Objective To investigate the levels and clinical significance of serum 25 -hydroxy vitamin D[25 (OH)D]in patients with chronic liver disease.Methods A total of 153 hospitalized patients with chronic liver disease in the First Affiliated Hospital of Jilin Univer-sity from June 2012 to September 2013 were enrolled in the study group.The levels of serum 25(OH)D were measured by liquid chromatog-raphy tandem mass spectrometry.The serum samples from 300 healthy volunteers who underwent physical examination in our hospital were used as controls.The study group was divided into three subgroups:non -cirrhosis,liver cirrhosis [Child -Pugh (CP)grades A,B,and C],and primary biliary cirrhosis.Comparison of continuous data between groups was made by t test and analysis of variance,and compari-son of categorical data was made by chi -square test.Correlation between different variables was investigated by Pearson linear regression a-nalysis.Results Of the 153 patients with chronic liver disease,the percentages of those who had vitamin D adequacy (≥30 ng/ml),in-sufficiency (20 -30 ng/ml),deficiency (10 -20 ng/ml),and severe deficiency (<10 ng/ml)were 20.3%,22.9%,35.9%,and 20.9%,respectively.The percentages of patients with vitamin D deficiency and severe deficiency were significantly higher in the cirrhosis subgroup than in the non -cirrhosis and primary biliary cirrhosis subgroups (41.7%,25.0% vs 27.5%,12.5% and 23.5%,17.6%,re-spectively;χ2 =6.261 -18.474,P =0.001 -0.012).The serum 25(OH)D levels in patients with cirrhosis were significantly lower com-pared with those in patients without cirrhosis and in controls (18.58 ±12.48 vs 23.78 ±11.81 and 25.69 ±12.39 ng/ml,P =0.029 and 0.001).CP class C cirrhotic patients had significantly lower serum levels of 25(OH)D compared with CP class A patients (P =0.009). Conclusion Serum 25(OH)D deficiency is common in patients with chronic liver disease.25(OH)D levels in cirrhotic patients,especial-ly in CP class C patients,are markedly lower than those in non -cirrhotic patients.

Objective:To clone human interleukin-33(hIL-33)and express it in E.coli efficiently.Methods:The primers were synthesized according to the hlL-33 cDNA sequence in GeneBank.The hIL-33 was amplified by RT-PCR from human fibroblast cell line(L929),the PCR product was inserted into pUC19 vector.The IL-33 cDNA confirmed by sequencing was inserted into expressing vector PQE30 and expressed in E.coli M15 strain.IL-33 protein expression was induced by IPTG and purified by Ni-NTA affinity chromatography.The recombinant IL-33 was identified by Immunoblot and its biological activity was analyzed.Results:DNA sequencing confirmed that the cloned cDNA was identical to the published sequence of hIL-33.The recombinant plasmid PQE/hIL-33 was transformed into M15.An expected 18KD protein of hIL-33 found mainly in the induced host strains about 25% of total bacteria lysis by SDS-PAGE and coomassie blue staining.The 18 KD protein could be recognized by anti-IL33 antibody in western blot.The recombinant protein was purified to more than 95% of total protein and induces the production of IL-4 and IL-5 in human peripheral blood mononuclear cells.Conclusion:We have successfully expressed hIL-33 protein in E.coli and the expressed product has IL-33 specific bioactivity.

Objective: To explore the related factors for primary hepatic carcinoma (PHC) caused by chronic hepatitis B (CHB) and hepatitis C (CHC). Methods: According to the principle of cross-sectional study, a cluster random sample method was used, a total of 366 chronic hepatitis patients in hospitals were recruited from three provincial tertiary hospitals in Shanxi, Henan and Jilin between July 2016 and October 2016, respectively. Using a self-designed unified questionnaire, face-to-face interviews was conducted on subjects, including sex, age, alcohol consumption, coffee consumption, green tea consumption, fish consumption, smoking, HBV/HCV diagnosis and treatment, diabetes mellitus, family history of PHC (whether PHC in first-degree relatives), etc. Multivariate unconditional logistic regression were performed to identify the related factors for PHC with CHB and CHC. According to the clinical diagnosis the patients were divided into a chronic hepatitis group (not developing to PHC) and a PHC group. Results: Among 366 cases patients, 287 (78.4%) cases were male, 79 cases were female (21.6%), average age was (52.7±9.3) years. 202 cases were chronic hepatitis group, 164 cases were PHC group. Multivariate unconditional logistics regression analysis indicated that alcohol consumption (odds ratio (OR)=2.11, 95%CI: 1.18-3.75), family history of PHC (OR=5.12, 95%CI: 2.60-10.08) were positively correlated with the development of PHC in chronic b, green tea consumption (OR=0.45, 95%CI: 0.23-0.88), antiviral treatment (OR=0.19, 95%CI: 0.11-0.32) were negatively correlated. Alcohol consumption (OR=3.98, 95%CI: 1.14-13.85) was positively correlated with the development of PHC in chronic c, antiviral treatment (OR=0.14, 95%CI: 0.04-0.50) was negatively correlated. Conclusion Alcohol consumption, family history of PHC, green tea consumption and antiviral treatment were the related factors for the development of PHC in chronic hepatitis b. Alcohol consumption and antiviral treatment were the related factors for the development of PHC in chronic hepatitis c.

There is are large number of patients with chronic hepatitis B virus (HBV) infection. HBV not only damages the liver, but also involves the kidney. Hepatitis B virus-associated glomerulonephritis (HBV-GN) is secondary glomerulonephritis caused by HBV infection, and it is one of the most common extrahepatic complications of HBV infection. HBV-GN is mainly observed in children and young and middle-aged adults, with varying degrees of proteinuria as the main clinical manifestation, and it may be accompanied by hematuria and hypertension. Membranous nephropathy is the most common pathological type, followed by membrano-proliferative glomerulonephritis and IgA nephropathy. HBV-GN has an insidious onset and lacks characteristic symptoms and pathological manifestations, and thus it may be easily confused with various types of glomerulonephritis, which may lead to missed diagnosis and misdiagnosis. HBV-GN has a complex pathogenesis involving various links such as immune disorders, direct viral damage, and genetics, among which the theory of immune complex deposition has been widely recognized. In recent years, some important advances have been made in the research on the pathogenesis, diagnosis, and treatment of HBV-GN. This article summarizes the above issues, so as to provide a reference for clinical diagnosis and treatment.