Background Transient elastography is a non‐invasive method for staging liver fibrosis. The meta‐analysis using the hierarchical models to evaluate the diagnostic accuracy of transient elastography for the staging of liver fibrosis in patients with chronic hepatitis B was rarely reported. Aim A meta‐analysis using the hierarchical models was performed to assess transient elastography for diagnosing and stage liver fibrosis in patients with chronic hepatitis B. Methods Electronic databases were searched and studies were identified to assess the diagnostic accuracy of transient elastography in CHB patients for staging fibrosis F ≥ 2, F ≥ 3 and F = 4 with liver biopsy as a reference standard. The hierarchical summary receiver operating characteristic curve and the bivariate models were performed to evaluate the diagnostic accuracy of transient elastography, and meta‐regression analyses were performed to explore the heterogeneity. The quality Assessment of Diagnostic Accuracy Studies‐2 tool was used to assess the quality of studies. Results Twenty‐seven studies with a total of 4386 patients were included in the meta‐analysis. The summary sensitivity of transient elastography for staging fibrosis F ≥ 2, F ≥ 3 and F = 4 was 0.806 (95% CI, 0.756–0.847), 0.819 (95% CI, 0.748–0.874) and 0.863 (95% CI, 0.818–0.898), respectively, and the summary specificity was 0.824 (95% CI, 0.761–0.873), 0.866 (95% CI, 0.824–0.899) and 0.875 (95% CI, 0.840–0.903), respectively. The corresponding area under the summary receiver operating characteristic curve was 0.88 (95% CI, 0.85–0.91), 0.91 (95% CI, 0.88–0.93) and 0.93 (95% CI, 0.91–0.95), respectively. Meta‐regression showed that patient age contributed to heterogeneity. Conclusions Transient elastography performs well to diagnose liver fibrosis in patients with chronic hepatitis B, which may reduce the use of liver biopsy.

The female vaginal environment contains diverse microorganisms, and their interactions play significant roles in health and disease. Lactobacillus species are the predominant vaginal microorganisms in healthy women and relevant as a barrier to defense against pathogens, including Candida albicans. The yeast-to-hyphae transition is believed to be a determinant of C. albicans pathogenesis. In this study, we investigated the effects of vaginal isolates of L. crispatus (7 strains), L. gasseri (6 strains) and L. jensenii (5 strains) on growth, hyphal formation and virulence-related genes expression of C. albicans ATCC 10231. We found that the L. crispatus showed the most significant antimicrobial activities in microplate-based liquid medium assay (P 60%. The effects might be due to their productions of some secretory antimicrobial compounds in addition to H2O2 and organic acids. Furthermore, each of the CFS of Lactobacillus strains was found to significantly suppress the yeast-to-hyphae transition of C. albicans under hyphae-inducing conditions (RPMI 1640 medium supplemented with 10% fetal bovine serum). The hyphae inhibition rates of C. albicans treated by CFS from L. crispatus, L. gasseri and L. jensenii were 88.3 ± 3.02 %, 84.9 ± 6.0% and 81.9 ± 6.2 %, respectively. Moreover, the expression of hyphae-specific genes (ALS3, HWP1, ECE1, EAP1 and SAP5) and transcriptional regulatory genes (EFG1, TEC1 and NRG1) were analyzed using quantitative real-time PCR. The results demonstrated that L. crispatus CFS significantly down-regulated the expression of hyphae-specific genes ALS3 (0.140-fold)), HWP1 (0.075-fold) and ECE1 (0.045-fold), while up-regulated the expression of the negative transcriptional regulator gene NRG1 with 1.911-fold. The antimicrobial compounds from L. crispatus B145 against Candida growth were heat stable and protease resistance, but those against hyphal formation were partially sensitive to the same treatments. Our novel findings suggest that L. crispatus, a dominant Lactobacillus species associated with a healthy vagina, could strongly inhibit C. albicans growth and hyphal formation. L. crispatus might repress the expression of hyphae-specific genes (ALS3, HWP1 and ECE1) in a NRG1-dependent manner. Besides, L. crispatus B145 is highly worthwhile for probiotic investigation.

