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Objective@#To understand the epidemiological characteristics of influenza A(H1N1)pdm09 virus in Sichuan population during the monitoring period of 2018-2019, and to clarify the antigenic variation, the gene characteristics and the matching of current epidemic strains, vaccine strains, representative strains at home and abroad.@*Methods@#A total of 118 strains of influenza A(H1N1)pdm09 virus isolated in Sichuan region influenza network laboratory from April 2018 to March 2019 were selected. The hemagglutination inhibition (HI) assay was conducted for antigen analysis. The HA and NA genes of 16 strains with low-response strains were sequenced. Phylogenetic analysis and amino acid locus variation analysis were applied using BioEdit and MEGA5.0 software.@*Results@#The result of the antigen analysis demonstrated that more than 95% of the A(H1N1) pdm09 influenza viruses detected were similar to the WHO recommended vaccine strain A/Michigan/45/2015. The analysis of HA gene characteristics showed that some low-response strains had amino acid site variation in the Sa, Sb and Cb regions of the HA protein. A total of 15 low-response strains belonged to the 6B.1 branch. And their evolutionary relationship were close to the representative strains A/beijin-xicheng/SWL1633/2018 and A/brisbane/02/2018, which were popular at home and abroad. Compared with A/sichuan/1/2009, there are mutations involving 6, 14 and 1 amino acid sites in the antigen-determining regions (Sa, Sb, Ca and Cb), non-determined regions and receptor binding site(RBS) respectively. No amino acid site mutations related to resistance to NA gene were found.@*Conclusions@#In 2018-2019, the epidemic A(H1N1) pdm09 influenza virus in Sichuan is consistent with the global epidemic characteristics, which also matched with vaccine strains recommended by WHO in the northern hemisphere. Compared with A/sichuan/1/2009 which was the first isolated in China in 2009, there were amino acid sites mutations in antigen-determining region and receptor binding site of the HA protein, and the transmembrane region of the NA protein, drug and antibody binding sites.
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Objective@#To investigate the genotype and genetic characteristics of the pathogens associated with the epidemic outbreak of acute gastroenteritis(AGE) in Guangyuan city, Sichuan province.@*Methods@#Eighteen stool samples and 15 anal swab samples from 4 AGE outbreaks were collected from Feb 2017 to May 2017. Norovirus (NoV) nucleic acid was detected by Real-time PCR method , and the positive samples were amplified by conventional reverse transcription-polymerase chain reaction (RT-PCR) and nucleotide sequencing.@*Results@#Four AGE outbreaks were all caused by NoV. And 20 (60.6%) samples were positive for NoV GⅡ. Gene sequence comparison and phylogenetic analysis showed that 4 AGE outbreaks were all caused by GⅡ.P16/GⅡ.2 NoV. All the strains of GⅡ.P16/GⅡ.2 NoV shared high homology in nucleotides. One of the outbreaks was caused by GⅡ.P16/GⅡ.2 and GⅡ.P7/GⅡ.14 NoV co-infection.@*Conclusions@#The 4 outbreaks of AGE in Guangyuan city, Sichuan province were major caused by GⅡ.P16/GⅡ.2 NoV, meanwhile GⅡ.P16/GⅡ.2 and GⅡ.P7/GⅡ.14 NoV co-infection existed.
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<p><b>OBJECTIVE</b>To investigate the role of oxidative stress in impaired intermediate-conductance Ca(2+)-activated potassium channels (IKCa)- and small-conductance Ca(2+)-activated potassium channels (SKCa)-mediated relaxation in diabetic resistance arteries.</p><p><b>METHODS</b>Rat diabetic model was induced by a high fat and high glucose diet and streptozotocin (STZ) injection. Endothelial function of mesenteric arteries was assessed with the use of wire myography. The expression levels of IKCa and SKCa in cultured human umbilical vein endothelial cells (HUVECs) treated with H2O2 and/or antioxidant alpha lipoic acid (ALA) were measured using Western blotting.</p><p><b>RESULTS</b>IKCa- and SKCa-mediated vasodilatation in response to acetylcholine was impaired in the third-order mesenteric arterioles of diabetic rats. In cultured HUVECs, H2O2 significantly decreased the protein expression of IKCa and SKCa. ALA alleviated the impairment of both vasodilatation function of the mesenteric arterioles ex vivo and enhanced the expression of IKCa and SKCa challenged with H2O2 in cultured HUVECs.</p><p><b>CONCLUSION</b>Our data demonstrated for the first time that impaired IKCa- and SKCa-mediated vasodilatation in diabetes was induced, at least in part, by oxidative stress via down-regulation of IKCa and SKCa channels.</p>