Objective To evaluate the effect of remifentanil on Toll-like receptor 2 (TLR2) mRNA expression during renal ischemia-reperfusion (Ⅰ/R) in rats.Methods Fifty-four male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n=18 each) using a random number table:sham operation group (group S),Ⅰ/R group and remifentanil group (group R).Renal Ⅰ/R injury was produced by clamping the bilateral renal arteries for 45 min followed by reperfusion in Ⅰ/R and R groups.Bilateral renal arteries were only exposed but not clamped in group S.Remifentanil 1.0 μg · kg-1 · min-1 was infused via the tail vein starting from 15 min before ischemia until 30 min of reperfusion in group R,while the equal volume of normal saline was given instead in S and Ⅰ/R groups.The animals were sacrificed at 15 min before ischemia and 6 and 24 h of reperfusion,and the renal specimens were obtained for examination of the pathological changes (with light microscope) and for determination of the contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) (by ELISA) and expression of TLR2 mRNA (by RT-PCR) and cell apoptosis (by double staining and flow eytometry).The apoptotic rate was calculated.Results Compared with group S,TLR2 mRNA expression was significantly up-regulated,and the contents of TNF-α and IL-6 and apoptotic rate were increased at 6 and 24 h of reperfusion in Ⅰ/R and R groups.Compared with group Ⅰ/R,TLR2 mRNA expression was significantly down-regulated,and the contents of TNF-α and IL-6 and apoptotic rate were decreased at 6 and 24 h of reperfusion in group R.The pathological changes were significantly attenuated in group R as compared with group Ⅰ/R.Conclusion The mechanism by which remifentanil reduces renal Ⅰ/R injury is related to down-regulation of TLR2 expression and decrease in TLR2 activity and inhibition of inflammatory responses in renal tissues and cell apoptosis in rats.

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Objective The current study is aimed to investigate the association of single nucleotide polymorphisms and gene expression in peptidylarginine deiminase Ⅳ (PADI4) with rheumatoid arthritis (RA).Methods The gene expression of PADI4 was examined using real-time quantitative reverse transcription-polymcrase chain reaction (RT-PCR) in 70 patients with RA and 81 healthy controls. Four exonie SNPs of the PADI4 gene (PADI4_89, _90, _92, _104) were genotyped using DNA sequencing and TA cloning.Results The distribution of PADI4_89, _90, _104 SNPs in RA was different from that of healthy controls. The increased RA susceptibility was significantly associated with minor alleles. When haplotypes were construe -ted with 4 SNPs, two major haplotypes, ACCC and GTGT were found in all samples, and GTGT haplo-type (carrying only the minor alleles) was significandy associated with increased RA susceptibility (P<0.01)in comparison with the reference haplotype ACCC. There was over expression of PADI4 in RA than controls(P<0.05). C, enotypes carrying the minor alleles had higher expression level of PADI4 in RA and controls than those with the common alleles. Conclusion PADI4 SNPs and haplotypes are associated with RA susceptibility in Chinese. PADI4 is over-expressed in the blood of RA patients, and there is significant association between the haplotypes and expression level of the PADI4 gene.

Objective: To study the epidemiologic and genetic characteristics of coxackievirus A6(CV-A6) strains isolated in Shenyang. Methods: Enterovirus strains positive for neither enterovirus A71 (EV-A71) nor CV-A16 were isolated from Shenyang during 2013 to 2017 to screen for CV-A6 isolates by real-time PCR. The entire sequences of viral genes encoding VP1 of CV-A6 positive samples were amplified and sequenced. The phylogenetic analysis was performed. Results: CV-A6 strains accounted for 27.83% (575/2 066) of the non-EV-A71 and non-CV-A16 enterovirus strains isolated in Shenyang during the years 2013 to 2017. And CV-A6 strains were the predominant enterovirus strains with positive rate of 68.38 % (240/351) in 2015. The CV-A6 isolates from Shenyang during 2013 to 2017 could be classified into the cluster D3a in the phylogenetic tree. Subtype D3a.1 strains circulated during 2013 to 2014 and subtype D3a.2 strains circulated during 2015 to 2017. Conclusions CV-A6 strains were the predominant enterovirus strains among non-EV-A71 and non-CV-A16 enterovirus strains circulated in Shenyang from 2013 to 2017. The CV-A6 isolates from Shenyang during 2013 to 2017 could be classified into the cluster D3a in the phylogenetic tree and subtype D3a.2 strains were evolved from subtype D3a.1 strains.

Objective To explore the influencing factors of microcirculation dysfunction in patients with anterior wall acute myocardial infarction(AMI)and to establish a relevant prediction model.Methods A total of 130 patients with anterior wall AMI,whose microcirculation function was assessed by caIMR after receiving percutaneous coronary intervention(PCI)at Shanghai Sixth People's Hospital of China from January 2017 to September 2020,were enrolled in this study.The patients were divided into abnormal microcirculation resistance group(n=52)and normal microcirculation resistance group(n=78).The clinical data were compared between the two groups.The regression analysis was used to analyze the influencing factors of microcirculation dysfunction.Results In the abnormal microcirculation resistance group the contrast agent consumption,the onset-to-operation time,the Gensini total score and the LAD Gensini score were(121.92±31.37)mL,(10.51±5.12)min,(97.91±31.77)points and(69.36±13.15)points respectively,which were significantly higher than(109.03±28.2)mL,(4.94±2.94)min,(81.05±35.22)points and(54.45±23.48)points respectively in the normal microcirculation resistance group,the differences in the above indexes between the two groups were statistically significant(all P＜0.05).A prediction model covering interventional strategies was established,and its accuracy was higher than that of a conventional model,its AUC compared with the conventional model was 0.91 to 0.87,indicating that this model could well predict the risk of microcirculation dysfunction in patients with AMI after receiving PCI.Conclusion This prediction model can promptly identify high-risk microcirculation dysfunction patients with anterior wall AMI after receiving PCI.

Objective:To identify the etiology and genetics of the human parainfluenza virus type 3 (HPIV3) virus which caused an acute respiratory tract infection outbreak in a primary school in Shenyang.Methods:Throat swab samples were collected from 17 students of the primary school where the epidemic of acute respiratory infection outbreak in December 2020 in Shenyang, Liaoning province. TaqMan low-density arrays (TLDA) real-time PCR was performed to simultaneously detect multiple respiratory pathogens. The HN gene was amplified using nested RT-PCR and sequenced, followed by phylogenetic analysis for those HPIV3 positive samples.Results:Of the 17 specimens, 10 were HPIV3 positive by TLDA Real-time PCR, and were accompanied by conditional pathogen infection, consequently, amplification result ed in 7 complete HN sequences. Phylogenetic analysis showed that the infected HPIV3 virus of the outbreak belonged to HPIV subtype C3a. All the 7 strains detected in this study belonged to subbranch C3a.1 evolutionary branch, with a nucleotide homology of 99.9%, a nucleotide homology of 94.56 with the prototype strain Wash/47885/57 and 99.5% with the most phylogenetically close strain of ZJ/11-s-165/KP690785/CHN/11.Conclusions:The HPIV3 virus caused the acute respiratory tract infection outbreak in Shenyang in 2020 and HPIV subtype C3a1 was detected firstly in Northeast China.