High-throughput sequencing-based analysis of gene expression of hepatitis B virus infection-associated human hepatocellular carcinoma.

Hepatitis B virus (HBV) infection is a critical factor for the initiation and progression of hepatocellular carcinoma (HCC). Gene expression profiles for HBV-associated HCC may provide valuable insight for the diagnosis and treatment of this type of HCC. The present study aimed to screen the differential genes in human HCC tissues based on high-throughput sequencing and to predict the potential therapeutic targets. Total mRNA was extracted from human HCC tissues and paracancerous tissues and sequenced using the Hiseq4000 sequencing platform. Differential gene expressions were screened and further analyzed using quantitative PCR and immunohistochemistry. A total of 2,386 differentially expressed genes were screened. Of these, 1119 were upregulated and 1,267 were downregulated in paracancerous tissues compared with tumor tissues. Gene Ontology term analysis demonstrated that differentially expressed genes were involved in carboxylic acid catabolism, monocarboxylic acid metabolic processes and α-amino acid metabolic processes. Molecular functional analysis revealed that the differentially expressed genes functioned in oxidoreductase activity, for example acting on CH-OH group of donors and permitting identical protein binding, anion binding, coenzyme binding and monocarxylic acid transporter activity. The Kyoto Encyclopedia of Genes and Genomes analysis reported that the differentially expressed genes were primarily concentrated in 20 signaling pathways, such as valine, leucine and leucine degradation, retinol metabolism and the cell cycle. Differential expression of proteins regulating the cell cycle, including stratifin, cyclin B1 and cyclin-dependent kinase 1, were significantly higher in tumor tissue compared with those in paracancerous tissue at both the mRNA and protein levels. These results were consistent with those obtained from high-throughput sequencing, indicating the reliability of the high-throughput sequencing. Together, these results identified differentially expressed genes and predicted the subsequent signaling pathways, which may be involved in the occurrence and development of HCC. Therefore, the present study may provide novel implications in the therapeutic and diagnosis of HCC.

A totally implantable venous access port associated with bloodstream infection caused by Mycobacterium fortuitum: A case report.

RATIONALE: Rapidly growing mycobacteria (RGM) are well-known causative agents of human infections, particularly in immunocompromised hosts. However, Mycobacterium fortuitum, a predominant organism, in catheter-associated infections, has rarely been documented in totally implantable venous access port (TVIAP)-associated bloodstream infections. PATIENT CONCERNS: A 25-year-old woman with breast cancer presented to hospital with repeated fever for several days. The patient first refused to remove the TVIAP in her body, and had a relapse of M. fortuitum bacteraemia four months later. DIAGNOSES: Bacteria isolated from patient's blood and TVIAP were identified as M. fortuitum by Matrix-assisted laser desorption/ionization-time of flight spectrometry and bacterial 16s rDNA sequencing. The patient was diagnosed as a TVIAP-associated bloodstream infection. INTERVENTIONS: The TVIAP was eventually surgically removed, and M. fortuitum was found to have localized on the tip of the catheter. The patient was treated by anti-infection therapy. OUTCOMES: The patient was treated with 4 weeks of intravenous amikacin and levofloxacin followed by 4 weeks of oral levofloxacin. No episodes of fever occurred during the follow-up to date. LESSONS: RGM infections remain a challenging issue for TIVAPs. Accurate species identification, timely intravascular catheter removal and appropriate antibiotic therapy are recommended to ensure successful outcomes.

Association of Interferon Gamma +874T/A Polymorphism and Leukemia Risk: A Meta-Analysis.

Interferon gamma (IFN-γ) has antitumor and antiproliferative effects, and previous studies indicated IFN-γ +874T/A (rs2430561) polymorphism were related to the risk of many types of cancer. However, the association between IFN-γ +874T/A polymorphism and leukemia risk remained controversial.We performed a comprehensive meta-analysis based on the Preferred Reporting Items for Systematic Reviews and Meta-analyses statement (PRISMA). Electronic database of Embase, Pubmed, and the Cochrane Library were searched for eligible articles published up to December 13, 2015. The association between genetic polymorphisms and leukemia risk was measured by odds ratios (ORs) and its corresponding 95% confidence intervals (CIs).A total of 8 studies amounting to 420 patients and 767 control subjects were retrieved for this study. Although associations between IFN-γ +874T/A polymorphism and overall leukemia risks were lacking, decreased chronic lymphocytic leukemia (CLL) risk was detected in the allelic model (T vs A, OR=0.660, 95%CI = 0.483-0.902, P = 0.009, I = 0.0% and P = 0.863 for heterogeneity), the codominant model (TT vs AA, OR = 0.472, 95%CI = 0.247-0.902, P = 0.023, I = 0.0% and P = 0.994 for heterogeneity), and dominant model (TT + TA vs AA, OR = 0.457, 95%CI = 0.285-0.734, P = 0.001, I = 40.3% and P = 0.195 for heterogeneity) by using fixed-effect model separately. On the contrary, results indicated T carries have an increased chronic myelogenous leukemia (CML) risk in dominant model (TT + TA vs AA, OR = 1.783, 95%CI = 1.236-2.573, P = 0.002, I = 19.0% and P = 0.295 for heterogeneity).This study suggests IFN-γ +874T/A polymorphism are related to CML and CLL risk. In addition, our work also points out IFN-γ +874T/A polymorphism may play dual contrasting role in leukemia risk.

Association Between IL-4 Polymorphisms and Risk of Liver Disease: An Updated Meta-Analysis.

Interleukin-4 (IL-4) polymorphisms have been reported to influence an individual's susceptibility to liver disease as it is a central anti-inflammatory Th2 cytokine; however, these results remain controversial.A comprehensive meta-analysis of the relevant literature was thus performed to better estimate the relationship between IL-4 polymorphisms and liver disease.Systematic searches of various databases (PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure) for studies published before July 5, 2015 were performed. Odds ratios (ORs) with 95% confidence intervals (CIs) calculated in fixed or random-effects models were used to estimate the strength of the association. Subgroup analyses, meta-regression, Galbraith plots, and sensitivity analyses were also performed.A total of 16 case-control studies, of which 15 involved the -590C/T polymorphism and 3 involved the -33T/C polymorphism, were included in the study. With respect to the -590C/T polymorphism, a significantly increased risk of liver diseases was found in the overall population (TT + CT vs CC: OR = 1.25, 95% CI = 1.06-1.49, P = 0.009 and CT vs CC: OR = 1.22, 95% CI = 1.00-1.48, P = 0.048) and the Asian population (TT + CT vs CC: OR = 1.28, 95% CI = 1.04-1.57, P = 0.020). Further subgroup analyses also showed significant associations between the -590C > T polymorphism and the risk of hepatitis C infection and hepatocellular carcinoma. However, no association was found between the -33T/C polymorphism and risk of liver diseases in all comparison models.This meta-analysis suggested that the IL-4 -590C > T polymorphism is associated with an increased risk of hepatitis C infection and hepatocellular carcinoma, especially among the Asian population.