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4
4th edition Metabolism & Cancer, Virtual, 2021
== Program ==
:::: [https://www.metabolism-cancer.com/program/ here]
== Organizers ==
:::: The list of organizers can be found [https://www.metabolism-cancer.com/under-construction/ here]
== Registration ==
:::: [https://www.metabolism-cancer.com/registration/ Registration and more information]
== Oroboros at MetaboCancer 2021==
:::: [[Gnaiger Erich]]: Oroboros Instruments innovations - NextGen-O2k and Bioenergetics Communications, ''May 28th at 11:25''
=== Booth ===
:::: The Oroboros team is looking forward to welcome you at our Oroboros booth which will be available at this conference.
== Support ==
[[File:Template NextGen-O2k.jpg|right|350px|link=NextGen-O2k]]
[[Category:NextGen-O2k]]
:::: Supported by project NextGen-O2k which has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 859770.
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5
5th Academic Symposium of Metabolic Biology Branch of Chinese Biophysical Society, Zunyi, China, 2022 +
5th International Mitochondrial Medicine Conference Mitochondrial, Online, 2021 +
5th edition Metabolism & Cancer, Nice, France, 2023
== Venue ==
:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 How to get there]
== Program ==
:::: Program available [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]
== Organizers ==
:::: The list of organizers can be found [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]
== Registration ==
:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 Registration and more information] +
6
6th Annual Conference of Chinese Society for Neurobiological Control of Metabolism 2024 Quanzhou CN +
6<sup>th</sup> Annual Conference of Chinese Society for Neurobiological Control of Metabolism, Quanzhou, China, 2024 +
6th Biannual Meeting on Mitochondria Apoptosis & Cancer, Prague, Czech Republic, 2019 +
6th EU-Cardioprotection WG Meeting CA16625 on mito and metabolism as targets for cardioprotection., Virtual Event, 2021 +
6th International Conference on Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging and Therapeutic Targets, Chania, Crete, Greece, 2019 +
6th Research Day, Innsbruck, Austria, 2023 +
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77th Annual Meeting of the Japanese Cancer Association at the Osaka International Convention Center and RIHGA, Osaka, Japan, 2018 +
7th European Phycological Congress, Zagreb, Croatia, 2019 +
7th Molecular Mechanisms of Axon Degeneration Meeting, Loch Lomond, Scotland, Great Britain, 2019 +
7th World Congress on Targeting Microbiota, Krakow, Poland, 2019
== Venue ==
:::: Park Inn by Radisson Krakow Hotel
:::: Ul. Monte Cassino 2 PL
:::: 30337 - Krakow - Poland
:::: [https://www.microbiota-site.com/venue.html More information]
== Organizer ==
:::: [https://www.microbiota-site.com/committee.html Information available here]
== Programme ==
:::: [https://www.microbiota-site.com/images/2019/PDF/Targeting_Microbiota_2019_Agenda_-_V7.pdf Agenda]
== Speakers ==
:::: List of speakers can be found [https://www.microbiota-site.com/microbiota-2019-speakers.html here]
== Registration ==
:::: [https://www.microbiota-site.com/registrations.html Registration and more information] +
8
8th SMRM and Mitochondria-Metabolism Network Meeting, Pune, India, 2020
== General information ==
:::: Flyer available for [https://www.mitoeagle.org/images/b/b2/8th_SMRM_and_Mitochondria-Metabolism_Network_Meeting_Poster.pdf download]
== Venue ==
:::: Indian Institute of Science Education and Research (ISER Pune)
:::: Dr. Homi Bhabha Road
:::: Pashan, Pune 411 008
:::: INDIA
::::[http://www.iiserpune.ac.in/facilities/guesthouse-cum-convention-centre Hotel and Travel]
== Programme ==
:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=12&confId=7288 here]
== Speakers ==
:::: List of speakers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=0&confId=7288 here]
== Organizers ==
:::: The list of organizers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=9&confId=7288 here]
