Search

Metabolic remodeling in heart failure (HF) is a type of overload cardiomyopathy caused by insufficient energy supply or an imbalance of glucose and lipid metabolism. Therefore, metabolic pathways may serve as potential targets for HF treatment. BRM-associated factor (BAF) 60c (also known as smarcd3) promotes the transformation of oxidative muscle fibers to glycolytic muscle fibers. Our study aimed to test whether BAF60c and the PGC1[alpha]--PPAR[alpha]--mTOR pathway interact to affect myocardial metabolism in HF rats. Established rat models of HF were injected with BAF60c low or overexpression plasmids to assess cardiac contractile proteins, energy metabolism, oxidative metabolism, glycolysis, high-energy phosphate content, mitochondrial function, and apoptosis. BAF60c overexpression/siRNA plasmid was transfected into H9C2 cells. These results suggest that HF rats present decreased levels of BAF60c, increased glycolysis, and reduced levels of cardiac contractile proteins, PGC1[alpha], PPAR[alpha], and oxidative metabolism. Overexpression of BAF60c maintained the balance between oxidative metabolism and glycolysis and activated the PGC1[alpha]-PPAR[alpha]-mTOR pathway. PGC1[alpha] interacted with BAF60c, and overexpression of PGC1[alpha] decreased BAF60c knockdown, damaging H9C2 cells. Collectively, overexpression of BAF60c activated the PGC1[alpha]-PPAR[alpha]-mTOR pathway, maintained the oxidative metabolism/glycolysis balance, and improved mitochondrial function in HF rats. This study offers novel insights into HF treatment. Key words: heart failure, oxidative metabolism/glycolysis equilibrium, mitochondrial function, BAF60c, PGC1[alpha]-PPARa-mTOR pathway, myocardial hypertrophy. BAF60c (BRM-associated factor 60c) favorise la glycolyse dans le muscle et ameliore l'homeostasie du glucose. Cette etude a explore le mecanisme d'action de BAF60c dans l'insuffisance cardiaque (IC). Des modeles d'insuffisance cardiaque chez le rat foetal/adulte ont ete etablis, et les niveaux de proteines contractiles cardiaques et de facteurs lies au metabolisme energetique, au metabolisme oxydatif et a la glycolyse ont ete detectes. Un plasmide de surexpression ou un petit ARNi de BAF60c ont ete injectes a des rats adultes atteints d'IC pour evaluer le captage de glucose par le myocarde, le contenu en phosphate a haute energie, la fonction mitochondriale, la proliferation cellulaire et l'apoptose. Le plasmide de surexpression ou le petit ARNi de BAF60c ont ete transfectes dans des cellules hypertrophiques cardiaques H9C2 afin d'en explorer les effets in vitro. L'interaction entre BAF60c et PGC1[alpha] a ete examinee. Les resultats suggeraient que les rats adultes atteints d'IC presentent des niveaux accrus de proteines foetales (ssTnI et fTnT), de BAF60c et de facteurs lies a la glycolyse, et des niveaux reduits de proteines contractiles cardiaques, de PGC1[alpha], de PPAR[alpha] et de facteurs lies au metabolisme oxydatif. La suppression de BAF60c ameliorait le captage du glucose, maintenait l'equilibre entre le metabolisme oxydatif et la glycolyse, favorisait la proliferation des cellules H9C2 et inhibait l'apoptose. PGC1[alpha] interagissait avec BAF60c. La suppression de BAF60c activait egalement la voie PGC1[alpha]/PPAR[alpha]/mTOR. La surexpression de PGC1[alpha] diminuait les dommages causes aux cellules H9C2 par BAF60c. Dans l'ensemble, la regulation a la baisse de BAF60c activait la voie PGC1[alpha]/PPAR[alpha]/mTOR, maintenait l'equilibre entre le metabolisme oxydatif et la glycolyse et ameliorait la fonction mitochondriale dans des modeles d'IC chez le rat. Cette etude peut offrir de nouvelles perspectives pour le traitement de l'IC. [Traduit par la Redaction] Mots-cles : insuffisance cardiaque, equilibre metabolisme oxydatif/glycolyse, fonction mitochondriale, BAF60c, voie PGC1[alpha]/PPAR[alpha]/mTOR, hypertrophie myocardique., Introduction Although 'energy deficiency' is considered a factor in the transition from functional compensatory hypertrophy to heart failure (HF), the details of the metabolic reconstruction and the determination of the [...]

Carbon fiber reinforced silicon carbide matrix composites (Cf/SiC composites) are lightweight, high strength, wear-resistant, and heat-resistant, making them widely used in aerospace and other industries. However, machining holes in Cf/SiC composites is a great challenge due to the anisotropy and high hardness of the material. In this paper, a brazed diamond grinding rod was employed to grind 1 mm diameter holes in Cf/SiC composites, and the influence of grinding parameters on grinding force, hole entrance/exit defects, and hole wall quality was investigated. In addition, the material removal mechanism of Cf/SiC composites and the wear mechanism of the diamond grinding rod were explored. The findings showed that the damage at the hole entrance and exit predominantly manifests as tearing and burring. The damage factor at the hole exit is 3.5% larger than that at the hole entrance, and the damage factor at both the hole entrance and exit reduces with the growth of spindle speed and the decrease of feed rate. In addition, the diameter errors of the hole entrances and exits are all less than 10%, and the entrance diameter is 2.9% larger than the exit. The hole wall defects include fiber fracture, silicon carbide matrix peeling, and inherent porosity, with poorer surface quality at fiber orientation angles (FOA) of 90° to 180°. The main wear mechanisms were identified as abrasive wear and the spalling of abrasive grains. [ABSTRACT FROM AUTHOR]

This paper concentrates on the general birth–death processes with two different types of catastrophes. The Laplace transform of transition probability function for birth–death processes with two-type catastrophes is successfully expressed with the Laplace transform of transition probability function of the birth–death processes without catastrophe. The first effective catastrophe occurrence time is considered. The Laplace transform of its probability density function, expectation and variance are obtained. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Phospholipid scramblase 1 interacts with influenza A virus NP, impairing its nuclear import and thereby suppressing virus replication." The correction addresses errors in the figures of the original article, including the reuse of data and incorrect images. The corrected figures are provided in the notice, and the original unadjusted images are available as supplementary material. The authors apologize for the errors and provide an updated Data Availability statement. [Extracted from the article]