic research and, potentially, also for therapeutic purposes.<br />
|editor=[[Plangger M]]<br />
|mipnetlab=DE Frankfurt Osiewacz HD<br />
}}<br />
{{Labeling<br />
|area=Respiration, mt-Membrane<br />
|organism=Fungi<br />
|preparations=Isolated mitochondria<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Glombik_2023_Int_J_Mol_SciGlombik 2023 Int J Mol Sci2024-03-13T13:38:23Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Glombik K, Kukla-Bartoszek M, Curzytek K, Detka J, Basta-Kaim A, Budziszewska B (2023) The effects of prenatal dexamethasone exposure on brain metabolic homeostasis in adulthood: implications for depression. Int J Mol Sci 24:1156. https://doi.org/10.3390/ijms24021156<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/36674678 PMID: 36674678 Open Access]<br />
|authors=Glombik Katarzyna, Kukla-Bartoszek Magdalena, Curzytek Katarzyna, Detka Jan, Basta-Kaim Agnieszka, Budziszewska Boguslawa<br />
|year=2023<br />
|journal=Int J Mol Sci<br />
|abstract=Since depression produces a long-term negative impact on quality of life, understanding the pathophysiological changes implicated in this disorder is urgent. There is growing evidence that demonstrates a key role for dysfunctional energy metabolism in driving the onset of depression; thus, bioenergetic alterations should be extensively studied. Brain metabolism is known to be a glucocorticoid-sensitive process, but the long-lasting consequences in adulthood following high levels of glucocorticoids at the early stages of life are unclear. We examined a possible association between brain energetic changes induced by synthetic glucocorticoid-dexamethasone treatment in the prenatal period and depressive-like behavior. The results show a reduction in the oxidative phosphorylation process, Krebs cycle impairment, and a weakening of the connection between the Krebs cycle and glycolysis in the frontal cortex of animals receiving dexamethasone, which leads to ATP reduction. These changes appear to be mainly due to decreased expression of pyruvate dehydrogenase, impairment of lactate transport to neurons, and pyruvate to the mitochondria. Acute stress in adulthood only slightly modified the observed alterations in the frontal cortex, while in the case of the hippocampus, prenatal exposure to dexamethasone made this structure more sensitive to future adverse factors.<br />
|keywords=Animal model, Bioenergetics, Brain, Depression, Dexamethasone<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration, Developmental biology<br />
|diseases=Other<br />
|organism=Rat<br />
|tissues=Nervous system<br />
|preparations=Isolated mitochondria<br />
|couplingstates=LEAK, OXPHOS, ET<br />
|pathways=N, S, NS, ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Verma_2023_Int_J_Mol_SciVerma 2023 Int J Mol Sci2024-03-13T13:15:46Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Verma A, Azhar G, Zhang X, Patyal P, Kc G, Sharma S, Che Y, Wei JY (2023) ''P. gingivalis''-LPS induces mitochondrial dysfunction mediated by neuroinflammation through oxidative stress. Int J Mol Sci 24:950. https://doi.org/10.3390/ijms24020950<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/36674463 PMID: 36674463 Open Access]<br />
|authors=Verma Ambika, Azhar Gohar, Zhang Xiaomin, Patyal Pankaj, Kc Grishma, Sharma Shakshi, Che Yingni, Wei Jeanne Y<br />
|year=2023<br />
|journal=Int J Mol Sci<br />
|abstract=''Porphyromonas gingivalis'' (''P. gingivalis''), a key pathogen in periodontitis, is associated with neuroinflammation. Periodontal disease increases with age; 70.1% of adults 65 years and older have periodontal problems. However, the ''P. gingivalis''- lipopolysaccharide (LPS)induced mitochondrial dysfunction in neurodegenerative diseases remains elusive. In this study, we investigated the possible role of ''P. gingivalis''-LPS in mitochondrial dysfunction during neurodegeneration. We found that ''P. gingivalis''-LPS treatment activated toll-like receptor (TLR) 4 signaling and upregulated the expression of Alzheimer's disease-related dementia and neuroinflammatory markers. Furthermore, the LPS treatment significantly exacerbated the production of reactive oxygen species and reduced the mitochondrial membrane potential. Our study highlighted the pivotal role of ''P. gingivalis''-LPS in the repression of serum response factor (SRF) and its co-factor p49/STRAP that regulate the actin cytoskeleton. The LPS treatment repressed the genes involved in mitochondrial function and biogenesis. ''P. gingivalis''-LPS negatively altered oxidative phosphorylation and glycolysis and reduced total adenosine triphosphate (ATP) production. Additionally, it specifically altered the mitochondrial functions in complexes I, II, and IV of the mitochondrial electron transport chain. Thus, it is conceivable that ''P. gingivalis''-LPS causes mitochondrial dysfunction through oxidative stress and inflammatory events in neurodegenerative diseases.<br />
|keywords=P. gingivalis-LPS, Mitochondrial dysfunction, Neuroinflammation, Oxidative stress<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|diseases=Neurodegenerative<br />
|organism=Human<br />
|tissues=Endothelial;epithelial;mesothelial cell<br />
|preparations=Permeabilized cells, Intact cells<br />
|couplingstates=LEAK, ROUTINE, OXPHOS, ET<br />
|pathways=N, S, CIV, ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Bassot_2023_Cell_RepBassot 2023 Cell Rep2024-03-13T12:37:05Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Bassot A, Chen J, Takahashi-Yamashiro K, Yap MC, Gibhardt CS, Le GNT, Hario S, Nasu Y, Moore J, Gutiérrez T, Mina L, Mast H, Moses A, Bhat R, Ballanyi K, Lemieux H, Sitia R, Zito E, Bogeski I, Campbell RE, Simmen T (2023) The endoplasmic reticulum kinase PERK interacts with the oxidoreductase ERO1 to metabolically adapt mitochondria. Cell Rep 42:111899. https://doi.org/10.1016/j.celrep.2022.111899<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/36586409 PMID: 36586409 Open Access]<br />
|authors=Bassot Arthur, Chen Junsheng, Takahashi-Yamashiro Kei, Yap Megan C, Gibhardt Christine Silvia, Le Giang NT, Hario Saaya, Nasu Yusuke, Moore Jack, Gutierrez Tomas, Mina Lucas, Mast Heather, Moses Audric, Bhat Rakesh, Ballanyi Klaus, Lemieux Helene, Sitia Roberto, Zito Ester, Bogeski Ivan, Campbell Robert E, Simmen Thomas<br />
|year=2023<br />
|journal=Cell Rep<br />
|abstract=Endoplasmic reticulum (ER) homeostasis requires molecular regulators that tailor mitochondrial bioenergetics to the needs of protein folding. For instance, calnexin maintains mitochondria metabolism and mitochondria-ER contacts (MERCs) through reactive oxygen species (ROS) from NADPH oxidase 4 (NOX4). However, induction of ER stress requires a quick molecular rewiring of mitochondria to adapt to new energy needs. This machinery is not characterized. We now show that the oxidoreductase ERO1⍺ covalently interacts with protein kinase RNA-like ER kinase (PERK) upon treatment with tunicamycin. The PERK-ERO1⍺ interaction requires the C-terminal active site of ERO1⍺ and cysteine 216 of PERK. Moreover, we show that the PERK-ERO1⍺ complex promotes oxidization of MERC proteins and controls mitochondrial dynamics. Using proteinaceous probes, we determined that these functions improve ER-mitochondria Ca<sup>2+</sup> flux to maintain bioenergetics in both organelles, while limiting oxidative stress. Therefore, the PERK-ERO1⍺ complex is a key molecular machinery that allows quick metabolic adaptation to ER stress.<br />
|keywords=CP: Metabolism, CP: Molecular biology, ER, ER stress, ERO1, MAMs, MERCs, PERK, Bioenergetics, Endoplasmic reticulum, Mitochondria, Mitochondria-associated membranes, Mitochondria-endoplasmic reticulum contacts, Oxidoreductase<br />
|editor=[[Plangger M]]<br />
|mipnetlab=CA Edmonton Lemieux H<br />
}}<br />
{{Labeling<br />
|area=Respiration, Genetic knockout;overexpression<br />
|organism=Human, Mouse<br />
|tissues=HEK, Fibroblast<br />
|preparations=Intact cells<br />
|couplingstates=LEAK, ROUTINE, ET<br />
|pathways=ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Dabrowska_2023_Int_J_Mol_SciDabrowska 2023 Int J Mol Sci2024-03-13T12:22:08Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Dabrowska A, Zajac M, Bednarczyk P, Lukasiak A (2023) Effect of quercetin on mitoBK<sub>Ca</sub> channel and mitochondrial function in human bronchial epithelial cells exposed to particulate matter. Int J Mol Sci 24:638. https://doi.org/10.3390/ijms24010638<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/36614079 PMID: 36614079 Open Access]<br />
|authors=Dabrowska Adrianna, Zajac Miroslaw, Bednarczyk Piotr, Lukasiak Agnieszka<br />
|year=2023<br />
|journal=Int J Mol Sci<br />
|abstract=Particulate matter (PM) exposure increases reactive oxygen species (ROS) levels. It can lead to inflammatory responses and damage of the mitochondria thus inducing cell death. Recently, it has been shown that potassium channels (mitoK) located in the inner mitochondrial membrane are involved in cytoprotection, and one of the mechanisms involves ROS. To verify the cytoprotective role of mitoBK<sub>Ca</sub>, we performed a series of experiments using a patch-clamp, transepithelial electrical resistance assessment (TEER), mitochondrial respiration measurements, fluorescence methods for the ROS level and mitochondrial membrane potential assessment, and cell viability measurements. In the human bronchial epithelial cell model (16HBE14σ), PM < 4 μm in diameter (SRM-PM4.0) was used. We observed that PM decreased TEER of HBE cell monolayers. The effect was partially abolished by quercetin, a mitoBK<sub>Ca</sub> opener. Consequently, quercetin decreased the mitochondrial membrane potential and increased mitochondrial respiration. The reduction of PM-induced ROS level occurs both on cellular and mitochondrial level. Additionally, quercetin restores HBE cell viability after PM administration. The incubation of cells with PM substantially reduced the mitochondrial function. Isorhamnetin had no effect on TEER, the mitoBK<sub>Ca</sub> activity, respiratory rate, or mitochondrial membrane potential. Obtained results indicate that PM has an adverse effect on HBE cells at the cellular and mitochondrial level. Quercetin is able to limit the deleterious effect of PM on barrier function of airway epithelial cells. We show that the effect in HBE cells involves mitoBK<sub>Ca</sub> channel-activation. However, quercetin’s mechanism of action is not exclusively determined by modulation of the channel activity.<br />
