ABSTRACT
SOX17,a member of the SOX family of transcription factors,is conserved in many species and plays an important role in the formation of embryo endoderm.A number of studies have found that SOX17 gene expression is silenced or decreased might be due to promoter bypermethylation,which plays a vital role in tumorigenesis and tumor progression,and may contribute to aberrant activation of canonical Wnt signaling pathway in several human malignant tumors.
ABSTRACT
<p><b>OBJECTIVE</b>To study the pathogenic effect of hepatitis G virus (HGV) infection on hepatic failure.</p><p><b>METHODS</b>Using 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.</p><p><b>RESULTS</b>There 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<P<0.05).</p><p><b>CONCLUSIONS</b>The virulence of HGV is mild, and the HGV infection does not aggravate hepatic failure.</p>