Objective To analyze the characteristics of drug resistance to quinolones and erythromycin of clinical Campylobacter jejuni (C .jejuni) strains and to further investigate its molecular mechanisms .Methods A total of 193 clinical C .jejuni strains were isolated from feces of patients with diarrhea .Drug susceptibilities to ciprofloxacin (CIP ) , gentamycin (GEN ) , azithromycin (AZI ) , erythromycin (ERY) ,chloromycetin (CHL) ,doxycycline (DOX) and tetracycline (TET) were tested using standard agar dilution method . gyrA , gyrB and parC genes were amplified by polymerase chain reaction (RCR) and analyzed for molecular mechanisms of quinolones resistance ,and 23S rRNA , rplD and rplV genes for erythromycin resistance .Chi‐square test or Fisher′s exact two‐tailed tests were used to perform the statistical analysis .Results A total of 193 clinical C . jejuni strains were isolated during 1994—2010 ,among which 43 C .jejuni strains were isolated in 1994—1999 ,80 in 2000—2005 and 70 in 2006—2010 .The drug resistance rates for CIP increased significantly from 55 .8% in 1994—1999 to 95 .0% in 2000—2005 and 94 .3% in 2005—2010 (χ2=41 .94 ,P<0 .01) .The drug resistance rates for GEN were 0 in 1994—1999 ,11 .3% in 2000—2005 and 10 .0% in 2006—2010 ,but with no statistic difference (χ2=5 .078 , P=0 .08) .The drug resistance rates for AZI were 0 in 1994—1999 ,3 .8% in 2000—2005 and 4 .3% in 2006—2010 (χ2=1 .81 ,P=0 .40) .The drug resistance rates for ERY were 0 in 1994—1999 ,1 .3% in 2000—2005 and 4 .3% in 2006—2010 (χ2 = 2 .87 , P= 0 .24 ) . T he drug resistance rates for CHL were 2 .3% in 1994—1999 ,11 .3% in 2000—2005 and 20 .0% in 2006—2010 (χ2 =7 .82 ,P=0 .02) .The drug resistance rates for DOX were 60 .5% in 1994‐1999 ,86 .3% in 2000—2005 and 82 .9% in 2006—2010 (χ2 =12 .18 ,P<0 .01) .The drug resistance rates for TET were 74 .4%in 1994—1999 ,95 .0% in 2000—2005 and 94 .3% in 2006—2010 (χ2 = 15 .46 , P< 0 .01 ) .T he drug resistance rates for CIP‐DOX‐TET were 37 .2% in 1994—1999 ,83 .8% in 2000—2005 and 80 .0% in 2006—2010 (χ2 =33 .53 ,P<0 .01) .The drug resistance rates for CHL‐CIP‐DOX‐TET were 0 in 1994—1999 ,7 .5% in 2000—2005 and 20 .0% in 2006—2010 (χ2=12 .68 ,P<0 .01) .The drug resistance rates for GEN‐CIP‐DOX‐TET were 0 in 1994—1999 ,7 .5% in 2000—2005 and 8 .6% in 2006—2010 (χ2 =3 .74 ,P=0 .15) .All 163 CIP‐resistant C .jejuni strains had C257T mutation on gyrA gene .Mutations on gyrB gene were silent .ParC gene was absent in C .jejuni .Four ERY resistant C .jejuni strains had no mutation on rplD and rplV genes , but 3 of them had A2075G mutation on 23S rRNA gene . Conclusions The antimicrobial resistance rates for C .jejuni increase remarkably over the periods .C257T mutation on gyrA gene and A2075G mutation on 23S rRNA gene are main mechanisms for quinolones resistance and erythromycin resistance ,respectively .

Drug-induced liver injury (DILI) is one of the most common and severe adverse drug reactions in humans, which may lead to liver failure and even death in some patients. Liver injury caused by different drugs has various clinical manifestations and severities, and most patients with DILI have no symptoms or have mild symptoms. There are various typing methods for DILI based on clinical features, course of disease, and pathogenesis. According to the R value, DILI can be classified into hepatocellular injury type (R ≥5), cholestasis type (R ≤2), and mixed type (2 < R < 5); according to the course of the disease, DILI can be classified into acute DILI and chronic DILI; according to the pathogenesis, DILI can be classified into intrinsic DILI, idiosyncratic DILI, and indirect DILI. A comprehensive understanding of the clinical manifestations and typing methods of DILI helps to reveal its pathogenesis and perform diagnosis and treatment in a timely manner.