|keywords=Epithelium, mitoBKCa channel, Mitochondria, Particulate matter, Quercetin<br />
|editor=[[Plangger M]]<br />
|mipnetlab=PL Warsaw Bednarczyk P<br />
}}<br />
{{Labeling<br />
|area=Respiration, mt-Membrane, Pharmacology;toxicology<br />
|injuries=Oxidative stress;RONS<br />
|organism=Human<br />
|tissues=Lung;gill, Endothelial;epithelial;mesothelial cell<br />
|preparations=Permeabilized cells, Intact cells<br />
|topics=Ion;substrate transport, mt-Membrane potential<br />
|couplingstates=LEAK, ROUTINE, OXPHOS, ET<br />
|pathways=S, ROX<br />
|instruments=Oxygraph-2k, O2k-Fluorometer<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Commun_Med_(Lond)Commun Med (Lond)2024-03-12T14:43:39Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://www.nature.com/commsmed Communications Medicine] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://www.nature.com/commsmed Communications Medicine]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Tsouka_2024_Commun_Med_(Lond)Tsouka 2024 Commun Med (Lond)2024-03-12T14:09:19Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Tsouka S, Kumar P, Seubnooch P, Freiburghaus K, St-Pierre M, Dufour JF, Masoodi M (2024) Transcriptomics-driven metabolic pathway analysis reveals similar alterations in lipid metabolism in mouse MASH model and human. Commun Med (Lond) 4:39. https://doi.org/10.1038/s43856-024-00465-3<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38443644 PMID: 38443644 Open Access]<br />
|authors=Tsouka Sofia, Kumar Pavitra, Seubnooch Patcharamon, Freiburghaus Katrin, St-Pierre Marie, Dufour Jean-Francois, Masoodi Mojgan<br />
|year=2024<br />
|journal=Commun Med (Lond)<br />
|abstract=Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disease worldwide, and can rapidly progress to metabolic dysfunction-associated steatohepatitis (MASH). Accurate preclinical models and methodologies are needed to understand underlying metabolic mechanisms and develop treatment strategies. Through meta-analysis of currently proposed mouse models, we hypothesized that a diet- and chemical-induced MASH model closely resembles the observed lipid metabolism alterations in humans.<br />
<br />
We developed transcriptomics-driven metabolic pathway analysis (TDMPA), a method to aid in the evaluation of metabolic resemblance. TDMPA uses genome-scale metabolic models to calculate enzymatic reaction perturbations from gene expression data. We performed TDMPA to score and compare metabolic pathway alterations in MASH mouse models to human MASH signatures. We used an already-established WD+CCl4-induced MASH model and performed functional assays and lipidomics to confirm TDMPA findings.<br />
<br />
Both human MASH and mouse models exhibit numerous altered metabolic pathways, including triglyceride biosynthesis, fatty acid beta-oxidation, bile acid biosynthesis, cholesterol metabolism, and oxidative phosphorylation. We confirm a significant reduction in mitochondrial functions and bioenergetics, as well as in acylcarnitines for the mouse model. We identify a wide range of lipid species within the most perturbed pathways predicted by TDMPA. Triglycerides, phospholipids, and bile acids are increased significantly in mouse MASH liver, confirming our initial observations.<br />
<br />
We introduce TDMPA, a methodology for evaluating metabolic pathway alterations in metabolic disorders. By comparing metabolic signatures that typify human MASH, we show a good metabolic resemblance of the WD+CCl4 mouse model. Our presented approach provides a valuable tool for defining metabolic space to aid experimental design for assessing metabolism.<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration, Instruments;methods<br />
|diseases=Other<br />
|organism=Mouse<br />
|tissues=Liver<br />
|preparations=Isolated mitochondria<br />
|couplingstates=LEAK, OXPHOS, ET<br />
|pathways=N, S, CIV, NS, ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Perin_2023_Proc_Natl_Acad_Sci_U_S_APerin 2023 Proc Natl Acad Sci U S A2024-03-12T08:24:57Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Perin G, Bellan A, Michelberger T, Lyska D, Wakao S, Niyogi KK, Morosinotto T (2023) Modulation of xanthophyll cycle impacts biomass productivity in the marine microalga ''Nannochloropsis''. Proc Natl Acad Sci U S A 120:e2214119120. https://doi.org/10.1073/pnas.2214119120<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/37307488/ PMID: 37307488 Open Access]<br />
|authors=Perin Giorgio, Bellan A, Michelberger T, Lyska D, Wakao S, Niyogi KK, Morosinotto Tomas<br />
|year=2023<br />
|journal=Proc Natl Acad Sci U S A<br />
|abstract=Life on earth depends on photosynthetic primary producers that exploit sunlight to fix CO2 into biomass. Approximately half of global primary production is associated with microalgae living in aquatic environments. Microalgae also represent a promising source of biomass to complement crop cultivation, and they could contribute to the development of a more sustainable bioeconomy. Photosynthetic organisms evolved multiple mechanisms involved in the regulation of photosynthesis to respond to highly variable environmental conditions. While essential to avoid photodamage, regulation of photosynthesis results in dissipation of absorbed light energy, generating a complex trade-off between protection from stress and light-use efficiency. This work investigates the impact of the xanthophyll cycle, the light-induced reversible conversion of violaxanthin into zeaxanthin, on the protection from excess light and on biomass productivity in the marine microalgae of the genus Nannochloropsis. Zeaxanthin is shown to have an essential role in protection from excess light, contributing to the induction of nonphotochemical quenching and scavenging of reactive oxygen species. On the contrary, the overexpression of zeaxanthin epoxidase enables a faster reconversion of zeaxanthin to violaxanthin that is shown to be advantageous for biomass productivity in dense cultures in photobioreactors. These results demonstrate that zeaxanthin accumulation is critical to respond to strong illumination, but it may lead to unnecessary energy losses in light-limiting conditions and accelerating its reconversion to violaxanthin provides an advantage for biomass productivity in microalgae.<br />
|editor=Gnaiger E<br />
|mipnetlab=IT Padova Morosinotto T<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|organism=Algae<br />
|preparations=Intact cells<br />
|topics=Redox state<br />
|couplingstates=ROUTINE<br />
|instruments=Oxygraph-2k, NextGen-O2k<br />
|additional=PhotoBiology<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/J_Exerc_RehabilJ Exerc Rehabil2024-03-11T15:47:54Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://www.e-jer.org/ Journal of Exercise Rehabilitation] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://www.e-jer.org/ Journal of Exercise Rehabilitation]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Kim_2024_J_Exerc_RehabilKim 2024 J Exerc Rehabil2024-03-11T15:26:33Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Kim TW, Park SS, Kim SH, Kim MK, Shin MS, Kim SH (2024) Exercise before pregnancy exerts protective effect on prenatal stress-induced impairment of memory, neurogenesis, and mitochondrial function in offspring. J Exerc Rehabil 20:2-10. https://doi.org/10.12965/jer.2448068.034<br />
|info=[https://www.ncbi.nlm.nih.gov/pubmed/38433854 PMID: 38433854 Open Access]<br />
|authors=Kim Tae-Woon, Park Sang-Seo, Kim Sang-Hoon, Kim Myung-Ki, Shin Mal-Soon, Kim Seong-Hyun<br />
|year=2024<br />
|journal=J Exerc Rehabil<br />
|abstract=Stress during pregnancy has a negative effect on the fetus. However, maternal exercise has a positive effect on the cognitive function of the fetus and alleviates the negative effects of stress. This study aimed to demonstrate whether exercise before pregnancy has a protective effect on prenatal stress-induced impairment of memory, neurogenesis and mitochondrial function in mice offspring. In this experiment, immunohistochemistry, Western blot, measurement of mitochondria oxygen respiration, and behavior tests were performed. Spatial memory and short-term memory of the offspring from the prenatal stress with exercise were increased compared to the offspring from the prenatal stress. The numbers of doublecortin-positive and 5-bromo-2'-deoxyuridine-positive cells in the hippocampal dentate gyrus of the offspring from the prenatal stress with exercise were higher compared to the offspring from the prenatal stress. The expressions of brain-derived neurotrophic factor, postsynaptic density 95 kDa, and synaptophysin in the hippocampus of the offspring from the prenatal stress with exercise were enhanced compared to the offspring from the prenatal stress. Oxygen consumption of the offspring from the prenatal stress with exercise were higher compared to the offspring from the prenatal stress. Exercise before pregnancy alleviated prenatal stress-induced impairment of memory, neurogenesis, and mitochondrial function. Therefore, exercise before pregnancy may have a protective effect against prenatal stress of the offspring.<br />
|keywords=Exercise, Maternal stress, Memory, Offspring, Pregnancy<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Pilot_Feasibility_StudPilot Feasibility Stud2024-03-07T13:39:52Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://pilotfeasibilitystudies.biomedcentral.com/ Pilot and Feasibility Studies] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://pilotfeasibilitystudies.biomedcentral.com/ Pilot and Feasibility Studies]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Taylor_2024_Pilot_Feasibility_StudTaylor 2024 Pilot Feasibility Stud2024-03-07T13:38:39Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Taylor MK, Burns JM, Choi IY, Herda TJ, Lee P, Smith AN, Sullivan DK, Swerdlow RH, Wilkins HM (2024) Protocol for a single-arm, pilot trial of creatine monohydrate supplementation in patients with Alzheimer's disease. Pilot Feasibility Stud 10:42. https://doi.org/10.1186/s40814-024-01469-5<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38414003 PMID: 38414003 Open Access]<br />
