Brucellosis has extensive clinical spectrum, clinicians have insufficient understanding of the disease, and the misdiagnosis rate is still high. By collecting and analyzing the clinical characteristics of patients with brucellosis in Heilongjiang Province to provide guidance and reference for clinicians to make timely diagnosis and treatment. The demographic and epidemiological characteristics, clinical features, complications, laboratory findings were retrospectively evaluated in 850 brucellosis patients admitted in the Department of Infectious Diseases of the First Affiliated Hospital of Harbin Medical University and the Second Hospital of Daqing from 2012 to 2017. Of the 850 patients, the most common clinical manifestations were fever (93.3%), joint pain (69.8%), sweating (45.2%), fatigue (38.6%), and splenomegaly (34.0%). Peripheral arthritis, spondylitis and epididymal-orchitis were the common complications. Of the 398 patients who were followed up and completed treatment, 22 (5.5%) had relapse. Brucellosis is a multisystem disease with diverse clinical manifestations. In areas where brucellosis is endemic, the possibility of the disease should be considered in patients with unexplained fever and joints pain. In addition, the high rate of relapse is mainly due to the misdiagnosis of complications, so local CT or MRI examination is necessary for patients with joint pain and low back pain. Timely diagnosis, early detection of complications are essential to improve the prognosis and reduce relapse.

BackgroundHepatitis B virus (HBV) infection has a tendency to be chronic. The quasi species of HBV in the pre-S/S gene and mutations in enhancer II (EnhII)/core promoter (CP)/pre-C of HBV were studied in asymptomatic carrier (AsC) mothers and their children with different virus loads, to gain a better understanding of the pathogenic mechanisms of HBV MethodsQuasi species were analyzed using an established phylogenetic tree based on the sequences of the pre-S/S gene from 3 mother-child pairs. The mutations of EnhII/CP/pre-C were studied in 15 mother-child pairs ResultsSubstitution was the main mutation model. The phylogenetic tree indicated that the pre-S/S gene in every mother-child pair had the same root. The sequences of the pre-S/S gene of each patient were somewhat different from one another, but there was limited evolutionary distance between them. The evolutionary distances between the pre-S/S gene and the base of the tree in patients with low virus loads were greater than those in patients with high virus loads. The mutations in patients with low virus loads were much more frequent than those in patients with high virus loads and were not related to age, irrespective of whether the pre-S/S gene or EnhII/CP/pre-C was considered ConclusionsThere are HBV quasi species in the sera of AsCs, and the mutations are related to virus load and hepatitis B e antigen seroconversion, irrespective of age

Although the prognostic value of microRNA-122 (miR-122) for hepatocellular carcinoma (HCC) patients have been evaluated by numerous studies, the results of them were not completely consistent. The present study aims to comprehensively evaluate the predicting value of miR-122 on the prognosis of patients with HCC based on all eligible literatures. Numerous electronic databases (MEDLINE, Embase, Pubmed, Google Scholar, and China Biology Medicine disc) were applied to retrieve relevant studies. Overall survival (OS) and progression-free survival (PFS) were used as primary endpoints. All statistical analyses were performed by RevMan software version 5.3.5 and STATA software version 14.1. In addition, the results of this meta-analysis were validated by an independent dataset from the Cancer Genome Atlas (TCGA). A total of 11 studies containing 1124 patients were included in this meta-analysis. The pooled results showed that low miR-122 expression in HCC tissues significantly associated with unfavorable OS (hazard ratio [HR] = 1.48, 95% confidence interval [CI] 1.22–1.80, P < .001) and PFS (HR = 1.54, 95% CI 1.28–1.85, P < .001) in patients with HCC. However, the expression level of miR-122 in blood did not have the ability in predicting OS (HR = 0.75, 95% CI 0.44–1.28, P = .29) and PFS (HR = 0.84, 95% CI 0.58–1.20, P = .33) of HCC. Subgroup analysis further indicated that low expression of miR-122 in tumor tissues predicted poor OS in HCC patients who received curative liver resection (HR = 2.00, 95% CI 1.08–3.70, P = .03). Analysis using TCGA dataset suggested that low miR-122 expression in HCC tissues was significantly associated with OS (HR = 1.61, 95% CI 1.13–2.27, P = .008) other than PFS (HR = 1.30, 95% CI 0.96–1.75, P = .09). Low miR-122 expression in HCC tissues was a reliable indicator for predicting the OS of HCC patients who underwent curative resection. Owing to the disagreement between this meta-analysis and the TCGA dataset, the predictive value of miR-122 in tissues for PFS needs to be verified by future well-designed studies with large sample size.