== Registration ==
:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=6&confId=7288 Registration and more information] +
9
9th ÖGMBT Annual Meeting & 8th Life Science Meeting, Innsbruck, Austria +
A
46<sup>th</sup> All India Cell Biology Conference, Navi Mumbai, India, 2024 +
AlgaEurope 2018, Amsterdam, Netherlands, 2018 +
z-Scores were devised to provide a transparent but widely-applicable scoring system for participants in proficiency tests for analytical laboratories. The essential idea is to provide an appropriate scaling of the difference between a participant’s result and the ‘assigned value’ for the concentration of the analyte. Interpretation of a z-score is straightforward but some aspects need careful attention to avoid misconception. Over time several related scores have been devised to cope with a diversified range of applications. The main types of score have recently been codified in ISO 13528 (2015). +
64<sup>th</sup> Annual International Conference of the Associate of Microbiologists of India, Jhansi, India, 2023 +
'''APS Conference: Physiological Bioenergetics: Mitochondria from Bench to Bedside, Bioenergetics17'''. San Diego CA, USA; 2017 August. +
32nd APS Annual Convention, Chicago, USA, 2020 +
AVRO - Association for Research in Vision and Ophthalmology, Honolulu, Hawaii, USA, 2018 +
Joint ASMRM and J-mit Conference, Fukuoka, Japan, 2019 +
9<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine and 5<sup>th</sup> Conference of Chinese Society of Mitochondrial Research and Medicine (Chinese-Mit), [http://asmrm2012.csp.escience.cn/dct/page/65540 ASMRM 2012], Bejing CN +
10<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine - [http://asmrm2013.com/common_files/mess.asp ASMRM 2013], Seoul KR +
12<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine - [http://www.ig.zju.edu.cn/ASMRM/EN/ ASMRM 2015], Hangzhou CN +
[[File:ASMRM2016.jpg|500px|right]]
'''13<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine and the 16<sup>th</sup> Conference of the Japanese Society of Mitochondrial Research and Medicine (J-mit). The world of mitochondrial diseases: Their diversity and heterogeneity. Shinagawa JP.''' +
'''14<sup>th</sup>Conference of the Asian Society of Mitochondrial Research and Medicine'''. Xi'an, Shaanxi, China; 2017 September. +
15th Conference of the Asian Society of Mitochondrial Research and Medicine, Busan, South Korea, 2018. +
ASMRM 2020, Singapore, SG, 2021 +
ATSPB 2023, Hall in Tirol, Austria, 2023 +
Endurance exercise on a regular basis induces skeletal and cardiac muscle performance adaptation, lower mean arterial blood pressure and metabolic adaptation in a number of organs [1,2]. The latter has been shown to involve mitochondrial biogenesis. Upon injury when training intensity decreases, as well as in aging, these events tend to reverse [2,3]. The aim of the present study was to investigate whether the level of aerobic performance affects mitochondrial respiration in platelets.
Six male and female athletes were subjected to magnetic resonance imaging (MRI) of the heart and blood sampling within three days following an anterior cruciate ligament (ACL) injury. An initial follow-up was performed at the start of rehabilitation training and a late follow up at eight months following injury. The latter exams also included a maximal incremental exercise test with gas analysis. Platelets were isolated by centrifugation and mitochondrial respiration was analyzed using a substrate-uncoupler-inhibitor-protocol.
The total heart volume (THV) was significantly lower following the period of reduced exercise intensity from the time of injury to initial follow-up (p = 0.042, n = 6). There was no significant difference in THV between initial and late follow-up. The maximal ''V''<sub>O2</sub> uptake showed a trend toward increase from initial to late follow-up (p = 0.086, n = 4). There were, however, no significant differences or any discernable trends in respiratory parameters between the time points studied.