|authors=Taylor Matthew K, Burns Jeffrey M, Choi In-Young, Herda Trent J, Lee Phil, Smith Aaron N, Sullivan Debra K, Swerdlow Russell H, Wilkins Heather M<br />
|year=2024<br />
|journal=Pilot Feasibility Stud<br />
|abstract=Impaired brain bioenergetics is a pathological hallmark of Alzheimer's disease (AD) and is a compelling target for AD treatment. Patients with AD exhibit dysfunction in the brain creatine (Cr) system, which is integral in maintaining bioenergetic flux. Recent studies in AD mouse models suggest Cr supplementation improves brain mitochondrial function and may be protective of AD peptide pathology and cognition.<br />
<br />
The Creatine to Augment Bioenergetics in Alzheimer's disease (CABA) study is designed to primarily assess the feasibility of supplementation with 20 g/day of creatine monohydrate (CrM) in patients with cognitive impairment due to AD. Secondary aims are designed to generate preliminary data investigating changes in brain Cr levels, cognition, peripheral and brain mitochondrial function, and muscle strength and size.<br />
<br />
CABA is an 8-week, single-arm pilot study that will recruit 20 patients with cognitive impairment due to AD. Participants attend five in-person study visits: two visits at baseline to conduct screening and baseline assessments, a 4-week visit, and two 8-week visits. Outcomes assessment includes recruitment, retention, and compliance, cognitive testing, magnetic resonance spectroscopy of brain metabolites, platelet and lymphocyte mitochondrial function, and muscle strength and morphology at baseline and 8 weeks.<br />
<br />
CABA is the first study to investigate CrM as a potential treatment in patients with AD. The pilot data generated by this study are pertinent to inform the design of future large-scale efficacy trials.<br />
|keywords=Alzheimer’s disease, Bioenergetics, Brain, Creatine, Pilot trial<br />
|editor=[[Plangger M]]<br />
|mipnetlab=US KS Kansas City Swerdlow RH, US KS Kansas City Wilkins H<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|diseases=Alzheimer's<br />
|organism=Human<br />
|tissues=Lymphocyte, Platelet<br />
|preparations=Permeabilized cells<br />
|instruments=Oxygraph-2k, O2k-Fluorometer<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Ransy_2020_Int_J_Mol_SciRansy 2020 Int J Mol Sci2024-03-07T08:09:49Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Ransy C, Vaz C, Lombès A, Bouillaud F (2020) Use of H<sub>2</sub>O<sub>2</sub> to cause oxidative stress, the catalase issue. Int J Mol Sci 21:9149. https://doi.org/10.3390/ijms21239149<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/33266350/ PMID: 33266350 Open Access]<br />
|authors=Ransy C, Vaz C, Lombès A, Bouillaud F<br />
|year=2020<br />
|journal=Int J Mol Sci<br />
|abstract=Addition of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) is a method commonly used to trigger cellular oxidative stress. However, the doses used (often hundreds of micromolar) are disproportionally high with regard to physiological oxygen concentration (low micromolar). In this study using polarographic measurement of oxygen concentration in cellular suspensions we show that H<sub>2</sub>O<sub>2</sub> addition results in O<sub>2</sub> release as expected from catalase reaction. This reaction is fast enough to, within seconds, decrease drastically H<sub>2</sub>O<sub>2</sub> concentration and to annihilate it within a few minutes. Firstly, this is likely to explain why recording of oxidative damage requires the high concentrations found in the literature. Secondly, it illustrates the potency of intracellular antioxidant (H<sub>2</sub>O<sub>2</sub>) defense. Thirdly, it complicates the interpretation of experiments as subsequent observations might result from high/transient H2O2 exposure and/or from the diverse possible consequences of the O<sub>2</sub> release.<br />
<br />
|editor=Gnaiger E<br />
|mipnetlab=FR Paris Bouillaud F<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|injuries=Oxidative stress;RONS<br />
|tissues=CHO<br />
|preparations=Permeabilized cells, Intact cells<br />
|couplingstates=ROUTINE<br />
|instruments=Oxygraph-2k<br />
|additional=Catalase<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Torcasio_2024_J_Transl_MedTorcasio 2024 J Transl Med2024-03-05T15:28:37Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Torcasio R, Gallo Cantafio ME, Veneziano C, De Marco C, Ganino L, Valentino I, Occhiuzzi MA, Perrotta ID, Mancuso T, Conforti F, Rizzuti B, Martino EA, Gentile M, Neri A, Viglietto G, Grande F, Amodio N (2024) Targeting of mitochondrial fission through natural flavanones elicits anti-myeloma activity. J Transl Med 22:208. https://doi.org/10.1186/s12967-024-05013-0<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38413989 PMID: 38413989 Open Access]<br />
|authors=Torcasio Roberta, Gallo Cantafio Maria Eugenia, Veneziano Claudia, De Marco Carmela, Ganino Ludovica, Valentino Ilenia, Occhiuzzi Maria Antonietta, Perrotta Ida Daniela, Mancuso Teresa, Conforti Filomena, Rizzuti Bruno, Martino Enrica Antonia, Gentile Massimo, Neri Antonino, Viglietto Giuseppe, Grande Fedora, Amodio Nicola<br />
|year=2024<br />
|journal=J Transl Med<br />
|abstract=Mitochondrial alterations, often dependent on unbalanced mitochondrial dynamics, feature in the pathobiology of human cancers, including multiple myeloma (MM). Flavanones are natural flavonoids endowed with mitochondrial targeting activities. Herein, we investigated the capability of Hesperetin (Hes) and Naringenin (Nar), two aglycones of Hesperidin and Naringin flavanone glycosides, to selectively target Drp1, a pivotal regulator of mitochondrial dynamics, prompting anti-MM activity.<br />
<br />
Molecular docking analyses were performed on the crystallographic structure of Dynamin-1-like protein (Drp1), using Hes and Nar molecular structures. Cell viability and apoptosis were assessed in MM cell lines, or in co-culture systems with primary bone marrow stromal cells, using Cell Titer Glo and Annexin V-7AAD staining, respectively; clonogenicity was determined using methylcellulose colony assays. Transcriptomic analyses were carried out using the Ion AmpliSeq™ platform; mRNA and protein expression levels were determined by quantitative RT-PCR and western blotting, respectively. Mitochondrial architecture was assessed by transmission electron microscopy. Real time measurement of oxygen consumption was performed by high resolution respirometry in living cells. ''In vivo'' anti-tumor activity was evaluated in NOD-SCID mice subcutaneously engrafted with MM cells.<br />
<br />
Hes and Nar were found to accommodate within the GTPase binding site of Drp1, and to inhibit Drp1 expression and activity, leading to hyperfused mitochondria with reduced OXPHOS. ''In vitro'', Hes and Nar reduced MM clonogenicity and viability, even in the presence of patient-derived bone marrow stromal cells, triggering ER stress and apoptosis. Interestingly, Hes and Nar rewired MM cell metabolism through the down-regulation of master transcriptional activators (SREBF-1, c-MYC) of lipogenesis genes. An extract of Tacle, a Citrus variety rich in Hesperidin and Naringin, was capable to recapitulate the phenotypic and molecular perturbations of each flavanone, triggering anti-MM activity ''in vivo''.<br />
<br />
Hes and Nar inhibit proliferation, rewire the metabolism and induce apoptosis of MM cells via antagonism of the mitochondrial fission driver Drp1. These results provide a framework for the development of natural anti-MM therapeutics targeting aberrant mitochondrial dependencies.<br />
|keywords=Flavanones, Hesperitin, Mitochondrial dynamics, Multiple myeloma, Naringenin<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration, mt-Structure;fission;fusion, Pharmacology;toxicology<br />
|diseases=Cancer<br />
|organism=Human<br />
|tissues=Blood cells<br />
|preparations=Intact cells<br />
|couplingstates=LEAK, ROUTINE, ET<br />
|pathways=ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Romagnolo_2024_Acta_NeuropatholRomagnolo 2024 Acta Neuropathol2024-03-05T14:22:26Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Romagnolo A, Dematteis G, Scheper M, Luinenburg MJ, Mühlebner A, Van Hecke W, Manfredi M, De Giorgis V, Reano S, Filigheddu N, Bortolotto V, Tapella L, Anink JJ, François L, Dedeurwaerdere S, Mills JD, Genazzani AA, Lim D, Aronica E (2024) Astroglial calcium signaling and homeostasis in tuberous sclerosis complex. Acta Neuropathol 147:48. https://doi.org/10.1007/s00401-024-02711-3<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38418708 PMID: 38418708 Open Access]<br />
|authors=Romagnolo Alessia, Dematteis Giulia, Scheper Mirte, Luinenburg Mark J, Muehlebner Angelika, Van Hecke Wim, Manfredi Marcello, De Giorgis Veronica, Reano Simone, Filigheddu Nicoletta, Bortolotto Valeria, Tapella Laura, Anink Jasper J, Francois Liesbeth, Dedeurwaerdere Stefanie, Mills James D, Genazzani Armando A, Lim Dmitry, Aronica Eleonora<br />
|year=2024<br />
|journal=Acta Neuropathol<br />
|abstract=Tuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by the development of benign tumors in various organs, including the brain, and is often accompanied by epilepsy, neurodevelopmental comorbidities including intellectual disability and autism. A key hallmark of TSC is the hyperactivation of the mechanistic target of rapamycin (mTOR) signaling pathway, which induces alterations in cortical development and metabolic processes in astrocytes, among other cellular functions. These changes could modulate seizure susceptibility, contributing to the progression of epilepsy and its associated comorbidities. Epilepsy is characterized by dysregulation of calcium (Ca<sup>2+</sup>) channels and intracellular Ca<sup>2+</sup> dynamics. These factors contribute to hyperexcitability, disrupted synaptogenesis, and altered synchronization of neuronal networks, all of which contribute to seizure activity. This study investigates the intricate interplay between altered Ca<sup>2+</sup> dynamics, mTOR pathway dysregulation, and cellular metabolism in astrocytes. The transcriptional profile of TSC patients revealed significant alterations in pathways associated with cellular respiration, ER and mitochondria, and Ca<sup>2+</sup> regulation. TSC astrocytes exhibited lack of responsiveness to various stimuli, compromised oxygen consumption rate and reserve respiratory capacity underscoring their reduced capacity to react to environmental changes or cellular stress. Furthermore, our study revealed significant reduction of store operated calcium entry (SOCE) along with strong decrease of basal mitochondrial Ca<sup>2+</sup> concentration and Ca<sup>2+</sup> influx in TSC astrocytes. In addition, we observed alteration in mitochondrial membrane potential, characterized by increased depolarization in TSC astrocytes. Lastly, we provide initial evidence of structural abnormalities in mitochondria within TSC patient-derived astrocytes, suggesting a potential link between disrupted Ca<sup>2+</sup> signaling and mitochondrial dysfunction. Our findings underscore the complexity of the relationship between Ca<sup>2+</sup> signaling, mitochondria dynamics, apoptosis, and mTOR hyperactivation. Further exploration is required to shed light on the pathophysiology of TSC and on TSC associated neuropsychiatric disorders offering further potential avenues for therapeutic development.<br />
