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Aim To investigate whether CTSB is involved in hypoxia-induced injury of cardiac microvascular endothelial cells.Methods A hypoxia-induced endothelial cell injury model was used.Cardiac microvascular endothelial cells were isolated from CTSB gene knockout mice.CTSB was overexpressed by adenovirus delivery system, and bafilomycin was used to block autophagy.ELISA was used to detect the release of inflammatory factors.Tunel staining was used to detect the number of cell apoptosis.caspase-3 kit was used to detect the activity of cell caspase-3.Cells were infected with LC3-GFP-mCherry double-labeled adenovirus todetect cell autophagy flow.Results CTSB gene knockout could significantly aggravate the inflammation and apoptosis of endothelial cells induced by hypoxia, and increased autophagy.Overexpression of CTSB reduced the inflammation and apoptosis of endothelial cells induced by hypoxia, and increased autophagy.But bafilomycin treatment could significantly offset the inhibitory effect of CTSB overexpression on cell inflammation and apoptosis and the protective effect on cell autophagy.Conclusions CTSB knockout aggravates inflammation and apoptosis induced by hypoxia in endothelial cells; while the overexpression of CTSB ameliorates endothelial cell injury induced by hypoxia.CTSB maintains normal autophagy degradation in endothelial cells.BAF blocks the protective effect of CTSB on endothelial cells by inhibiting autophagy degradation.
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Phylogenetic methods have been widely used to detect the evolution of influenza viruses.However, previous phylogenetic studies of influenza viruses do not make full use of the genetic information at the protein level and therefore cannot distinguish the subtle differences among viral genes. Proteotyping is a new approach to study influenza virus evolution. It aimed at mining the potential genetic information of the viral gene at the protein level by visualizing unique amino acid signatures (proteotypes). Neuraminidase gene fragments of some H5N1 avian influenza viruses were used as an example to illustrate how the proteotyping method worked. Bayesian analysis confirmed that the NA gene tree was mainly divided into three lineages. The NA proteotype analysis further suggested there might be multiple proteotypes within these three lineages and even within single genotypes. At the same time, some proteotypes might even involve more than one genotype. In particular, it also discovered some amino acids of viruses of some genotypes might co-reassort. All these results proved this approach could provide additional information in contrast to results from standard phylogenetic tree analysis.
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0.05). Accessory pathway antegrade and retrograde effective refractory period values were shorter in patients with PAF attacks (P
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AIM: To investigate the possibility of dauricine (DAU) to inhibit the irreversible platelet aggregation of patients with acute myocardial infarction (AMI). METHODS: Glycoprotein IV (GP IV) and thrombospondin(TSP) levels on the membrane surface of the stationary platelet or platelet activated by thrombin(50,100, 500, 1 000 U·L-1) in 12 patients with AMI were measured with a washed platelet flowcytometric assay and compared with those of the healthy (n = 14). RESULTS: The GP IV, TSP level of stationary platelet and activated platelet in patients with AMI were higher than those in the healthy significantly (P<0.05, 0.01), DAU (50 μmol·L-1) inhibited the GPIV membrane redistribution and the release of TSP from intracellular αgranules induced by thrombin (50 U·L-1, 100 U·L-1, 500 U·L-1) apparently (P<0.05, 0.01), inhibitory effect of DAU was not found in platelets activated with high concentraction of thrombin (1 000 U·L-1). CONCLUSION: The activity and reactivity to thrombin of platelets increased in patients with AMI and DAU may have a blocking effect on the consolidation of platelet aggregation in AMI.