Expression of FHIT genes in CIN and cervical carcinoma and the relationship between FHIT gene and p53 and HPV16/18 / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the role and significance of FHIT genes depletion, p53 overexpression and HPV16/18 infection in cervical intraepithelial neoplasia (CIN) and cervical carcinoma (CC).</p><p><b>METHODS</b>Tumor samples taken from 52 cases of CIN and 69 cases of CC were processed by immunohistochemistry (SP) to determine the expression of FHIT genes and p53 protein, by in situ hybridization to detect HPV16/18 infection, and were compared with those in 18 cases of normal cervical tissues as control.</p><p><b>RESULTS</b>(1) The FHIT expression was positive in normal cervical tissue with no depletion occurred, and was 30.8% in CIN. It was significantly higher in CIN III and carcinoma groups than that in normal and CIN I/II groups (P < 0.01). The depleted expression of FHIT in infiltrating cervical carcinoma group was 66.7% (46/69), significantly higher than that in normal and CIN groups (P < 0.01). Along with the decreasing of cell differentiation, the negative rate of FHIT raised. (2) The positive expression of p53 in CC group was 56.5% (39/69) and the HPV16/18 was 84.1% (58/69), both higher than that in CIN and normal groups (P < 0.05). (3) In CIN and CC groups, the positive rate of p53 in cases with positive or negative FHIT expression was similar (P > 0.05). (4) There is a negative correlation between FHIT and p53 expression. The rate of HPV16/18 infection in the depleted expression of FHIT group was significantly higher than that in FIHT normal expression group (P < 0.01).</p><p><b>CONCLUSION</b>(1) The FHIT-depletion is related with cervical carcinogenesis. It may be used as a marker to serve mass screening of CIN-high risk subjects and diagnostic indicator for early cervical carcinoma. (2) Depleted expression of FHIT is frequently associated with p53 over-expression in CIN and CC subjects, but there is no direct correlation between them. (3) HPV16/18 infection may probably be the common cause leading to altered FHIT and p53 expression.</p>

Effect and mechanism of chimonin on pulmonary hypertention of chronic hypoxia and hypercapnic rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of chimonin on chronic hypoxia and hypercapnic pulmonary hypertension and to explore its mechanism.</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group (C). HO-1 and HO-1 mRNA was observed in pulmonary arterioles of rats by the technique of immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>(1) mPAP was significantly higher in rats of B group than that of A and C group. Differences of mCAP were not significant in three groups. (2) Blood CO concentration was significantly higher in rats of B group than that of A group, it was significantly higher in rats of C group than that of B group. (3) Light microscopy showed that WA/TA (vessel wall area/total area), SMC (the density of medial smooth muscle cell) and PAMT (the thickness of medial smooth cell layer) were significantly higher in rats of B group than those of A and C group. (4) Electron microscopy showed proliferation of medial smooth muscle cells and collagenous fibers of pulmonary arterioles in rats of B group, and chimonin could reverse the changes mentioned above. (5) HO-1 and HO-1 mRNA in pulmonary arterioles was significantly higher in rats of B group than that of A group, they were significantly higher in rats of C group than that of B group.</p><p><b>CONCLUSION</b>Chimonin can inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling by further increasing the expression of HO-1 mRNA.</p>