|keywords=Astrocytes, Calcium signaling, Epilepsy, Mitochondria, Tuberous sclerosis complex, mTOR<br />
|editor=[[Plangger M]]<br />
|mipnetlab=IT Novara Filigheddu N<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|diseases=Other<br />
|organism=Human<br />
|tissues=Nervous system<br />
|preparations=Intact cells<br />
|topics=Calcium<br />
|couplingstates=LEAK, ROUTINE, ET<br />
|pathways=ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-03<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Pakkiriswami_ShanmugasundaramPakkiriswami Shanmugasundaram2024-03-05T13:28:12Z<p>Plangger Mario: </p>
<hr />
<div>{{Person<br />
|lastname=Pakkiriswami<br />
|firstname=Shanmugasundaram<br />
|title=PhD<br />
|institution=:::::::::::::::[[File:Pakkiriswami_S.jpg|right|180px|Pakkiriswami Shanmugasundaram]] <br />
Liu Lab, Department of Integrative Biology and Physiology, University of Minnesota<br />
|city=Minneapolis-Saint Paul<br />
|state=Minnesota (MN)<br />
|country=USA<br />
|mailaddress=spakkiri@umn.edu<br />
}}<br />
{{Labelingperson}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Empson_1930_Chatto_and_WindusEmpson 1930 Chatto and Windus2024-03-03T12:29:19Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Empson W (1930) Seven types of ambiguity. Chatto and Windus, London.<br />
|info=[https://magdlibs.com/2016/07/14/william-empson/ Hughes MEJ]<br />
|authors=Empson William<br />
|year=1930<br />
|journal=Chatto and Windus<br />
|abstract=First published in 1930, Seven Types of Ambiguity has long been recognized as a landmark in the history of English literary criticism. Revised twice since it first appeared, it has remained one of the most widely read and quoted works of literary analysis. Ambiguity, according to Mr. Empson, includes “any verbal nuance, however slight, which gives room for alternative reactions to the same piece of language.” From this definition, broad enough by his own admission sometimes to seem “stretched absurdly far,” he launches into a brilliant discussion, under seven classifications of differing complexity and depth, of such works, among others, as Shakespeare’s plays and the poetry of Chaucer, Donne, Marvell, Pope, Wordsworth, G. M. Hopkins, and T. S. Eliot.<br />
<br />
Empson was working in the weeks before his expulsion on what was to be his best-known book, Seven Types of Ambiguity. It is original, startling in places and hugely influential in the teaching of English nowadays not only at university but at school too; and it offers in many ways the intellectual positioning implied by Richards’s more empirical and experimental interest in the processes of reading and understanding.<br />
|editor=Gnaiger E<br />
}}<br />
== Seven types ==<br />
Source: https://en.wikipedia.org/wiki/Seven_Types_of_Ambiguity <br />
<br />
:::: We have ambiguity when "alternative views might be taken without sheer misreading." <br />
<br />
::::# The first type of ambiguity is the metaphor, that is, when two things are said to be alike which have different properties. This concept is similar to that of metaphysical conceit.<br />
::::# Two or more meanings are resolved into one. Empson characterizes this as using two different metaphors at once.<br />
::::# Two ideas that are connected through context can be given in one word simultaneously.<br />
::::# Two or more meanings that do not agree but combine to make clear a complicated state of mind in the author.<br />
::::# When the "author is discovering his idea in the act of writing..." Empson describes a simile that lies halfway between two statements made by the author.<br />
::::# When a statement says nothing and the readers are forced to invent a statement of their own, most likely in conflict with that of the author.<br />
::::# Two words that within context are opposites that expose a fundamental division in the author's mind.<br />
<br />
== Book ==<br />
::::* https://www.londonreviewbookshop.co.uk/stock/seven-types-of-ambiguity-william-empson<br />
<br />
{{Labeling<br />
|additional=Ambiguity crisis<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Ossa-Richardson_2019_Princeton_Univ_PressOssa-Richardson 2019 Princeton Univ Press2024-03-02T10:57:17Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Ossa-Richardson A (2019) A history of ambiguity. Princeton Univ Press https://doi.org/10.2307/j.ctv80cd3c.<br />
|info=[https://www.jstor.org/stable/j.ctv80cd3c Princeton Univ Press]<br />
|authors=Ossa-Richardson A<br />
|year=2019<br />
|journal=Princeton Univ Press<br />
|abstract=Ever since it was first published in 1930, William Empson'sSeven Types of Ambiguity has been perceived as a milestone in literary criticism-far from being an impediment to communication, ambiguity now seemed an index of poetic richness and expressive power. Little, however, has been written on the broader trajectory of Western thought about ambiguity before Empson; as a result, the nature of his innovation has been poorly understood.<br />
<br />
A History of Ambiguity remedies this omission. Starting with classical grammar and rhetoric, and moving on to moral theology, law, biblical exegesis, German philosophy, and literary criticism, Anthony Ossa-Richardson explores the many ways in which readers and theorists posited, denied, conceptualised, and argued over the existence of multiple meanings in texts between antiquity and the twentieth century. This process took on a variety of interconnected forms, from the Renaissance delight in the 'elegance' of ambiguities in Horace, through the extraordinary Catholic claim that Scripture could contain multiple literal-and not just allegorical-senses, to the theory of dramatic irony developed in the nineteenth century, a theory intertwined with discoveries of the double meanings in Greek tragedy. Such narratives are not merely of antiquarian interest: rather, they provide an insight into the foundations of modern criticism, revealing deep resonances between acts of interpretation in disparate eras and contexts.A History of Ambiguity lays bare the long tradition of efforts to liberate language, and even a poet's intention, from the strictures of a single meaning.<br />
|editor=Gnaiger E<br />
}}<br />
== Selected quotes ==<br />
https://pup-assets.imgix.net/onix/images/9780691167954/9780691228440.pdf<br />
<br />
::::* Doubt and plurality, or plenty, are the twin poles of ambiguity as it is studied in this book. .. The perception of plenty in a word, in a line, in a poem, makes us doubt which meaning is the right one.<br />
<br />
::::* What Empson meant by ambiguity should not be taken for granted. His infamous definition is ‘any verbal nuance, however slight, which gives room for alternative reactions to the same piece of language’. .. A few pages later he specifies both the subjective and the objective, doubt and plenty: ‘Ambiguity’ itself can mean an indecision as to what you mean, an intention to mean several things, a probability that one or other or both of two things has been meant, and the fact that a statement has several meanings.<br />
<br />
::::* The emphasis on context to resolve apparent ambiguity is almost universal in works of classical hermeneutics, for instance in theology and law.<br />
<br />
::::* .. the basic unit of this history is not the ambiguous phrase but the act of seeing ambiguity in a phrase. <br />
<br />
{{Labeling<br />
|additional=Ambiguity crisis<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Donnelly_2024_EU-METAHEART_MC2_MeetingDonnelly 2024 EU-METAHEART MC2 Meeting2024-03-01T14:56:45Z<p>Plangger Mario: </p>
<hr />
<div>{{Abstract<br />
|title=Donnelly C, Komlódi T, Cecatto C, Cardoso LHD, Kayser B, Place N, Gnaiger E (2024) Functional hypoxia in cardiac mitochondria: effects on oxidative phosphorylation, mitochondrial membrane potential, redox state of coenzyme Q, and calcium uptake. EU-METAHEART MC2 Meeting 2024 Antalya TR.<br />
|info=[[EU-METAHEART]]<br />
|authors=Donnelly Chris, Komlodi Timea, Cecatto Cristiane, Cardoso Luiza HD, Kayser Bengt, Place Nicolas, Gnaiger Erich<br />
|year=2024<br />
|event=EU-METAHEART MC2 Meeting 2024 Antalya TR<br />
|abstract=How changes in respiration under functional hypoxia - i.e., when intracellular O<sub>2</sub> levels limit mitochondrial respiration [1] - are relayed by the electron transfer system to impact mitochondrial adaption and remodeling after hypoxic exposure remains poorly defined. This is largely due to challenges integrating findings under controlled and defined O<sub>2</sub> levels in studies of isolated mitochondria. Performing steady-state respirometry with isolated mouse cardiac mitochondria [2] we found that oxygen limitation of respiration reduced electron flow and oxidative phosphorylation, lowered the mitochondrial membrane potential difference, caused progressive reduction of coenzyme Q, and decreased mitochondrial calcium influx. Our results suggest that by regulating calcium uptake the mitochondrial electron transfer system is a hub for coordinating cellular adaption under functional hypoxia [3].<br />
|editor=[[Plangger M]]<br />
|mipnetlab=AT Innsbruck Oroboros, CH Lausanne Place N, AT Innsbruck Gnaiger E<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|injuries=Hypoxia<br />