In conclusion, there was no difference in platelet mitochondrial respiration in response to alterations in exercise level in this small pilot study. +
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
Within a drug discovery program derived from a project for a pharmacological treatment of mitochondrial complex I deficiency, we have developed cell-permeable prodrugs of succinate (NV118) and malonate (NV161) suitable for research use in intact cells. Succinate is an intermediate of the Krebs’ cycle and acts as mitochondrial energy substrate by providing reducing equivalents to complex II (succinate dehydrogenase) of the mitochondrial oxidative phosphorylation pathway. As succinate is converted to malate by complex II, electrons are transferred down the pathway leading to proton pumping and ATP-synthesis. Succinate, as a dicarboxylic acid, is not cell-permeable and for exogenous succinate to enter cells the cell membrane requires permeabilization, using e.g. digitonin or perfringolysin. NV118 allows the researcher to deliver succinate to the cytoplasm without disrupting the plasma membrane. Malonate is a competitive inhibitor of complex II that binds to the active site of succinate dehydrogenase, thus preventing succinate from being metabolized. Like succinate, malonate is a dicarboxylic acid that does not readily permeate through the cell membrane. By using the same prodrug strategy as for NV118, the cell-permeable analogue of malonate, NV161, has been synthesized. NV118 and NV161 are rapidly metabolized, likely by the action of carboxyesterases, releasing succinate and malonate respectively.
Cell-permeable succinate and malonate were tested in a range of human cells and tissues, such as blood cells, fibroblasts, immortalized liver cells and human heart fibers either in the Oroboros O2k-FluoRespirometer (Oroboros Instruments, Innsbruck, Austria) or in the Seahorse Bioscience XFe96 Extracellular Flux Analyser (Seahorse Bioscience, North Billerica, USA). Dose-response curves for both prodrugs were obtained in human complex I inhibited platelets and primary fibroblasts.
NV118 and NV161 dose-dependently support and inhibit succinate-linked mitochondrial respiration in intact human platelets and fibroblasts. NV161 completely inhibits succinate-linked mitochondrial respiration at about ten times lower concentration as compared to malonate. Dimethyl succinate and dimethyl malonate have previously been reported to be cell-permeable, but did not show strong evidence of efficient cell penetration in this study.
We believe that NV118 and NV161 may prove valuable as scientific tools in mitochondrial research, enabling evaluation of complex II in intact cells and tissues. Analogues of both the succinate and malonate series optimized for ''in vivo'' use are simultaneously being developed.
::[http://bioblast.at/images/0/0f/Aasander_Frostner_Poster_MiP2017.pdf '''Poster link''']
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] +
Primary mitochondrial diseases are a heterogeneous group of rare genetic disorders affecting approximately 125 persons per million. Mutations underlying these diseases give rise to biological changes (including decrease in cellular energy production and increase in reactive oxygen species), leading to organ failure, and commonly early morbidity. Mitochondrial diseases often present in early childhood and lead to the development of severe symptoms, with severe fatigue and myopathy being some of the most prevalent and debilitating clinical signs.
There are currently no cures for mitochondrial diseases, nor any approved pharmaceutical treatments for multisystemic disorders.
Current drug development in mitochondrial diseases focuses mainly on modulation of oxidative stress, regulation of the expression of genes involved in metabolic pathways, modulation of coenzymes, induction of mitochondrial biogenesis, and energy replacement.
In this short review, we present the current landscape of mitochondrial disease drug development, focusing on small molecules in clinical trials conducted by industrial sponsors. +
[[File:BEC.png|25px|link=https://doi.org/10.26124/bec:2022-0004]] https://doi.org/10.26124/bec:2022-0004
Primary mitochondrial diseases are a heterogeneous group of rare genetic disorders affecting approximately 125 persons per million. Mutations underlying these diseases give rise to biological changes (including decrease in cellular energy production and increase in reactive oxygen species), leading to organ failure, and commonly early morbidity. Mitochondrial diseases often present in early childhood and lead to the development of severe symptoms, with severe fatigue and myopathy being some of the most prevalent and debilitating clinical signs.
There are currently no cures for mitochondrial diseases, nor any approved pharmaceutical treatments for multisystemic disorders.
Current drug development in mitochondrial diseases focuses mainly on modulation of oxidative stress, regulation of the expression of genes involved in metabolic pathways, modulation of coenzymes, induction of mitochondrial biogenesis, and energy replacement.
