Objective To study the diagnosis, treatment, etiology and prognosis of scrotum gangrene. Method We did a retrospective analysis of the data of 78 patients with scrotum gangrene who hospitalized during August 2007 and August 2011 in Jinja Hospital in Uganda.Results Among 78 patients, 73 patients were cured, with 93.6%of the cure rate. After early debridement and second phase reconstruction, patients recovered after the treatment. Conclusion On the basis of systemic antibiotic drug use and local debridement processing, penis-scrotum revascularization has good curative effect on scrotum gangrene.We hope to provide reference and help to foreign health medical team of aid work in Yunnan province.

Objective To construct antisense survivin eukaryotic expression vector pIRES2-EGFP-SVVas and detect its expression in human malignant glioma cell line SHG-44 cells. Methods The antisense survivin eukaryotic expression vector pIRES2-EGFP-SVVas was constructed and then transfected into SHG-44 cells with lipofectamine. The expression of survivin on the cells was measured by RT-PCR and Western blotting. Results The mRNA and protein expression of survivin decreased in the transfected cells. Conclusion pIRES2-EGFP-SVVas can decrease the expression of survivin in the cells transfected with the vector.

AIM: To determine the effects of Angiotensin II(AngII) on migration of rat smooth muscle cells and to investigate the mechanisms underlying Ang II action in the development of injured vascular disease. METHODS: VSMCs isolated from aortic media of Wistar rats and cultured by the modified explant method were adopted. In prersence and absence of AngII, the expression of AngII receptor and reorganization of the actin cytoskeleton of VSMCs were studied by immunocytochemistry technique, fluorocytochemistry technique. The migration assays were performed by a modified Boyden's chamber. And the effects of AT 1R antagonist (CV-11974), AT 2R antagonist (PD123319) on aforementioned target were studied. RESULTS: VSMCs migration was stimulated by addition of AngII. The dynamic reorganization of actin cytoskeleton may be an important mechanism by which AngII facilitates VSMC motility. The expression of AT 1R in VSMCs can be upregulated after treatment with AngII initially, then decreased gradually. The expression of AT 1R was downregulated by AT 1R antagonist. The effect of AngII on VSMCs migration was mediated by AT 1R, while AT 2R had no significant effect. CONCLUSION: The dynamic reorganization of actin cytoskeleton is required for AngII-induced VSMC migration, and this effect is mediated by AT 1R .