Rent species of bacteria; technique employed to ascertain the electricalhttps://doi.org/10.1021/acssensors.2c02166 ACS Sens. 2023, 8, 1101ACS Sensorspubs.acs.org/acssensorsArticleMIC; photograph of the final experimental setup displaying a chip with six sensors; and plot from the magnitude of impedance and phase angle for MH1 medium as a function of frequency (PDF)AUTHOR INFORMATIONCorresponding AuthorHywel Morgan College of Electronics and Computer Science, and Institute for Life Sciences, University of Southampton, Southampton SO17 1BJ, U.K.; orcid.org/0000000348505676; Email: [email protected] Spencer College of Electronics and Laptop Science, and Institute for Life Sciences, University of Southampton, Southampton SO17 1BJ, U.K. Yuetao Li School of Electronics and Laptop or computer Science, and Institute for Life Sciences, University of Southampton, Southampton SO17 1BJ, U.K. Yiling Zhu Technologies Development Group, Investigation and Evaluation, UK Overall health Safety Agency (UKHSA), Salisbury SP4 0JG, U.K. J. Mark Sutton Technology Development Group, Analysis and Evaluation, UK Overall health Safety Agency (UKHSA), Salisbury SP4 0JG, U.K.; Institute of Pharmaceutical Science, School of Cancer Pharmaceutical Sciences, King’s College London, London SE1 9NH, U.K.; orcid.org/0000000222880446 Total contact info is accessible at: https://pubs.acs.org/10.1021/acssensors.2cNotesThe authors declare no competing monetary interest. The information that assistance the findings of this study are openly obtainable in University of Southampton repository at https:// doi.Price of 1310405-06-1 org/10.2-Chloro-5-nitropyrazine uses 5258/SOTON/D2538.PMID:35954127 ACKNOWLEDGMENTS The authors would prefer to acknowledge funding from the Wessex Academic Health Science Network (AHSN).
ORIGINAL RESEARCHAcute Inhibition of Excessive Mitochondrial Fission After Myocardial Infarction Prevents Longterm Cardiac DysfunctionMarieHlne Disatnik, PhD; Julio C.B. Ferreira, PhD; Juliane Cruz Campos, MSc; Ktia Sampaio Gomes, BSc; ee a Paulo M.M. Dourado, MD, PhD; Xin Qi, PhD; Daria MochlyRosen, PhDBackgroundIschemia and reperfusion (IR) injury remains a significant cause of morbidity and mortality and a number of molecular and cellular pathways have already been implicated in this injury. We determined no matter whether acute inhibition of excessive mitochondrial fission at the onset of reperfusion improves mitochondrial dysfunction and cardiac contractility postmyocardial infarction in rats. Procedures and ResultsWe made use of a selective inhibitor from the fission machinery, P110, which we’ve not too long ago made. P110 therapy inhibited the interaction of fission proteins Fis1/Drp1, decreased mitochondrial fission, and enhanced bioenergetics in three various rat models of IR, like major cardiomyocytes, ex vivo heart model, and an in vivo myocardial infarction model. Drp1 transiently bound for the mitochondria following IR injury and P110 therapy blocked this Drp1 mitochondrial association. Compared with control therapy, P110 (1 lmol/L) decreased infarct size by 28 and enhanced adenosine triphosphate levels by 701 soon after IR relative to handle IR in the ex vivo model. Intraperitoneal injection of P110 (0.5 mg/kg) in the onset of reperfusion in an in vivo model resulted in improved mitochondrial oxygen consumption by 68 when measured 3 weeks after ischemic injury, enhanced cardiac fractional shortening by 35 , reduced mitochondrial H2O2 uncoupling state by 70 , and improved all round mitochondrial functions. ConclusionsTogether, we show that excessive mitochondrial fission at.
