ObjectiveTo investigate the distribution of HCV genotypes in 383 patients with HIV/HCV coinfection in Guizhou, China and the effect of coinfection on HIV viral load, CD4+ T lymphocytes, and platelet count (PLT), and to provide a basis for individualized treatment of patients with HIV/HCV coinfection. MethodsRelated clinical data were collected from 383 patients with HIV/HCV coinfection who were treated in Guiyang Public Health Clinical Center from March 2015 to December 2019, and HCV genotype, HIV viral load, CD4+ T lymphocytes, and PLT were determined. A total of 1068 patients with HIV alone were enrolled as control. The Kruskal-Wallis H test was used for comparison between multiple groups, the Wilcoxon rank-sum test was used for comparison between two groups, and the Bonferroni method was used for further comparison between two groups; the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. ResultsAmong the 4664 patients with HIV infection, 383 (8.21%) had HCV coinfection, and the main HCV genotypes were genotype 6a (35.51%), genotype 3b (27.42%), and genotype 1b (21.41%), followed by genotypes 3a (1332%), 1a (1.31%), 2a (0.52%), 6n (0.26%), and 6xa (0.26%). The most common route of infection was intravenous drug addiction (72.59%), followed by sexual contact (24.80%). Compared with the patients with HIV infection alone, the patients with HIV/HCV coinfection had a significantly higher HIV RNA load and significantly lower CD4+ T lymphocytes and PLT (Z=6.716, 11.813, and 9.192, all P＜0.05). Among the patients with coinfection, the patients with HCV genotype 3b had the highest HIV RNA load and the lowest CD4+ T lymphocytes and PLT, while the patients with HCV genotype 1a had the lowest HIV RNA load and the highest CD4+ T lymphocytes (all P＜0.05). Among the patients with different clinical stages, the patients with compensated cirrhosis had the highest HIV RNA load, the patients with chronic hepatitis C had the lowest HIV RNA load, the patients with end-stage liver disease had the lowest count of CD4+ T lymphocytes, and the patients with chronic hepatitis C had the highest PLT (all P＜0.05). ConclusionThe distribution of HCV genotypes is diverse in the patients with HIV/HCV coinfection in Guizhou, and HCV strains with genotypes 6a, 3b, and 1b are the main epidemic strains. Intravenous drug addiction is the main route of infection. Coinfection may affect HIV replication and immune status, with a significantly marked effect on HCV genotype 3b and liver cirrhosis or end-stage liver disease.

Objective To explore the risk factors on the symptoms of lumbar intervertebral disc herniation so as to develop a predictive model for the disease. Methods With a populationbased case-control study, 303 of 50 123 residents were diagnosed as having lumbar intervertebral disc herniation symptoms. 152 cases and 167 healthy controls, matched by gender and age, were randomly chosen as case and control groups. Questionnaires were used to collect information on the exposure to risk factors and logistic predictive model was then established. Results Through non-conditional logistic regression analysis, data showed that the positive family history of lumbar vertebra disorder, lumbar treatment or surgery, mental stress, acute low back injury, permanent work pose, and body mass index ≥23.0 kg/m2 were the risk factors among residents from the countryside. The area under the receiver operator characteristic curve of logistic predictive model was 0.809. When 0.4 was set as the classification cutoff, the total predictive correct rate, sensitivity, and specificity were 74.0%, 73.7%, and 74.3% respectively. Conclusion The occurrence of lumbar disk herniationcan in countryside population was affected by multi-variables including genetic and environmental, and could be predicted with the logistic regression model established by our group.The positive predictive results could be used to alarm the patients and doctors for prevention and treatment of the disease.

[摘 要] 目的：探讨碱性核蛋白1（BNC1）对食管鳞状细胞癌（ESCC）细胞增殖、迁移、侵袭、细胞周期和凋亡的影响及其作用机制。方法：通过qPCR法检测ESCC细胞和正常食管上皮细胞中BNC1 mRNA的表达水平，免疫组织化学染色法检测10例ESCC患者癌及癌旁组织中BNC1的蛋白表达水平。利用siRNA敲低BNC1在KYSE-150和KYSE-30细胞中的表达，CCK-8法、划痕愈合实验、Transwell实验和流式细胞术检测BNC1对细胞增殖、迁移、侵袭、细胞周期和凋亡等的影响。通过CHIP-seq实验和GEPIA在线网站数据分析并结合敲低BNC1后的转录组测序数据分析筛选BNC1调控的下游靶基因，qPCR法验证BNC1敲低后靶基因的表达变化，并用双荧光素酶报告基因实验验证BNC1对靶基因的调控作用。结果：BNC1 mRNA和蛋白水平在ESCC组织中较癌旁组织高表达（均P<0.01）。敲低BNC1可明显抑制KYSE-150、KYSE-30细胞的增殖、迁移和侵袭能力（P<0.05或P<0.01），将细胞阻滞于G1期并促进细胞的凋亡（均P<0.01）。CHIP-seq实验结果和在线网站GEPIA数据分析结合敲低BNC1后的转录组测序数据显示，G蛋白通路抑制因子1（GPS1）可能为BNC1正向调控的致癌靶基因。qPCR法和双荧光素酶报告基因实验结果显示，BNC1对GPS1有调控作用（P<0.01）。结论：BNC1在ESCC组织和细胞中高表达，干扰BNC1可显著抑制ESCC细胞的增殖、迁移和侵袭能力，阻滞细胞于G1期并促进细胞凋亡，其机制可能是BNC1通过靶向GPS1调控ESCC细胞的恶性生物学行为。