In this short review, we present the current landscape of mitochondrial disease drug development, focusing on small molecules in clinical trials conducted by industrial sponsors.<br><br> +
[[Aasander Frostner 2022 Abstract Bioblast]]: Primary mitochondrial diseases are a heterogeneous group of rare genetic disorders affecting approximately 125 persons per million. Mutations underlying these diseases give rise to biological changes (including decrease in energy production and increase in reactive oxygen species), leading to organ failure, and commonly early morbidity. Mitochondrial diseases often present in early childhood and lead to the development of severe symptoms, with severe fatigue and myopathy being some of the most prevalent and debilitating ones.
There is currently no cure for primary mitochondrial diseases, nor any approved pharmaceutical treatments for multisystemic disorders.
Present drug development in mitochondrial diseases focuses mainly on modulation of oxidative stress, regulation of the expression of genes involved in metabolic pathways, modulation of coenzymes, induction of mitochondrial biogenesis, and energy replacement.
In this short review, we present the current landscape of mitochondrial disease drug development, focusing on small molecules in clinical trials conducted by industrial sponsor. +
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
Altered myocardial metabolism and cardiac inefficiency are hallmarks of the diabetic heart, and may play a central role in the pathogenesis of diabetes related cardiac dysfunction (diabetic cardiomyopathy). Although high levels of fatty acids has been demonstrated to have adverse effects in the normal heart, its effect in the obese/diabetic heart is less clear. In the present study we have examined how an acute fat-load on the heart diet-induced obese (DIO) mice (20 week on a high-fat diet) and age-matched controls (CON) will influence mitochondrial respiration.
We found reduced OXPHOS respiration in isolated mitochondrial from DIO as compared to CON hearts. By subjecting CON hearts to a high fat-load (elevated levels of fatty acids prior to mitochondrial isolation), OXPHOS respiration and RCR (respiratory coupling ratio) were reduced. These changes were not observed in mitochondria from DIO hearts, which may suggest that in diabetes, the heart undergoes adaptation to chronic exposure of elevated circulating fatty acids, which protect these hearts from the adverse effects of an acute fat-load. +
Preprints in science are nothing new. They are well established in the physical sciences, and experiments with preprints in medical sciences date back to the 1990s. When scientists imagine the future of scientific communication, preprints are inevitably an important component. The future, in this case, was slow to arrive but it is definitely here now. A preprint is a version of a scientific article that precedes its publication in a peer-reviewed journal. At one extreme, a preprint may be unedited, never peer-reviewed, or never published in a scholarly journal but simply posted on a preprint archive. The intention, however, is that by posting an article on a preprint archive, the article is freely accessible and will receive comments from the scientific community so that it can be improved before submission to a journal. +
Cancer and Metabolism conference, Cambridge, United Kingdom, 2018 +
Abcam Mitochondria Meeting 2014, London, UK; [http://www.abcam.com/index.html?pageconfig=resource&rid=16185&viapagetrap=mitochondriafeb Abcam Mitochondria Meeting 2014] +
NADPH oxidase (Nox) is emerging as one of the major sources of cellular reactive oxygen species (ROS). While controlled ROS generation by Nox is involved in the redox regulation of physiological cellular processes, excessive ROS production leads to tissue damage [1]. Nox over-reactivity has been shown to mediate the pathogenesis of tissue injury in neurodegenerative disorders [2], ischemia-reperfusion and cardiovascular disorders. Because of the short-lived nature of ROS, it is challenging to assess and monitor ROS levels in biological specimens. Thus, the development of a method to measure NADPH oxidase-derived ROS generation would be a valuable research tool to understand mechanisms relevant to neurodegeneration and tissue injury. Furthermore, this approach might be of relevance for screening of novel Nox inhibitors, which may selectively reduce disease-related Nox-mediated ROS generation without modifying ROS physiological signaling function.
