Sovrem Tekhnologii Med
March 2025
Unlabelled: Hypoxia is a part of many pathological and some physiological processes. It also occurs as a result of surgical techniques associated with limiting the blood supply to the operated organs and tissues. Hypoxia leads to a significant decrease in the ability of cells to implement energy-dependent processes due to a reduced contribution of mitochondria to the synthesis of adenosine triphosphate (ATP).
View Article and Find Full Text PDFNeurodevelopmental disorders result from interactions between genetic predisposition and environmental risk factors, with infancy being the most vulnerable period. We designed a longitudinal study to determine how short-term antibiotic exposure during early postnatal life impacts the gut microbiome, neurodevelopment, and behavior, and whether these alterations were exacerbated by the neurodevelopmental disorder-associated 16p11.2 microdeletion (16pDel) mutation.
View Article and Find Full Text PDFThe branching fraction ratios of B[over ¯]^{0}→D^{+}τ^{-}ν[over ¯]_{τ} and B[over ¯]^{0}→D^{*+}τ^{-}ν[over ¯]_{τ} decays are measured with respect to their muonic counterparts, using a data sample corresponding to an integrated luminosity of 2.0 fb^{-1} collected by the LHCb experiment in proton-proton collisions at sqrt[s]=13 TeV. The reconstructed final states are formed by combining D^{+} mesons with τ^{-}→μ^{-}ν[over ¯]_{μ}ν_{τ} candidates, where the D^{+} is reconstructed via the D^{+}→K^{-}π^{+}π^{+} decay.
View Article and Find Full Text PDFDisuse has a negative impact on the postural muscles of the trunk and legs. Different leg muscles demonstrate a differentiated and conservative response to disuse, in terms of a decrease in muscle mass, strength, aerobic performance, and changes in gene expression. We aimed to identify transcription factors regulating gene expression at baseline and after disuse in human m.
View Article and Find Full Text PDFAtherosclerosis is a complex inflammatory process associated with high-mortality cardiovascular diseases. Today, there is a growing body of evidence linking atherosclerosis to mutations of mitochondrial DNA (mtDNA). But the mechanism of this link is insufficiently studied.
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