The study was designed to investigate whether serum hepatitis B virus (HBV) RNA is a strong surrogate marker for intrahepatic HBV covalently closed circular DNA (cccDNA) compared with serum HBV DNA, hepatitis B surface antigen (HBsAg), and hepatitis B e antigen (HBeAg) in HBeAg-positive chronic hepatitis B (CHB) patients. Serum HBV RNA, HBV DNA, HBsAg, HBeAg, and intrahepatic cccDNA were quantitatively detected at baseline ( n = 82) and 96 weeks ( n = 62) after treatment with nucleos(t)ide analogue (NUC) in HBeAg-positive CHB patients. The correlations among serum HBV RNA, HBV DNA, HBsAg, HBeAg, and intrahepatic cccDNA levels were then statistically analyzed. The results showed that pretreatment intrahepatic cccDNA levels correlated better with serum HBV DNA levels ( r = 0.36, P < 0.01) than with serum HBV RNA levels ( r = 0.25, P = 0.02), whereas no correlations were found between pretreatment intrahepatic cccDNA levels and HBsAg ( r = 0.15, P = 0.17) or HBeAg ( r = 0.07, P = 0.56) levels. At 96 weeks after NUC treatment, intrahepatic cccDNA levels correlated well with HBsAg levels ( r = 0.39, P < 0.01) but not with serum HBV RNA, HBV DNA, and HBeAg levels (all P > 0.05). Besides, the decline in the intrahepatic cccDNA level from baseline to week 96 correlated better with the reduction in the serum HBsAg levels than with the decreases in the levels of the other markers (for the HBsAg decline, r = 0.38, P < 0.01; for the HBV DNA decline, r = 0.35, P = 0.01; for the HBV RNA decline, r = 0.28, P < 0.05; for the HBeAg decline, r = 0.18, P = 0.19). In conclusion, the baseline serum HBV RNA level or its decline after 96 weeks of NUC therapy correlated with the corresponding intrahepatic cccDNA level, while it was less than that seen with serum HBV DNA at baseline and HBsAg (or its decline) at 96 weeks after treatment, respectively.

BACKGROUND: Recent research has suggested that the oncomir microRNA 155 (miR‐155) is up‐regulated in hepatocellular carcinoma (HCC). In this study, the authors investigated the tumorigenic mechanism of this oncomir in the development of HCC.METHODS: Quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) was conducted to analyze the expressions of miR‐155 and its potential target genes in paired tumor tissues and adjacent tumor‐free tissues and in disease‐free liver tissue samples. The in silico predicted target genes of miR‐155 were assessed by dual‐luciferase reporting assay, real‐time RT‐PCR, and Western blot analyses. U6 promoters that drive miR‐155 precursor overexpression and miR‐155 tough decoy knock‐down constructs were used to study its affects on cell proliferation in vitro and on tumor formation in nude mice.RESULTS: Quantitative RT‐PCR demonstrated a gradual ascension of miR‐155 expression in cirrhotic liver tissues and in HCC tumor tissues compared with low expression levels in normal liver tissues. Ectopic expression of miR‐155 in HepG2 cells enhanced its tumorigenesis, whereas depletion of the endogenous miR‐155 reversed these tumorigenic properties. Ectopic expression of sex‐determining region Y box 6 (SOX6) was able to reverse the growth‐promoting property of miR‐155. Concordantly, the results demonstrated for the first time that SOX6 is a direct target of miR‐155. Further analysis revealed that SOX6 reduced cell growth by up‐regulating p21waf1/cip1 expression in a p53‐dependent manner. In addition, a decline in p21waf1/cip1 expression caused by miR‐155 could be reversed by SOX6 expression.CONCLUSIONS: The current data indicated that SOX6 is a novel target of miR‐155 and that miR‐155 enhances liver cell tumorigenesis at least in part through the novel miR‐155/SOX6/p21waf1/cip1 axis. These findings suggest that miR‐155 may be a potential target for HCC treatment. Cancer 2012. © 2011 American Cancer Society.