OBJECTIVE: In order to improve the accuracy and reliability in sudden cardiac death, the pathogenesis and relationship between the viral myocarditis and dilated cardiomyopathy were investigated. METHODS: Improved immunohistochemical technique was adopted to detect the expression of the dystrophin in myocardium from 25 viral myocarditis, 28 dilated cardiomyopathy and 17 control cases including normal, coronary atherosclerotic heart disease and hypertension heart disease as control. RESULTS: The positive rate of dystrophin protein expression in control group was 100%, that in viral myocarditis was 88%, and that in dilated cardiomyopathy was 57%, There were significant differences among three groups (P<0.05), and the correlation between viral myocarditis and dilated cardiomyopathy group (r = -0.526)were also found. CONCLUSION The myocardial cytoskeletal protein is disrupted in viral myocarditis and dilated cardiomyopathy, and the dystrophin protein may be involved in the pathogenesis of viral myocarditis and dilated cardiomyopathy. The viral infect and impair heart functions by cleaving host dystrophin proteins may ultimately contributes to the viral myocarditis to the converting from dilated cardiomyopathy.
Cardiomyopathy, Dilated/metabolism* ; Case-Control Studies ; Death, Sudden, Cardiac ; Dystrophin/metabolism* ; Enterovirus Infections/complications* ; Female ; Humans ; Immunohistochemistry ; Male ; Myocarditis/virology* ; Myocardium/pathology* ; Staining and Labeling

Objective: To study the correlation between the level of T-bet expression and liver damage in peripheral plasma cells of patients with autoimmune hepatitis (AIH) in order to provide reference for the study of pathogenesis and development of diseases. Methods: The peripheral venous blood and clinical examination data of 29 cases with AIH and 6 healthy volunteers were collected. The percentage of subpopulations of peripheral blood B cells and the proportion of T-bet⁺ cells in each subgroup were detected by flow cytometry. Plasma cells (CD19⁺CD10^-CD27^hiCD38^hi), primary B cells (CD19⁺CD10^-CD27^-IgD⁺), transitional B cells (CD19⁺CD10⁺), and memory B cells (CD19⁺CD10^-CD27⁺IgD^-) were the included subsets of B cells. Serum immunoglobulin G (IgG) and alanine aminotransferase (ALT) levels, the proportion of B cells in peripheral blood subsets and IgG level, the proportion of T-bet⁺ cells in each subset and the proportion of T-bet⁺ plasma cells in each subset in B cells, the proportion of T-bet⁺ plasma cells and the level of serum ALT were analyzed for correlation analysis. Statistical analysis was performed using two independent sample t-tests and linear regression. Results: The serum IgG level of AIH patients with abnormal ALT (19.47 ± 1.039)g/L was significantly higher than that of normal ALT patients (15.5 ± 1.069)g/L, and the difference was statistically significant (t = 2.65, P < 0.05). The percentage of peripheral plasma cells in B cells of AIH patients (2.80 ± 0.14) % was higher than that of healthy volunteers (0.73 ± 0.09) %, and the difference was statistically significant (P < 0.01). The percentage of T-bet⁺ cells in peripheral plasma cells of AIH patients (23.54 ± 1.61) % was higher than that of healthy volunteers (6.59±0.59) % , and the difference was statistically significant (P < 0.01). The correlation analysis showed that the proportion of T-bet⁺ cells in peripheral plasma cells of AIH patients was positively correlated with the proportion of plasma cells to B cells (r = 0.224 7, P < 0.01), and the percentage of peripheral plasma cells to B cells was positively correlated with the level of serum IgG (r = 0.299 1, P < 0.01). Serum IgG level was correlated with the level of ALT, reflecting an indicator of liver damage (t = 2.65, P < 0.05). Conclusion The increase of T-bet expression in the peripheral plasma cells of AIH patients is associated with liver damage, which is a new mechanism of AIH pathogenesis and disease progression.

Objective: To explore the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection who received entecavir alone or in combination with anluohuaxianwan for 78 weeks. Methods: Patients with chronic HBV infection were randomly treated with entecavir alone or in combination with anluohuaxian for 78 weeks. Ishak fibrosis score was used for blind interpretation of liver biopsy specimens. The improvement in liver fibrosis condition before and after the treatment was compared. Student's t test and non-parametric test (Mann-Whitney U-Test and Kruskal-Wallis test) were used to analyze the measurement data. The categorical variables were analyzed by Chi-square test method and Spearman’s rank correlation coefficient was used to test bivariate associations. Results: Liver fibrosis improvement rate after 78 weeks of treatment was 36.53% (80/219) and the progression rate was 23.29% (51/219). The improvement of liver fibrosis was associated to the degree of baseline fibrosis and treatment methods (P < 0.05). The improvement rate of hepatic fibrosis in patients treated with anluohuaxianwan combined with entecavir at baseline F < 3 (54.74%, 52/95) was significantly higher than that in patients treated only with entecavir (33.33%, 16/48), P = 0.016 and the progression rate of hepatic fibrosis (13.68%, 13/95) was lower than that in patients treated alone (18.75%, 9/48), P = 0.466. In patients with baseline F < 3, the proportion of patients with improved and stable liver fibrosis in the combined treatment group (68.1%, 32/47) was higher than that in the treatment group alone (51.7%, 15/29). Conclusion Combined anluohuaxianwan and entecavir treatment can significantly improve the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection. Furthermore, it has the tendency to improve the stability rate and reduce the rate of progression of liver fibrosis.