A proper triage for detecting women with high-risk human papillomavirus genotypes other than HPV16/18.

OBJECTIVE: To evaluate the effect of human papillomavirus (HPV) L1 capsid protein detection in cervical exfoliated cells as a proper triage for women with high-risk human papillomavirus (hrHPV) genotypes other than HPV 16/18. STUDY DESIGN: From January 2013 to June 2015, a total of 513 women aged 30-65 years infected with non-16/18 hrHPV were enrolled into the study. Primary HPV testing, HPV 16/18 genotyping and Papanicolaou (Pap) test were performed in all eligible women. HPV L1 capsid protein was detected by immunocytochemistry in cervical exfoliated cells. All hrHPV positive women underwent colposcopy and further biopsy if indicated. Relationships between HPV L1 capsid protein expression and histologic diagnosis, as well as cytology were analyzed. RESULTS: The positive expression rate of HPV L1 capsid protein in CIN2+ group was significantly lower than that in CIN1 or better group (16.3% vs. 66.7%, P=0.000). Compared with the Pap test, HPV L1 detection achieved higher sensitivity (83.7% vs. 51.2%, P=0.000), higher negative predictive value (NPV) (95.3% vs. 88.6%, P=0.002), and significant lower specificity (66.7% vs.76.1%, P=0.002) while identifying CIN2+. Compared with the Pap test, HPV L1 detection achieved higher sensitivity (89.7% vs. 51.7%, P=0.008), higher NPV (99.0% vs. 96.2%, P=0.043), and significant lower specificity (61.2% vs.73.8%, P=0.000) while identifying CIN3+. CONCLUSION: Because of its higher sensitivity and NPV than that of Pap test, HPV L1 capsid protein detection in cervical exfoliated cells reduces the missed identification of high-grade cervical intraepithelial neoplasia (CIN) in women with hrHPV genotypes other than HPV 16/18. HPV L1 capsid protein detection could be a potential triage for women with non-16/18 hrHPV infection.

Effects of bicyclol on dimethylnitrosamine-induced liver fibrosis in mice and its mechanism of action.

The aim was to investigate the suppressive effect of bicyclol on hepatic fibrosis induced by dimethylnitrosamine (DMN) in mice and the mechanism of its action. Hepatic fibrosis was established by intraperitoneal injection of 8 mg kg(-1) day(-1) on three consecutive days of each week for 4 or 5 weeks. In the prophylactic experiment, bicyclol (100 and 200mg.kg(-1)) was administered by gavage in association with DMN injection. For the therapeutic experiment, mice were firstly injected with DMN for 5 weeks as in the prophylactic experiment, and then the mice in drug groups were orally administered bicyclol (100 and 200mg.kg(-1)) once daily for 5 weeks. As a result, the levels of alanine aminotransferase (ALT), total bilirubin, hydroxyproline (Hyp), prolidase, tumor necrosis factor-alpha (TNFalpha), transforming growth factor beta-1 (TGFbeta(1)), type I collagen in serum and the score of liver fibrosis all significantly increased in the hepatic fibrosis model group in comparison with those in control group. The treatment with bicyclol markedly reduced all the above criteria. Bicyclol also attenuated the decrease of body weight of mice, serum total protein and albumin. In addition, bicyclol treatment inhibited liver TGFbeta(1) and tissue inhibitor of metalloproteinase 1 (TIMP-1) mRNA expression in the prophylactic experiment. Similarly, bicyclol reduced TIMP-1 levels in liver and serum and increased collagenase activity in the liver in the therapeutic experiment. The result suggest that bicyclol attenuates DMN-induced hepatic fibrosis in mice. Its mechanisms of action may be related to the hepatoprotective and anti-inflammation properties, the down-regulation of liver TGFbeta(1) and TIMP-1 expression and the increase of net collagenase activity in liver.