|organism=Mouse<br />
|tissues=Heart<br />
|preparations=Isolated mitochondria<br />
|instruments=Oxygraph-2k<br />
}}<br />
== Affiliations ==<br />
<br />
<br />
== References ==<br />
::::#Donnelly C, Schmitt S, Cecatto C, Cardoso LHD, Komlódi T, Place N, Kayser B, Gnaiger E (2022) The ABC of hypoxia – what is the norm. Bioenerg Commun 2022.12.v2. https://doi.org/10.26124/bec:2022-0012.v2<br />
::::#Harrison DK, Fasching M, Fontana-Ayoub M, Gnaiger E (2015) Cytochrome redox states and respiratory control in mouse and beef heart mitochondria at steady-state levels of hypoxia. J Appl Physiol 119:1210-8. https://doi.org/10.1152/japplphysiol.00146.2015<br />
::::#Donnelly C, Komlódi T, Cecatto C, Cardoso LHD, Compagnion A-C, Matera A, Tavernari D, Campiche O, Paolicelli RC, Zanou N, Kayser B, Gnaiger E, Place N (2024) Functional hypoxia reduces mitochondrial calcium uptake. Redox Biol 71:103037. https://doi.org/10.1016/j.redox.2024.103037</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Ioannidis_2023_JAMAIoannidis 2023 JAMA2024-02-29T09:08:08Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Ioannidis JPA, Berkwits M, Flanagin A, Bloom T (2023) Peer review and scientific publication at a crossroads: call for research for the 10th International Congress on Peer Review and Scientific Publication. JAMA 330:1232-5. https://doi.org/10.1001/jama.2023.17607<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/37738041/ PMID: 37738041 Open Access]<br />
|authors=Ioannidis John PA, Berkwits M, Flanagin A, Bloom T<br />
|year=2023<br />
|journal=JAMA<br />
|abstract=The way science is assessed, published, and disseminated has markedly changed since 1986, when the launch of a new Congress focused on the science of peer review was first announced. There have been 9 International Peer Review Congresses since 1989, typically running on an every-4-year cycle, and most recently in 2022 after a 1-year delay due to the COVID-19 pandemic.1 Here, we announce that the 10th International Congress on Peer Review and Scientific Publication will be held in Chicago, Illinois, on September 3-5, 2025.<br />
|editor=Gnaiger E<br />
}}<br />
== Selected quotes ==<br />
<br />
::::* .. scientific publishing is a huge market with one of the highest profit margins among all business enterprises, ..<br />
<br />
::::* Careful testing of the many proposals to improve peer review and publication and of interventions and processes to address threats to their integrity in a rigorous and timely manner are essential to the future of science and the scholarly publishing enterprise.<br />
<br />
::::* The premise of all Peer Review Congresses is that peer review and scientific publication must be properly examined, tested, and corrected in the same way the scientific method and its products are applied, vetted, weighted, and interpreted.<br />
<br />
::::* Fixed articles vs evolving versions and innovations to support updating of scientific articles and reviews.<br />
<br />
{{Labeling}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Ioannidis_2022_PLoS_MedIoannidis 2022 PLoS Med2024-02-29T08:56:42Z<p>Gnaiger Erich: Created page with "{{Publication |title=Ioannidis JPA (2022) Correction: Why most published research findings are false. PLoS Med 19:e1004085. https://doi.org/10.1371/journal.pmed.1004085. Errat..."</p>
<hr />
<div>{{Publication<br />
|title=Ioannidis JPA (2022) Correction: Why most published research findings are false. PLoS Med 19:e1004085. https://doi.org/10.1371/journal.pmed.1004085. Erratum for: PLoS Med 2005 2:e124<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/36007233/ PMID: 36007233 Open Access]<br />
|authors=Ioannidis JPA<br />
|year=2022<br />
|journal=PLoS Med<br />
|abstract=This corrects the article https://doi.org/10.1371/journal.pmed.0020124.<br />
|editor=Gnaiger E<br />
}}<br />
{{Labeling}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Nizami_H_LNizami H L2024-02-28T08:35:09Z<p>Marinkovic Biljana: Marinkovic Biljana moved page Nizami H L to Nizami Hina Lateef</p>
<hr />
<div>{{Person<br />
|lastname=Nizami<br />
|firstname=Hina Lateef<br />
|title=<br />
|institution=Oklahoma Medical Research Foundation<br />
|address=825 N.E. 13th Street<br />
|area code=73104<br />
|city=Oklahoma City<br />
|state=Oklahoma (OK)<br />
|country=USA<br />
|mailaddress=Hina-Nizami@omrf.org<br />
}}<br />
{{Labelingperson}}<br />
== Participated at ==</div>Marinkovic Biljanahttps://wiki.oroboros.at/index.php/Laiz%C4%81ne_LLaizāne L2024-02-28T08:14:35Z<p>Marinkovic Biljana: Marinkovic Biljana moved page Laizāne L to Laizāne Linda</p>
<hr />
<div>{{Person<br />
|lastname=Laizāne<br />
|firstname=Linda<br />
|title=<br />
|institution=[[File:Linda Laizane.jpeg|right|180px|Linda Laizane]] Riga Stradins University, LV<br />
|address=16 Dzirciems street<br />
|area code=1007<br />
|city=Riga<br />
|country=Latvia<br />
|mailaddress=Linda.Laizane@rsu.lv<br />
}}<br />
{{Labelingperson}}<br />
<br />
== Participated at ==</div>Marinkovic Biljanahttps://wiki.oroboros.at/index.php/Cefis_2024_Acta_Physiol_(Oxf)Cefis 2024 Acta Physiol (Oxf)2024-02-27T13:17:02Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Cefis M, Dargegen M, Marcangeli V, Taherkhani S, Dulac M, Leduc-Gaudet JP, Mayaki D, Hussain SNA, Gouspillou G (2024) MFN2 overexpression in skeletal muscles of young and old mice causes a mild hypertrophy without altering mitochondrial respiration and H<sub>2</sub>O<sub>2</sub> emission. Acta Physiol (Oxf) [Epub ahead of print]. https://doi.org/10.1111/apha.14119<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38400630 PMID: 38400630 Open Access]<br />
|authors=Cefis Marina, Dargegen Manon, Marcangeli Vincent, Taherkhani Shima, Dulac Maude, Leduc-Gaudet Jean-Philippe, Mayaki Dominique, Hussain Sabah NA, Gouspillou Gilles<br />
|year=2024<br />
|journal=Acta Physiol (Oxf)<br />
|abstract=Sarcopenia, the aging-related loss of muscle mass and function, is a debilitating process negatively impacting the quality of life of affected individuals. Although the mechanisms underlying sarcopenia are incompletely understood, impairments in mitochondrial dynamics, including mitochondrial fusion, have been proposed as a contributing factor. However, the potential of upregulating mitochondrial fusion proteins to alleviate the effects of aging on skeletal muscles remains unexplored. We therefore hypothesized that overexpressing Mitofusin 2 (MFN2) in skeletal muscle ''in vivo'' would mitigate the effects of aging on muscle mass and improve mitochondrial function.<br />
<br />
MFN2 was overexpressed in young (7 mo) and old (24 mo) male mice for 4 months through intramuscular injections of an adeno-associated viruses. The impacts of MFN2 overexpression on muscle mass and fiber size (histology), mitochondrial respiration, and H<sub>2</sub>O<sub>2</sub> emission (Oroboros fluororespirometry), and various signaling pathways (qPCR and western blotting) were investigated.<br />
<br />
MFN2 overexpression increased muscle mass and fiber size in both young and old mice. No sign of fibrosis, necrosis, or inflammation was found upon MFN2 overexpression, indicating that the hypertrophy triggered by MFN2 overexpression was not pathological. MFN2 overexpression even reduced the proportion of fibers with central nuclei in old muscles. Importantly, MFN2 overexpression had no impact on muscle mitochondrial respiration and H<sub>2</sub>O<sub>2</sub> emission in both young and old mice. MFN2 overexpression attenuated the increase in markers of impaired autophagy in old muscles.<br />
<br />
MFN2 overexpression may be a viable approach to mitigate aging-related muscle atrophy and may have applications for other muscle disorders.<br />
|keywords=Autophagy, Mitochondria, Mitochondrial dynamics, Mitochondrial fusion, Mitofusin 2, Sarcopenia, Skeletal muscle aging<br />
|editor=[[Plangger M]]<br />
|mipnetlab=CA Montreal Gouspillou G<br />
}}<br />
{{Labeling<br />
|area=Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style<br />
|diseases=Aging;senescence<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, NS, ROX<br />
|instruments=Oxygraph-2k, O2k-Fluorometer<br />
|additional=2024-02, AmR<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Donnelly_2024_Redox_BiolDonnelly 2024 Redox Biol2024-02-25T09:47:22Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Donnelly C, Komlódi T, Cecatto C, Cardoso LHD, Compagnion A-C, Matera A, Tavernari D, Campiche O, Paolicelli RC, Zanou N, Kayser B, Gnaiger E, Place N (2024) Functional hypoxia reduces mitochondrial calcium uptake. Redox Biol 71:103037. https://doi.org/10.1016/j.redox.2024.103037<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38401291/ PMID: 38401291 Open Access]<br />
|authors=Donnelly Chris, Komlodi Timea, Cecatto Cristiane, Cardoso Luiza HD, Compagnion Anne-Claire, Matera Alessandro, Tavernari Daniele, Campiche Olivier, Paolicelli Rosa Chiara, Zanou Nadege, Kayser Bengt, Gnaiger Erich, Place Nicolas<br />
|year=2024<br />
|journal=Redox Biol<br />
|abstract=Mitochondrial respiration extends beyond ATP generation, with the organelle participating in many cellular and physiological processes. Parallel changes in components of the mitochondrial electron transfer system with respiration render it an appropriate hub for coordinating cellular adaption to changes in oxygen levels. How changes in respiration under functional hypoxia (i.e., when intracellular O<sub>2</sub> levels limit mitochondrial respiration) are relayed by the electron transfer system to impact mitochondrial adaption and remodeling after hypoxic exposure remains poorly defined. This is largely due to challenges integrating findings under controlled and defined O<sub>2</sub> levels in studies connecting functions of isolated mitochondria to humans during physical exercise. Here we present experiments under conditions of hypoxia in isolated mitochondria, myotubes and exercising humans. Performing steady-state respirometry with isolated mitochondria we found that oxygen limitation of respiration reduced electron flow and oxidative phosphorylation, lowered the mitochondrial membrane potential difference, and decreased mitochondrial calcium influx. Similarly, in myotubes under functional hypoxia mitochondrial calcium uptake decreased in response to sarcoplasmic reticulum calcium release for contraction. In both myotubes and human skeletal muscle this blunted mitochondrial adaptive responses and remodeling upon contractions. Our results suggest that by regulating calcium uptake the mitochondrial electron transfer system is a hub for coordinating cellular adaption under functional hypoxia.<br />
