Objective The aim of the study was to investigate the effects of inflammation on the biological be-haviors of the VF -MSCs and provide the theoretic basis for the repair of the vocal folds which were damaged by in-flammation .Methods The inflammatory vocal fold tissues and normal vocal fold tissues were respectively derived from the vocal cord polyp and normal tissues of the hypopharyngeal carcinoma patients .The HE staining ,masson trichrome staining and elastin van gieson (EVG) staining were performed to detect the effects of inflammation on the collagenous fiber and elastic fibers of the vocal fold lamina propria .The cell colony formation analysis and MTT cell growth curve were used to detect the effects of inflammation on the proliferation of VF -MSCs .The effects of in-flammation on the multi-directional differentiation of VF -MSCs were evaluated by inducing the VF -MSCs to dif-ferentiate into osteoblasts and lipoblasts .Results The results of masson trichrome staining and EVG staining showed that in the inflammatory vocal fold lamina propria collagen fibers became thicker and the amount of collagen fibers increased ,while elastic fibers became thinner and the amount of elastic fibers decreased .Compared with the vocal fold mesenchymal stem cell (VF-MSCs) in normal vocal folds ,VF-MSCs in inflammatory vocal folds pro-liferated more significantly ,but the osteogenic differentiation and adipogenic differentiation of VF -MSCs in inflammatory vocal folds were restrained .Conclusion Inflammation enhanced the compressive resistance ,abated the elasticity , and restrained the multi -directional differentiation of VF -MSCs .

OBJECTIVETo study the pathogenic effect of hepatitis G virus (HGV) infection on hepatic failure.

METHODSUsing the RT-PCR and EIA techniques to detect HGV RNA and anti-HGV in sera of hepatic failure patients and compare them with their liver function and mortality rates.

RESULTSThere was no significant difference about the positive rates of HGV among acute hepatic failure, subacute hepatic failure and chronic hepatic failure groups (X(2)=2.54, P>0.05). The level of ALT in HGV-positive group was slightly lower than that in HGV-negative group. The concentration of bilirubin and globulin was higher in HGV-positive group than HGV-negative group, and the concentration of albumin in HGV-positive group was significantly lower than that in HGV-negative group (t=2.59, P<0.05). The mortality rate in HGV-positive group was significantly lower than that in HGV-negative group (X(2)=4.68, 0.01

CONCLUSIONSThe virulence of HGV is mild, and the HGV infection does not aggravate hepatic failure.

Adult ; Female ; Flaviviridae Infections ; complications ; GB virus C ; pathogenicity ; Hepatitis, Viral, Human ; complications ; Humans ; Liver Failure ; etiology ; Male ; Middle Aged