Objective To investigate the association between interleukin-23 receptor (IL-23R) gene rs1343151 single nucleotide polymorphism and ankylosing spondylitis (AS) in Chinese Han patients. Methods The genotypes of IL-23R SNP was detected in 104 Chinese AS patients and 95 ethnically matched blood donors by TaqMan probe assays. The allele and genotype frequencies and risk factors of AS were analyzed by Chi-square test in both groups. Results The rs 1343151 genotypes in AS patients consisted of homozygote C/C (90.4%),C/T (9.6%), while The rs1343151 genotypes in the controls were. composed of C/C (91.6%), C/T (8.4%). No significant difference was found in the distribution of rs1343151 genotypes between these two groups (x2=0.086, P>0.05). The frequency of rs1343151 allele in AS patients was also not significantly increased when compared with the control group (x2 =0.082,P>0.05). Conclusion There may be no association between the IL-23R gene rs1343151 SNP and ankylosing spondylitis in Chinese Hart population.

ObjectiveTo investigate the inhibitory effect of all-tram-retinoicacid (ATRA) on HCC cell growth and probe the potential molecular mechanism.MethodsHCC cell lines,HepG2 and SMMC-7721 were treated by ATRA and cell growth was analyzed by using MTT assay.The expression levels of miR-18a were evaluated in HepG2 and SMMC-7721,compared with the normal livers pool by using RealTime PCR analysis.Cell growth analysis by using MTT assay was performed on HepG2 and SMMC-7721 after transfection with anti-miR-18a.Rescued assay was designed to probe the mechanism of ATRA on cell growth by using ATRA with or without miR-18a mimic.ResultsHepG2 cell growth was suppressed about 74％ (P＜0.05,36 h),72％ (P＜0.01,48 h),and 67％ (P＜0.05,72 h) and SMMC-7721 cell growth was inhibited about 68％ (P＜0.05,48 h),and 64％ (P＜0.05,72 h) after treatment with ATRA,compared with the cells treated with Ethanol.MiR-18a expression was up-regulated in HepG2 and SMMC-7721 cell lines about 4.7- and 3.8-fold (P＜0.05),respectively.Endogenous miR-18a levels were down-regulated by ATRA about 67％ and 56％ (P＜0.05).The inhibitory effect of ATRA on HCC cell growth was reversed about 1.2-fold (P＜0.05,48 h) by overexpression of miR-18a in HepG2 cells and cell growth of SMMC-7721 was enhanced about 1.25- and 1.2-fold (P＜0.05,24 and 48 h) with ectopic expression of miR-18a.ConclusionHCC cells growth is suppressed by ATRA through miR-18a mediated network.

Objective To investigate the expression profile of miRNAs up-regualted in human extrahepatic and intrahepatic cholangiocarcinoma tissues and probe the effect on cell growth of four of these miRNAs in QBC939 cell line.Methods Up-regulated miRNAs in extrahepatic or intrahepatic cholangiocarcinoma tissues were analyzed by using miRNA-microarray,which was confirmed by using miRNA Real-Time PCR analysis.Based on these findings,four of these up-regulated miNRAs were chosen to perform function investigation.The specific miRNA inhibitors were transfected into QBC939 cells,respectively,and cell proliferation assay was performed by using MTT.Results 12 miRNAs were up-regulated both in two types of cholangiocarcinoma tissues,28 miRNAs and 21 miRNAs were up-regulated in extrahepatic cholangiocarcinoma and intrahepatic cholangiocarcinoma,respectively.MiR-125b and miR-19a expression levels were increased about 3.7 and 3.6 fold,compared with the matched normal bile duct tissues (P＜0.05).MiR-92a and miR-205 expression was upregulated about 4.S- and 3.5-fold,compared with the matched normal bile duct tissues (P＜0.05).MiR-125b,miR19a,miR-21,and miR 378* were inhibited in QBC939 cells,which indicated a significant inhibitory effect on cell growth.The ratio of inhibition was 71％,72％,69％,and 76％(P＜0.05)at 36 h,61％,63％,60％,and 59％(P＜0.01) at 48 h,and 61％、56％、60％ and 59％(P＜0.05) at 60 h.Conclusion The miRNAs expression patterns in human extrahepatic and intrahepatic cholangiocarcinoma tissues are different and uo-regulated miRNAs act as oncomirs on cholangiocarcinoma cell growth.

Clinical data of 655 patients with acute ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) in Luoyang Central Hospital during January 2017 to March 2020 were analyzed retrospectively. There were 425 cases who first visited PCI-capable hospital (PCI hospital group) and 230 cases who were transferred to PCI-capable hospital (transfer group). Compared with PCI hospital group, STEMI patients in the transfer group had a shorter first diagnosis time [2.0 (0.8, 4.2)h vs. 2.5(1.2, 4.1)h, Z=3.66, P<0.01], longer time from first medical contact to the balloon through (FMC2B) [175 (113, 344) min vs. 75 (57, 112) min, Z=-8.92, P<0.01], longer total ischemic time [5.4 (3.5, 9.8) h vs. 3.9 (2.4, 6.0) h, Z=-5.43, P<0.01]. There was no significant difference in the time from PCI hospital entry to balloon passage (DTB) between the two groups [43(29, 103) min vs. 46 (61, 94) min, Z=-0.56, P=0.573]. The compliance rate of FMC2B time<120 min in the transfer group was only 25.9% (50/193). However, the different first-visit hospital had no significant effect on the risk of heart failure ( OR=0.54, 95 %CI:0.16-1.79, P=0.311) and risk of death ( OR=1.14, 95 %CI:0.20-6.36, P=0.885). The results suggest that STEMI patients referred to PCI hospitals have considerable time delay, and the rate of compliance with FMC2B time<120 min is low.