|editor=Gnaiger E<br />
|mipnetlab=AT Innsbruck Oroboros, CH Lausanne Place N<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|injuries=Hypoxia<br />
|organism=Human, Mouse<br />
|tissues=Heart, Skeletal muscle<br />
|preparations=Intact organism, Isolated mitochondria, Intact cells<br />
|topics=Calcium, mt-Membrane potential, Oxygen kinetics, Redox state<br />
|couplingstates=LEAK, OXPHOS, ET<br />
|pathways=N, S, NS, ROX<br />
|instruments=Oxygraph-2k, O2k-Fluorometer, Ca, NextGen-O2k<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Meszaros_2024_Transpl_IntMeszaros 2024 Transpl Int2024-02-23T07:49:21Z<p>Gnaiger Erich: </p>
<hr />
<div>{{Publication<br />
|title=Meszaros AT, Weissenbacher A, Schartner M, Egelseer-Bruendl T, Hermann M, Unterweger J, Mittelberger C, Reyer BA, Hofmann J, Zelger BG, Hautz T, Resch T, Margreiter C, Maglione M, Komlódi T, Ulmer H, Cardini B, Troppmair J, Öfner D, Gnaiger E, Schneeberger S, Oberhuber R (2024) The predictive value of graft viability and bioenergetics testing towards the outcome in liver transplantation. Transpl Int 37. https://doi.org/10.3389/ti.2024.12380<br />
|info=[https://www.frontierspartnerships.org/articles/10.3389/ti.2024.12380/full?&utm_source=Email_to_authors_&utm_medium=Email&utm_content=T1_11.5e1_author&utm_campaign=Email_publication&field=&journalName=Transplant_International&id=12380 Open Access]<br />
|authors=Meszaros AT, Weissenbacher A, Schartner Melanie, Egelseer-Bruendl T, Hermann M, Unterweger J, Mittelberger C, Reyer BA, Hofmann Julia, Zelger BG, Hautz T, Resch T, Margreiter C, Maglione M, Komlodi Timea, Ulmer H, Cardini B, Troppmair J, Oefner D, Gnaiger Erich, Schneeberger Stefan, Oberhuber R<br />
|year=2024<br />
|journal=Transpl Int<br />
|abstract=Donor organ biomarkers with sufficient predictive value in liver transplantation (LT) are lacking. We herein evaluate liver viability and mitochondrial bioenergetics for their predictive capacity towards the outcome in LT. We enrolled 43 consecutive patients undergoing LT. Liver biopsy samples taken upon arrival after static cold storage were assessed by histology, real-time confocal imaging analysis (RTCA), and high-resolution respirometry (HRR) for mitochondrial respiration of tissue homogenates. Early allograft dysfunction (EAD) served as primary endpoint. HRR data were analysed with a focus on the efficacy of ATP production or ''P''-''L'' control efficiency, calculated as 1-''L''/''P'' from the capacity of oxidative phosphorylation ''P'' and non-phosphorylating respiration ''L''. Twenty-two recipients experienced EAD. Pre-transplant histology was not predictive of EAD. The mean RTCA score was significantly lower in the EAD cohort (−0.75 ± 2.27) compared to the IF cohort (0.70 ± 2.08; ''p'' = 0.01), indicating decreased cell viability. ''P''-''L'' control efficiency was predictive of EAD (0.76 ± 0.06 in IF vs. 0.70 ± 0.08 in EAD-livers; ''p'' = 0.02) and correlated with the RTCA score. Both RTCA and ''P''-''L'' control efficiency in biopsy samples taken during cold storage have predictive capacity towards the outcome in LT. Therefore, RTCA and HRR should be considered for risk stratification, viability assessment, and bioenergetic testing in liver transplantation.<br />
|editor=Gnaiger E<br />
|mipnetlab=AT Innsbruck Schneeberger S, AT Innsbruck Oroboros<br />
}}<br />
{{Labeling<br />
|area=Respiration, mt-Medicine, Patients<br />
|diseases=Other<br />
|injuries=Ischemia-reperfusion<br />
|organism=Human<br />
|tissues=Liver<br />
|preparations=Homogenate<br />
|topics=Coupling efficiency;uncoupling<br />
|couplingstates=LEAK, OXPHOS, ET<br />
|pathways=F, N, S, NS, ROX<br />
|instruments=Oxygraph-2k<br />
}}</div>Gnaiger Erichhttps://wiki.oroboros.at/index.php/Xiao_2024_Sci_AdvXiao 2024 Sci Adv2024-02-22T17:03:57Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Xiao L, Yin Y, Sun Z, Liu J, Jia Y, Yang L, Mao Y, Peng S, Xie Z, Fang L, Li J, Xie X, Gan Z (2024) AMPK phosphorylation of FNIP1 (S220) controls mitochondrial function and muscle fuel utilization during exercise. Sci Adv 10:eadj2752. https://doi.org/10.1126/sciadv.adj2752<br />
|info=[https://www.ncbi.nlm.nih.gov/pubmed/38324677 PMID: 38324677 Open Access]<br />
|authors=Xiao Liwei, Yin Yujing, Sun Zongchao, Liu Jing, Jia Yuhuan, Yang Likun, Mao Yan, Peng Shujun, Xie Zhifu, Fang Lei, Li Jingya, Xie Xiaoduo, Gan Zhenji<br />
|year=2024<br />
|journal=Sci Adv<br />
|abstract=Exercise-induced activation of adenosine monophosphate-activated protein kinase (AMPK) and substrate phosphorylation modulate the metabolic capacity of mitochondria in skeletal muscle. However, the key effector(s) of AMPK and the regulatory mechanisms remain unclear. Here, we showed that AMPK phosphorylation of the folliculin interacting protein 1 (FNIP1) serine-220 (S220) controls mitochondrial function and muscle fuel utilization during exercise. Loss of FNIP1 in skeletal muscle resulted in increased mitochondrial content and augmented metabolic capacity, leading to enhanced exercise endurance in mice. Using skeletal muscle-specific nonphosphorylatable FNIP1 (S220A) and phosphomimic (S220D) transgenic mouse models as well as biochemical analysis in primary skeletal muscle cells, we demonstrated that exercise-induced FNIP1 (S220) phosphorylation by AMPK in muscle regulates mitochondrial electron transfer chain complex assembly, fuel utilization, and exercise performance without affecting mechanistic target of rapamycin complex 1-transcription factor EB signaling. Therefore, FNIP1 is a multifunctional AMPK effector for mitochondrial adaptation to exercise, implicating a mechanism for exercise tolerance in health and disease.<br />
|editor=[[Plangger M]]<br />
|mipnetlab=CN Nanjing Gan Z<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, S<br />
|instruments=Oxygraph-2k<br />
|additional=2024-02, CN<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Hu_2024_Front_Endocrinol_(Lausanne)Hu 2024 Front Endocrinol (Lausanne)2024-02-21T14:40:16Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Hu Y, Fang B, Tian X, Wang H, Tian X, Yu F, Li T, Yang Z, Shi R (2024) Passive exercise is an effective alternative to HRT for restoring OVX induced mitochondrial dysfunction in skeletal muscle. Front Endocrinol (Lausanne) 15:1356312. https://doi.org/10.3389/fendo.2024.1356312<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38356957 PMID: 38356957 Open Access]<br />
|authors=Hu Yi, Fang Biqing, Tian Xu, Wang Haiwei, Tian Xiangyang, Yu Fangfang, Li Tao, Yang Zhijie, Shi Rengfei<br />
|year=2024<br />
|journal=Front Endocrinol (Lausanne)<br />
|abstract=Postmenopausal women are more prone to develop muscle weakness, which is strongly associated with impairment of mitochondrial function in skeletal muscle. This study aimed to examine the impact of a passive exercise modality, whole-body vibration training (WBVT), on muscle mitochondrial function in ovariectomized (OVX) mice, in comparison with 17β-estradiol (E<sub>2</sub>) replacement.<br />
<br />
Female C57BL/6J mice were assigned to four groups: sham operation control group (Sham), ovariectomized group (OVX), OVX with E<sub>2</sub> supplement group (OVX+E), and OVX with WBVT group (OVX+W). The estrous cycle, body weight, body composition, and muscle strength of the mice were monitored after the operation. Serum E<sub>2</sub> level was assessed by enzyme-linked immunosorbent assay (ELISA). The ATP levels were determined using a luciferase-catalyzed bioluminescence assay. The activity of mitochondrial respiration chain complexes was evaluated using high-resolution respirometry (O2K). Expression levels of oxidative phosphorylation (OXPHOS), peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and mitochondrial transcription factor A (TFAM) were detected using western blotting.<br />
<br />
We observed decreased muscle strength and impaired mitochondrial function in the skeletal muscle of OVX mice. The vibration training alleviated these impairments as much as the E<sub>2</sub> supplement. In addition, the vibration training was superior to the ovariectomy and the estradiol replacement regarding the protein expression of PGC-1α and TFAM.<br />
<br />
WBVT improves the OVX-induced decline in muscle strength and impairment of mitochondrial function in the skeletal muscle. This passive exercise strategy may be useful as an alternative to E<sub>2</sub> replacement for preventing menopausal muscular weakness. Further studies are needed to understand the effects of WBVT on various physiological systems, and precautions should be taken when implementing it in patient treatment.<br />
|keywords=17β-estradiol replacement, Hormone replacement therapy, Mitochondrial function, Muscle weakness, Ovariectomized mice, Passive exercise, Whole-body vibration training<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, S, CIV, NS, ROX<br />
|instruments=Oxygraph-2k<br />
|additional=2024-02, CN<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Opperdoes_2024_BMC_GenomicsOpperdoes 2024 BMC Genomics2024-02-21T13:15:31Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Opperdoes FR, Záhonová K, Škodová-Sveráková I, Bučková B, Chmelová Ľ, Lukeš J, Yurchenko V (2024) ''In silico'' prediction of the metabolism of ''Blastocrithidia nonstop'', a trypanosomatid with non-canonical genetic code. BMC Genomics 25:184. https://doi.org/10.1186/s12864-024-10094-8<br />
|info=[https://pubmed.ncbi.nlm.nih.gov/38365628 PMID: 38365628 Open Access]<br />
|authors=Opperdoes Fred R, Zahonova Kristina, Skodova-Sverakova Ingrid, Buckova Barbora, Chmelova Lubomira, Lukes Julius, Yurchenko Vyacheslav<br />
|year=2024<br />
|journal=BMC Genomics<br />
|abstract=Almost all extant organisms use the same, so-called canonical, genetic code with departures from it being very rare. Even more exceptional are the instances when a eukaryote with non-canonical code can be easily cultivated and has its whole genome and transcriptome sequenced. This is the case of ''Blastocrithidia nonstop'', a trypanosomatid flagellate that reassigned all three stop codons to encode amino acids.<br />
