Objective To investigate whether association of the genotype at the HLA A,B and DRB1, B3 B4 B5 loci with the Susceptipility to hemorrhagic fever with renal syndrome (HFRS) in Chinese Hans. Methods HLA A,B antigen types were detected by immunoserologic method and the genotypes of HLA DRB were identified by PCR/SSP method. Results The results showed that The Frequencies of A1, HLA DRB1 * (15,16) and DRB5 were increased in patients as compared to the healthy controls ( P

Objective To investigate the noninvasive indicators of indications for antiviral therapy in HBeAg-negative chronic hepatitis B virus (HBV) infection patients with alanine aminotransferase (ALT) ≤40 U/L under the guidance of liver pathology. MethodsA retrospective analysis was performed for the clinical data of 377 HBeAg-negative chronic HBV infection patients with ALT ≤40 U/L who were hospitalized in Affiliated Hospital of Yan’an University, from October 2013 to August 2018 and underwent liver biopsy, among whom the patients with inflammatory activity ＜A2 and fibrosis stage ＜F2 were enrolled as non-antiviral therapy group(n=266), and the patients with inflammatory activity ≥A2 or fibrosis stage ≥F2 were enrolled as antiviral therapy group(n=111). The chi-square test was used for comparison of categorical data between two groups; the t-test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups; univariate and multivariate binary logistic regression analyses were used to screen out the influencing factors for the initiation of antiviral therapy; the receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic efficiency of each indicator in determining the need for antiviral therapy in HBeAg-negative chronic HBV infection patients with ALT ≤40 U/L. ResultsOf all 377 patients, 266 (70.6%) did not need antiviral therapy for the time being, and 111 (29.4%) had marked liver damage and thus needed active antiviral therapy. The multivariate analysis showed that liver stiffness measurement (LSM) (odds ratio ［HR］=2.003, 95% confidence interval ［CI］: 1.647-2.437, P＜005), HBsAg (HR=1.563, 95% CI: 1.110-2.200, P＜0.05), HBV DNA (HR=1.519, 95% CI: 1173-1.966, P＜0.05), and albumin (HR=0.939, 95% CI: 0.884-0.998, P＜0.05) were independent influencing factors for the initiation of antiviral therapy. The ROC curve analysis showed that the area under the ROC curve (AUC) was 0.749 (95% CI: 0.699-0799) for LSM, 0642 (95% CI: 0.586-0.699) for HBV DNA, and 0.565 (95% CI: 0.507-0.623) for HBsAg, and the combination of LSM, HBV DNA, and HBsAg had a larger AUC of 0.779 (95% CI: 0.732-0.827). ConclusionThe levels of LSM, HBV DNA, and HBsAg have a reference value in determining the initiation of antiviral therapy in HBeAg-negative chronic HBV infection patients with ALT≤40 U/L.

The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system (CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells (OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that Foxg1 is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of Foxg1 in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of Foxg1 on demyelination and remyelination in the brain using a cuprizone (CPZ)-induced mouse model. In this work, 7-week-old Foxg1 conditional knockout and wild-type (WT) mice were fed a diet containing 0.2% CPZ w/w for 5 weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice, Foxg1-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that Foxg1 knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both in vivo and in vitro. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3β, a key regulatory kinase in the Wnt pathway, regulates the ability of β-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763, a selective inhibitor of GSK-3β activity, to further demonstrate the regulatory mechanism by which Foxg1 affects OPCs in vitro. The results showed that SB216763 clearly inhibited the expression of GSK-3β, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of Foxg1. These results suggest that Foxg1 is involved in the proliferation and differentiation of OPCs through the Wnt signaling pathway. The present experimental results are some of the first to suggest that Foxg1 is a new therapeutic target for the treatment of demyelinating diseases of the CNS.