By using the Oroboros Oxygraph-2k, we applied two different protocols for measuring oxygen consumption in parallel with ROS levels in freshly isolated synaptosomes. In parallel with spin trapping EPR spectroscopy, we employed this protocol to delineate the contribution of NADPH oxidase to ROS production in young female and male C57BL6 mice. The first protocol based on using a polarographic high resolution O2k sensor to measure oxygen consumption and a fluorescence-based module to monitor the rate of NADPH-mediated hydrogen peroxide production. Consistent Nox-dependent oxygen consumption was detected in synaptosomes following activation of Nox by 5 mM NADPH (3 doses). In parallel, we also employed a WPI -electrochemical sensor to determine H2O2 in the same sample. Although we didn't detect sex-dependent discrepancy in the rate of hydrogen peroxide production by Nox in isolated synaptosomes, the HRP/Amplex Red system was associated with greater oxygen consumption and higher rates of hydrogen peroxide generation, suggesting that HRP may be inducing Nox-like activity. We verified the Nox activity using spin trapping EPR spectroscopy. Our study revealed that the Oroboros Oxygraph-2k can be successfully used for assessment of Nox activity through the parallel detection of oxygen consumption and the resulting hydrogen peroxide generation. However, we have also found that HRP exhibit NADPH-dependent, oxygen-consuming, and H<sup>2</sup>O<sup>2</sup> -producing activity. Efforts are currently exerted to test other redox-sensitive dyes for the detection of ROS in the absence of HRP.
Disruption of cellular redox homeostasis is implicated in a wide variety of pathologic conditions and aging. A fundamental factor that dictates such balance is the ratio between mitochondria-mediated complete oxygen reduction into water and incomplete reduction into superoxide radical by mitochondria and NADPH oxidase (NOX) enzymatic activity. Here we determined mitochondrial as well as NOX-dependent rates of oxygen consumption in parallel with H<sub>2</sub>O<sub>2</sub> generation in freshly isolated synaptosomes using high-resolution respirometry combined with fluorescence or electrochemical sensory. Our results indicate that, although synaptic mitochondria exhibit substantially higher respiratory activities (8-82 folds greater than NOX oxygen consumption depending on mitochondrial respiratory state), NADPH-dependent oxygen consumption is associated with greater H<sub>2</sub>O<sub>2</sub> production (6-7 folds higher NOX-H<sub>2</sub>O<sub>2</sub>). We also show that, in terms of the consumed oxygen, while synaptic mitochondria ‘leaked’ 0.71% ± 0.12 H<sub>2</sub>O<sub>2</sub> during NAD<sup>+</sup>-linked resting, 0.21% ± 0.04 during NAD<sup>+</sup>-linked active, and 0.07% ± 0.02 during FAD<sup>+</sup>-linked active respirations, NOX converted 38% ± 13 of O<sub>2</sub> into H<sub>2</sub>O<sub>2</sub>. Our results indicate that NOX rather than mitochondria is the major source of synaptic H<sub>2</sub>O<sub>2</sub>. The present approach may assist in the identification of redox-modulating synaptic factors that underlie a variety of physiological and pathological processes in neurons. +
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]]
At the request of the author, this abstract is not made available online. +
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoeagle.org/index.php/MitoEAGLE|COST Action MitoEAGLE]]
At the request of the authors, this abstract is not made available online. +
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] +
Mitochondrial and immune dysfunctions are often implicated in the aetiology of autism spectrum disorder (ASD). Here, we studied for the first time the relationship between ASD severity measures and mitochondrial respiratory rates in freshly isolated platelets as well as the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) in isolated neutrophils. We also verified the impact of hyperbaric oxygen therapy (HBOT) on mitochondrial and immune functions as well as on ASD severity measures. Blood samples were collected from three age-matched male groups (Control (Norm-N), autistic (Aut-N), and autistic + HBOT (Aut-H); N = 10 per group). Using high resolution respirometry, we found that routine basal respiration, complex I- and complex I + II-dependent oxidative phosphorylation rate were significantly impaired in Aut-N platelets. Similarly, deficits in immune response of neutrophils were evidenced through lower rates of oxygen consumption and reactive oxygen species (ROS) production by phagocytic NOX. ASD-related behavioural outcomes were found to moderately correlate with platelets' mitochondrial bioenergetic parameters as well as with NOX-mediated activity in neutrophils. HBOT was not able to improve mitochondrial dysfunctions or to counteract ASD-related behavioral deficits. Although HBOT improved one measure of the immune response; namely, NOX-mediated superoxide burst, this was not associated with significant changes in trends of recurrent infections between groups. Taken together, our data suggest that ASD-associated mitochondria and immune deficits are detectable in platelets and neutrophils. We also found no evidence that HBOT confers any significant improvement of ASD-associated physiological or behavioural phenotypes. +
Incidents of myocardial infarction and sudden cardiac arrest vary with time of the day, but the mechanism for this effect is not clear. We hypothesized that diurnal changes in the ability of cardiac mitochondria to control calcium homeostasis dictate vulnerability to cardiovascular events.