BACKGROUND:Hepatitis B virus (HBV) is a hepatotropic virus that can infect extrahepatic tissue. Whether hematopoietic stem cells (HSCs) can be infected by HBV and serve as a potential virus reservoir is still unknown. In this study, the susceptibilit...

Background: Chronic alcohol consumption is more frequently associated with advanced, aggressive hepatocellular carcinoma (HCC) tumors. Alcohol adversely impacts ER/Golgi membrane trafficking and Golgi protein N‐glycosylation in hepatocytes; these effects have been attributed (in part) to dysregulated adenosine diphosphate‐ribosylation factor (ARF) GTPase signaling. Here, we investigated the role of the ARF GTPase guanine exchange factor PSD4 in HCC progression.Methods: R‐based bioinformatics analysis was performed on publicly available array data. Modulating gene expression was accomplished via lentiviral vectors. Gene expression was analyzed using quantitative real‐time PCR and immunoblotting. PSD4 promoter methylation was assessed using quantitative methylation‐specific PCR. Phospho‐p65(S276)/DNMT1 binding to the PSD4 promoter was analyzed via chromatin immunoprecipitation. We constructed ethanol/DEN‐induced and DEN only‐induced transgenic murine models of HCC.Results: We identified PSD4 as a hypermethylated, suppressed gene in alcohol‐related HCC tumors; however, PSD4 was not dysregulated in all‐cause HCC tumors. Certain HCC cell lines also displayed varying degrees of PSD4 downregulation. PSD4 overexpression or knockdown decreased and increased cell migration and invasiveness, respectively. Mechanistically, PSD4 transcription was repressed by TNF‐α‐induced phospho‐p65(S276)’s recruitment of DNA methyltransferase 1 (DNMT1), resulting in PSD4 promoter methylation. PSD4 inhibited pro‐EMT CDC42 activity, resulting in downregulation of E‐cadherin and upregulation of N‐cadherin and vimentin. Hepatocyte‐specific PSD4 overexpression reduced ethanol/DEN‐induced HCC tumor progression and EMT marker expression in vivo.Conclusions: PSD4 is a hypermethylated, suppressed gene in alcohol‐related HCC tumors that negatively modulated pro‐EMT CDC42 activity. Furthermore, we present a novel phospho‐NF‐κB p65(S276)/DNMT1‐mediated promoter methylation mechanism by which TNF‐α/NF‐κB signaling represses PSD4 transcription in HCC cells.

Although the existence of cancer stem cells (CSCs) has been suggested in diffuse large B cell lymphoma (DLBCL), there is still no definitive marker. CD45⁺CD19^- has been regarded as a potential marker of CSCs in mantle cell lymphoma (MCL). So, we explored the role of CD45⁺CD19^- in DLBCL. However, both CD45⁺CD19^- cells and CD45⁺CD19⁺ cells did not generate tumors until more than 100,000 cells were inoculated in NOD/SCID mice, even CD45⁺CD19⁺ cells generated more and larger tumors, as well as the soft agar colony formation in vitro; The aldehyde dehydrogenase (ALDH) activity was also identified in this study. Only 1,500 ALDH^high cells were enough to generate tumors in mice while the same number of ALDH^- cells were not. Moreover, both groups formed tumors when more cells were inoculated, but ALDH^high cells formed more and larger tumors. The similar result was obtained in vitro clonogenicity experiments. OCT4, SOX2, Nanog, and ABCG2 genes did not show any difference in CD45⁺CD19⁺, CD45⁺CD19^-, ALDH^high and ALDH^- cells. Taken together, CSCs are not enriched in the CD45⁺CD19^- cells but in the ALDH^high cells in DLBCL cell lines.