<br />
We ''in silico'' predicted the metabolism of ''B. nonstop'' and compared it with that of the well-studied human parasites ''Trypanosoma brucei'' and ''Leishmania major''. The mapped mitochondrial, glycosomal and cytosolic metabolism contains all typical features of these diverse and important parasites. We also provided experimental validation for some of the predicted observations, concerning, specifically presence of glycosomes, cellular respiration, and assembly of the respiratory complexes.<br />
<br />
In an unusual comparison of metabolism between a parasitic protist with a massively altered genetic code and its close relatives that rely on a canonical code we showed that the dramatic differences on the level of nucleic acids do not seem to be reflected in the metabolisms. Moreover, although the genome of ''B. nonstop'' is extremely AT-rich, we could not find any alterations of its pyrimidine synthesis pathway when compared to other trypanosomatids. Hence, we conclude that the dramatic alteration of the genetic code of ''B. nonstop'' has no significant repercussions on the metabolism of this flagellate.<br />
|keywords=Blastocrithidia, In silico, Metabolic predictions, Non-canonical genetic code, Trypanosomatid<br />
|editor=[[Plangger M]]<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|organism=Protists<br />
|preparations=Isolated mitochondria, Intact cells<br />
|couplingstates=LEAK, ROUTINE, OXPHOS, ET<br />
|pathways=S<br />
|instruments=Oxygraph-2k<br />
|additional=2024-02<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Al-Sabri_2024_Sci_RepAl-Sabri 2024 Sci Rep2024-02-20T13:54:58Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Al-Sabri MH, Ammar N, Korzh S, Alsehli AM, Hosseini K, Fredriksson R, Mwinyi J, Williams MJ, Boukhatmi H, Schiöth HB (2024) Fluvastatin-induced myofibrillar damage is associated with elevated ROS, and impaired fatty acid oxidation, and is preceded by mitochondrial morphological changes. https://doi.org/10.1038/s41598-024-53446-w<br />
|info=Sci Rep 14:3338. [https://pubmed.ncbi.nlm.nih.gov/38336990 PMID: 38336990 Open Access]<br />
|authors=Al-Sabri Mohamed H, Ammar Nourhane, Korzh Stanislava, Alsehli Ahmed M, Hosseini Kimia, Fredriksson Robert, Mwinyi Jessica, Williams Michael J, Boukhatmi Hadi, Schioeth Helgi B<br />
|year=2024<br />
|journal=Sci Rep<br />
|abstract=Previously, we showed that fluvastatin treatment induces myofibrillar damage and mitochondrial phenotypes in the skeletal muscles of ''Drosophila''. However, the sequential occurrence of mitochondrial phenotypes and myofibril damage remains elusive. To address this, we treated flies with fluvastatin for two and five days and examined their thorax flight muscles using confocal microscopy. In the two-day fluvastatin group, compared to the control, thorax flight muscles exhibited mitochondrial morphological changes, including fragmentation, rounding up and reduced content, while myofibrils remained organized in parallel. In the five-day fluvastatin treatment, not only did mitochondrial morphological changes become more pronounced, but myofibrils became severely disorganized with significantly increased thickness and spacing, along with myofilament abnormalities, suggesting myofibril damage. These findings suggest that fluvastatin-induced mitochondrial changes precede myofibril damage. Moreover, in the five-day fluvastatin group, the mitochondria demonstrated elevated H<sub>2</sub>O<sub>2</sub> and impaired fatty acid oxidation compared to the control group, indicating potential mitochondrial dysfunction. Surprisingly, knocking down Hmgcr (''Drosophila'' homolog of HMGCR) showed normal mitochondrial respiration in all parameters compared to controls or five-day fluvastatin treatment, which suggests that fluvastatin-induced mitochondrial dysfunction might be independent of Hmgcr inhibition. These results provide insights into the sequential occurrence of mitochondria and myofibril damage in statin-induced myopathy for future studies.<br />
|editor=[[Plangger M]]<br />
|mipnetlab=LV Riga Liepins E<br />
}}<br />
{{Labeling<br />
|area=Respiration, Pharmacology;toxicology<br />
|organism=Drosophila<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|couplingstates=LEAK, OXPHOS, ET<br />
|pathways=F, N, S, Gp, NS, ROX<br />
|instruments=Oxygraph-2k, O2k-Fluorometer<br />
|additional=2023-02, AmR<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/14th_Mitochondrial_Disease_Conference_2024_Padova_IT14th Mitochondrial Disease Conference 2024 Padova IT2024-02-20T12:08:22Z<p>Marinkovic Biljana: </p>
<hr />
<div>{{MitoGlobal header page name}}<br />
<br />
{{Publication<br />
|title='''Padova IT''', 2024 Oct 25-27. 14th Mitochondrial Disease Conference<br />
|info= [https://www.mitocon.it/convegno-nazionale-sulle-malattie-mitocondriali/ Conference website]<br />
|authors= tba<br />
|year=2024-10-25<br />
|journal=MitoGlobal<br />
|abstract= tba<br />
}}<br />
<br />
== Venue ==<br />
:::: BW Plus Hotel Galileo Padova, IT<br />
:::: Via Venezia 30 - 35131 - Padova<br />
<br />
== Program ==<br />
:::: tba<br />
<br />
== Oroboros at 14th Mitochondrial Disease Conference ==<br />
:::: [[Gnaiger Erich|Erich Gnaiger]]: Working title: High-resolution diagnostics of mitochondrial function in liquid biopsies<br />
<br />
<br />
{{Labeling<br />
|additional=2024, MitoGlobal, ORO, Next<br />
}}<br />
<br />
<br />
[[Image:MitoGlobal.jpg|right|80px|link=http://www.bioblast.at/index.php/MitoGlobal|MitoGlobal]] <br />
Listed under [[MitoGlobal Events]].</div>Marinkovic Biljanahttps://wiki.oroboros.at/index.php/Fehsenfeld_2024_Comp_Biochem_Physiol_A_Mol_Integr_PhysiolFehsenfeld 2024 Comp Biochem Physiol A Mol Integr Physiol2024-02-19T15:58:19Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Fehsenfeld S, Yoon GR, Quijada-Rodriguez AR, Kandachi-Toujas H, Calosi P, Breton S, Weihrauch D (2024) Short-term exposure to high pCO<sub>2</sub> leads to decreased branchial cytochrome C oxidase activity in the presence of octopamine in a decapod. https://doi.org/10.1016/j.cbpa.2024.111603<br />
|info=Comp Biochem Physiol A Mol Integr Physiol [Epub ahead of print]. [https://www.ncbi.nlm.nih.gov/pubmed/38346534 PMID: 38346534 Open Access]<br />
|authors=Fehsenfeld Sandra, Yoon Gwangseok R, Quijada-Rodriguez Alex R, Kandachi-Toujas Haluka, Calosi Piero, Breton Sophie, Weihrauch Dirk<br />
|year=2024<br />
|journal=Comp Biochem Physiol A Mol Integr Physiol<br />
|abstract=In a recent mechanistic study, octopamine was shown to promote proton transport over the branchial epithelium in green crabs, Carcinus maenas. Here, we follow up on this finding by investigating the involvement of octopamine in an environmental and physiological context that challenges acid-base homeostasis, the response to short-term high pCO2 exposure (400 Pa) in a brackish water environment. We show that hyperregulating green crabs experienced a respiratory acidosis as early as 6 h of exposure to hypercapnia, with a rise in hemolymph pCO2 accompanied by a simultaneous drop of hemolymph pH. The slightly delayed increase in hemolymph HCO3- observed after 24 h helped to restore hemolymph pH to initial values by 48 h. Circulating levels of the biogenic amine octopamine were significantly higher in short-term high pCO2 exposed crabs compared to control crabs after 48 h. Whole animal metabolic rates, intracellular levels of octopamine and cAMP, as well as branchial mitochondrial enzyme activities for complex I + III and citrate synthase were unchanged in posterior gill #7 after 48 h of hypercapnia. However, application of octopamine in gill respirometry experiments suppressed branchial metabolic rate in posterior gills of short-term high pCO2 exposed animals. Furthermore, branchial enzyme activity of cytochrome C oxidase decreased in high pCO2 exposed crabs after 48 h. Our results indicate that hyperregulating green crabs are capable of quickly counteracting a hypercapnia-induced respiratory acidosis. The role of octopamine in the acclimation of green crabs to short-term hypercapnia seems to entail the alteration of branchial metabolic pathways, possibly targeting mitochondrial cytochrome C in the gill. Our findings help advancing our current limited understanding of endocrine components in hypercapnia acclimation. SUMMARY STATEMENT: Acid-base compensation upon short-term high pCO2 exposure in hyperregulating green crabs started after 6 h and was accomplished by 48 h with the involvement of the biogenic amine octopamine, accumulation of hemolymph HCO3-, and regulation of mitochondrial complex IV (cytochrome C oxidase).<br />
|keywords=Acid-base homeostasis, Biogenic amine, Carcinus maenas, Enzyme activity, Gill, Green crab, Hypercapnia, Mitochondria, cAMP<br />
|editor=[[Plangger M]]<br />
|mipnetlab=CA Montreal Breton S<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|instruments=Oxygraph-2k<br />
|additional=2024-02<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Brunetta_2024_MitoFitBrunetta 2024 MitoFit2024-02-15T08:56:02Z<p>Cardoso Luiza: </p>
<hr />
<div>{{Publication<br />
|title=Brunetta HS, Holloway GP (2024) Methodological considerations for the determination of mitochondrial ADP sensitivity in skeletal muscle. MitoFit Preprints 2024. 1. https://doi.org/10.26124/mitofit:2024-0001<br />
|info=MitoFit Preprints 2024.1. [[File:MitoFit Preprints pdf.png|left|160px|link=https://wiki.oroboros.at/images/8/84/Brunetta_2024_MitoFit.pdf|MitoFit pdf]] [https://wiki.oroboros.at/images/8/84/Brunetta_2024_MitoFit.pdf Methodological considerations for the determination of mitochondrial ADP sensitivity in skeletal muscle]<br/><br />
|authors=Brunetta Henver Simionato, Holloway Graham P<br />
|year=2024<br />
|journal=MitoFit Prep<br />