Here we investigate mitochondrial calcium dynamics, respiratory function, and reactive oxygen species (ROS) production in mouse heart during different phases of wake versus sleep periods.
We assessed time-of-the-day dependence of calcium retention capacity of isolated heart mitochondria from young male C57BL6 mice. Rhythmicity of mitochondrial-dependent oxygen consumption, ROS production and transmembrane potential in homogenates were explored using the Oroboros O2k Station equipped with a fluorescence detection module. Changes in expression of essential clock and calcium dynamics genes/proteins were also determined at sleep versus wake time points.
Our results demonstrate that cardiac mitochondria exhibit higher calcium retention capacity and higher rates of calcium uptake during sleep period. This was associated with higher expression of clock gene Bmal1, lower expression of per2, greater expression of MICU1 gene (mitochondrial calcium uptake 1), and lower expression of the mitochondrial transition pore regulator gene cyclophilin D. Protein levels of mitochondrial calcium uniporter (MCU), MICU2, and sodium/calcium exchanger (NCLX) were also higher at sleep onset relative to wake period. While complex I and II-dependent oxygen utilization and transmembrane potential of cardiac mitochondria were lower during sleep, ROS production was increased presumably due to mitochondrial calcium sequestration.
Taken together, our results indicate that retaining mitochondrial calcium in the heart during sleep dissipates membrane potential, slows respiratory activities, and increases ROS levels, which may contribute to increased vulnerability to cardiac stress during sleep-wake transition. This pronounced daily oscillations in mitochondrial functions pertaining to stress vulnerability may at least in part explain diurnal prevalence of cardiac pathologies.
Lymphangioleiomyomatosis (LAM) is a rare and progressive systemic disease affecting mainly young women of childbearing age. A deterioration in lung function is driven by neoplastic growth of atypical smooth muscle-like LAM cells in the pulmonary interstitial space that leads to cystic lung destruction and spontaneous pneumothoraces. Therapeutic options for preventing disease progression are limited and often end with lung transplantation temporarily delaying an inevitable decline. To identify new therapeutic strategies for this crippling orphan disease, we have performed array based and metabolic molecular analysis on patient-derived cell lines. Our results point to the conclusion that mitochondrial biogenesis and mitochondrial dysfunction in LAM cells provide a novel target for treatment. +
Researchers in the life sciences are posting their work to preprint servers at an unprecedented and increasing rate, sharing papers online before (or instead of) publication in peer-reviewed journals. Though the popularity and practical benefits of preprints are driving policy changes at journals and funding organizations, there is little bibliometric data available to measure trends in their usage. Here, we collected and analyzed data on all 37,648 preprints that were uploaded to bioRxiv.org, the largest biology-focused preprint server, in its first five years. We find that preprints on bioRxiv are being read more than ever before (1.1 million downloads in October 2018 alone) and that the rate of preprints being posted has increased to a recent high of more than 2,100 per month. We also find that two-thirds of bioRxiv preprints posted in 2016 or earlier were later published in peer-reviewed journals, and that the majority of published preprints appeared in a journal less than six months after being posted. We evaluate which journals have published the most preprints, and find that preprints with more downloads are likely to be published in journals with a higher impact factor. Lastly, we developed Rxivist.org, a website for downloading and interacting programmatically with indexed metadata on bioRxiv preprints. +
.-20The-20world-20of-20mitochondrial-20diseases:-20Their-20diversity-20and-20heterogeneity.-20Shinagawa-20JP.-27-27%27){kind=link}