|abstract=In skeletal muscle, mitochondria adapt to physiological (i.e. exercise, aging) and pathological scenarios (i.e. insulin resistance, muscle atrophy). Due to the kinetic regulation by adenylates within the oxidative phosphorylation system, a small increase in free ADP (f[ADP]) within the cell results in a rapid compensatory increment in ATP production and oxygen consumption, conferring to mitochondria the unique ability to detect, and respond, to small changes in the energetic status of the cells. The advent of high-resolution oxygraphy potentiated the studies on mitochondrial bioenergetics where it is now possible to record mitochondrial O<sub>2</sub> consumption in real-time with high sensitivity in various tissues and substrate protocols. While most of the studies rely on saturating concentrations of substrates and ADP to test the maximal respiratory capacity of mitochondria, such approaches may not fully recapitulate physiological conditions by which these organelles are exposed within skeletal muscle cells. Over the years, we and others have employed a mitochondrial ADP sensitivity assay, where we determine mitochondrial bioenergetic responses to a wide range of ADP concentrations, scaling from the physiological levels found in resting skeletal muscle cells (μM) to saturating values (mM). Here, we reviewed this methodology by offering practical guidance and insights from experiments performed in our laboratory, as well as examples of the applicability of such a protocol. <br><br />
|keywords=mitochondrion, bioenergetics, oxidative phosphorylation, metabolism<br />
|editor=[[Tindle-Solomon Lisa]]<br />
|mipnetlab=CA Guelph Holloway GP<br />
}}<br />
{{Labeling<br />
|area=Respiration<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|topics=ADP<br />
|pathways=N, NS<br />
}}</div>Tindle Lisahttps://wiki.oroboros.at/index.php/Fitzgerald_2024_J_Cachexia_Sarcopenia_MuscleFitzgerald 2024 J Cachexia Sarcopenia Muscle2024-02-14T15:07:52Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Fitzgerald LF, Lackey J, Moussa A, Shah SV, Castellanos AM, Khan S, Schonk M, Thome T, Salyers ZR, Jakkidi N, Kim K, Yang Q, Hepple RT, Ryan TE (2024) Chronic aryl hydrocarbon receptor activity impairs muscle mitochondrial function with tobacco smoking. https://doi.org/10.1002/jcsm.13439<br />
|info=J Cachexia Sarcopenia Muscle [Epub ahead of print]. [https://pubmed.ncbi.nlm.nih.gov/38333944 PMID: 38333944 Open Access]<br />
|authors=Fitzgerald Liam F, Lackey Jacob, Moussa Ahmad, Shah Sohan V, Castellanos Ana Maria, Khan Shawn, Schonk Martin, Thome Trace, Salyers Zachary R, Jakkidi Nishka, Kim Kyoungrae, Yang Qinping, Hepple Russell T, Ryan Terence E<br />
|year=2024<br />
|journal=J Cachexia Sarcopenia Muscle<br />
|abstract=Accumulating evidence has demonstrated that chronic tobacco smoking directly contributes to skeletal muscle dysfunction independent of its pathological impact to the cardiorespiratory systems. The mechanisms underlying tobacco smoke toxicity in skeletal muscle are not fully resolved. In this study, the role of the aryl hydrocarbon receptor (AHR), a transcription factor known to be activated with tobacco smoke, was investigated.<br />
<br />
AHR related gene (mRNA) expression was quantified in skeletal muscle from adult controls and patients with chronic obstructive pulmonary disease (COPD), as well as mice with and without cigarette smoke exposure. Utilizing both skeletal muscle-specific AHR knockout mice exposed to chronic repeated (5 days per week for 16 weeks) cigarette smoke and skeletal muscle-specific expression of a constitutively active mutant AHR in healthy mice, a battery of assessments interrogating muscle size, contractile function, mitochondrial energetics, and RNA sequencing were employed.<br />
<br />
Skeletal muscle from COPD patients (N = 79, age = 67.0 ± 8.4 years) had higher levels of AHR (P = 0.0451) and CYP1B1 (P < 0.0001) compared to healthy adult controls (N = 16, age = 66.5 ± 6.5 years). Mice exposed to cigarette smoke displayed higher expression of Ahr (P = 0.008), Cyp1b1 (P < 0.0001), and Cyp1a1 (P < 0.0001) in skeletal muscle compared to air controls. Cigarette smoke exposure was found to impair skeletal muscle mitochondrial oxidative phosphorylation by ~50% in littermate controls (Treatment effect, P < 0.001), which was attenuated by deletion of the AHR in muscle in male (P = 0.001), but not female, mice (P = 0.37), indicating there are sex-dependent pathological effects of smoking-induced AHR activation in skeletal muscle. Viral mediated expression of a constitutively active mutant AHR in the muscle of healthy mice recapitulated the effects of cigarette smoking by decreasing muscle mitochondrial oxidative phosphorylation by ~40% (P = 0.003).<br />
<br />
These findings provide evidence linking chronic AHR activation secondary to cigarette smoke exposure to skeletal muscle bioenergetic deficits in male, but not female, mice. AHR activation is a likely contributor to the decline in muscle oxidative capacity observed in smokers and AHR antagonism may provide a therapeutic avenue aimed to improve muscle function in COPD.<br />
|keywords=Atrophy, Cigarette, Dioxin, Skeletal muscle<br />
|editor=[[Plangger M]]<br />
|mipnetlab=US FL Gainesville Hepple RT, US FL Gainesville Ryan TE<br />
}}<br />
{{Labeling<br />
|area=Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style<br />
|diseases=COPD<br />
|organism=Mouse<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue, Isolated mitochondria<br />
|topics=PCr;Cr<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, CIV, NS, ROX<br />
|instruments=Oxygraph-2k, O2k-Fluorometer<br />
|additional=2024-02<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/J_Sport_Health_SciJ Sport Health Sci2024-02-14T13:58:41Z<p>Plangger Mario: Created page with "{{Journal |Title=[https://www.sciencedirect.com/journal/journal-of-sport-and-health-science Journal of Sport and Health Science] }}"</p>
<hr />
<div>{{Journal<br />
|Title=[https://www.sciencedirect.com/journal/journal-of-sport-and-health-science Journal of Sport and Health Science]<br />
}}</div>Plangger Mariohttps://wiki.oroboros.at/index.php/Qiao_2024_J_Sport_Health_SciQiao 2024 J Sport Health Sci2024-02-14T13:57:58Z<p>Plangger Mario: </p>
<hr />
<div>{{Publication<br />
|title=Qiao YS, Blackwell TL, Cawthon PM, Coen PM, Cummings SR, Distefano G, Farsijani S, Forman DE, Goodpaster BH, Kritchevsky SB, Mau T, Toledo FGS, Newman AB, Glynn NW (2024) Associations of accelerometry-measured and self-reported physical activity and sedentary behavior with skeletal muscle energetics: The Study of Muscle, Mobility and Aging (SOMMA). https://doi.org/10.1016/j.jshs.2024.02.001<br />
|info=J Sport Health Sci [Epub ahead of print]. [https://pubmed.ncbi.nlm.nih.gov/38341136 PMID: 38341136 Open Access]<br />
|authors=Qiao Yujia Susanna, Blackwell Terri L, Cawthon Peggy M, Coen Paul M, Cummings Steven R, Distefano Giovanna, Farsijani Samaneh, Forman Daniel E, Goodpaster Bret H, Kritchevsky Stephen B, Mau Theresa, Toledo Frederico GS, Newman Anne B, Glynn Nancy W<br />
|year=2024<br />
|journal=J Sport Health Sci<br />
|abstract=Skeletal muscle energetics decline with age, and physical activity (PA) has been shown to offset these declines in older adults. Yet, many studies reporting these effects were based on self-reported PA or structured exercise interventions. Therefore, we examined the associations of accelerometry-measured and self-reported PA and sedentary behavior (SB) with skeletal muscle energetics and explored the extent to which PA and SB would attenuate the associations of age with muscle energetics.<br />
<br />
As part of the Study of Muscle, Mobility and Aging (SOMMA), enrolled older adults (n = 879), 810 (mean ± SD age = 76 ± 5 years old; 58% women) had maximal muscle oxidative capacity measured ''ex vivo'' via high-resolution respirometry of permeabilized myofibers (maximal oxidative phosphorylation (maxOXPHOS)) and ''in vivo'' by <sup>31</sup>Phosphorus magnetic resonance spectroscopy (maximal adenosine triphosphate (ATP<sub>max</sub>)). Accelerometry-measured SB, light activity, and moderate-to-vigorous PA (MVPA) were assessed using a wrist-worn ActiGraph GT9X over 7 days. Self-reported SB, MVPA, and all physical activity were assessed with the Community Healthy Activities Model Program for Seniors (CHAMPS) questionnaire. Linear regression models with progressive covariate adjustments evaluated the associations of SB and PA with muscle energetics as well as the attenuation of the age/muscle energetics association by MVPA and SB. As a sensitivity analysis, we also examined activPAL-measured daily step count and time spent in SB and their associations with muscle energetics.<br />
<br />
Every 30 min/day more of ActiGraph-measured MVPA was associated with 0.65 pmol/s × mg higher maxOXPHOS and 0.012 mM/s higher ATP<sub>max</sub> after adjusting for age, site/technician, and sex (p < 0.05). Light activity was not associated with maxOXPHOS or ATP<sub>max</sub>. Meanwhile, every 30 min/day spent in ActiGraph-measured SB was associated with 0.39 pmol/s × mg lower maxOXPHOS and 0.006 mM/s lower ATP<sub>max</sub> (p < 0.05). Only associations with ATP<sub>max</sub> held after further adjusting for socioeconomic status, body mass index, lifestyle factors, and multimorbidity. CHAMPS MVPA and all physical activity yielded similar associations with maxOXPHOS and ATP<sub>max</sub> (p < 0.05), but SB did not. Higher activPAL step count was associated with higher maxOXHPOS and ATP<sub>max</sub> (p < 0.05), but time spent in SB was not. Additionally, age was significantly associated with muscle energetics for men only (P < 0.05); adjusting for time spent in ActiGraph-measured MVPA attenuated the age association with ATP<sub>max</sub> by 58% in men.<br />
<br />
More time spent in accelerometry-measured or self-reported daily PA, especially MVPA, was associated with higher skeletal muscle energetics. Interventions aimed specifically at increasing higher intensity activity might offer potential therapeutic interventions to slow age-related decline in muscle energetics. Our work also emphasizes the importance of taking PA into consideration when evaluating associations related to skeletal muscle energetics.<br />
|keywords=Aging, Exercise, Mitochondria<br />
|editor=[[Plangger M]]<br />
|mipnetlab=US FL Orlando Goodpaster BH, US PA Pittsburgh DeLany JP<br />
}}<br />
{{Labeling<br />
|area=Respiration, Exercise physiology;nutrition;life style<br />
|diseases=Aging;senescence<br />
|organism=Human<br />
|tissues=Skeletal muscle<br />
|preparations=Permeabilized tissue<br />
|couplingstates=LEAK, OXPHOS<br />
|pathways=N, NS<br />
|instruments=Oxygraph-2k<br />
|additional=2024-02<br />
}}</div>Plangger Mario