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Objective To study the relationship between liver fibrosis degree and widths of portal vein(TPV) and spleen vein(SPV).Method Liver specimens from 151 patients with chronic viral hepatitis were divided into 4 groups from S 1 to S 4 according to the liver fibrosis degree.The diameters of TPV and SPV were measured by ultrasonic B.Results The diameters of TPV and SPV of groups S 1,S 2,S 3 and S 4 were (11 89?1 39)mm and (5 78?1 33)mm,(12 22?1 19)mm and (6 25?1 28)mm,(12 43?1 26)mm and (7 03?1 54)mm,(13 07?1 23)mm and (8 0?1 80)mm,respectively.The differences of diameter of TPV between group S 4 and group S 1,S 2 were significant(all P
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【Objective】 To study the relationship of pathologic changes and serologic markers of fibrosis in patients with viral hepatitis. 【Me thods】 Liver s pecimens were obtained by percutaneous needle biopsy under color Doppler ultras ound guidance in 299 patients with viral hepatitis. The specimens were stained b y hematoxylin and eosin (HE), Gordon and Sweet's reticulum methods (RT), in orde r to determine the degree and the stage of pathologic changes with microscopy. H yaluronic acid(HA), collagen type Ⅳ(Ⅳ-C) and human precollagen type Ⅲ（HPCⅢ ）as serum fibrous markers were detected by radioimmunoassay. 【Results】 The se rum levels serologic markers were slightly increased in 97 patients with mild ch ronic hepatitis, moderately increased in 126 patients with moderate chronic hepa titis, and significantly increased in 29 severe cases and 47 subjects with cirrh osis. Both the grade of inflammatory activity and the stage of fibrosis were clo sely related to the levels of serum fibrous markers. 【Conclusion】 Chronic vira l hepatitis pathologic feature and levels of serum markers of fibrosis change al ong with clinical process of patients. The combination of liver biopsy and detec tion of serum markers of fibrosis might be highly valuable for the diagnosis.
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【Objective】To construct the c-myb antisense RNA recombinant retroviral vector and its packaging cell line.【Methods】The segment of c-myb gene was cloned into pUC19 with TA cloning method after amplication by RT-PCR,and then was subcloned into retroviral vector pDOR.The recombinant retroviral vector named pDOR-myb was transfected into retroviral package cell line PA317 after selection with G418.【Results】Sequencing data indicated that the c-myb gene was exactly identical to the sequence in the GenBank.The segment of c-myb gene was inserted directionally into pDOR.Resistant colonies were obtained and the titers of pDOR-myb were 5.2×104～9.5×104 CFU/mL.【Conclusion】The recombinant retroviral vector containing c-myb gene is successfully constructed and its packaging cell line PA317/pDOR-myb was established.
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Objective To study the SEN-V DNA in liver tissue from patients with non A to E hepatitis in Guangzhou area. Methods A set of primers according to the original sequence from GenBank were designed , and SEN-V DNA sequence was amplified by in situ-PCR in liver tissue. Results Two of 6 patients with non A to E hepatitis were found to be SEN-V-DNA positive in liver tissue. While 8 patients with HBV infection and 6 of other liver diseases including 2 of autoimmune liver disease, 1 of Dubin Johnson syndrome, 1 of fatty liver, 1 of the primary biliary cirrhosis and 1 of drug induced hepatitis were all SEN-V DNA negative. SEN-V DNA were mainly distributed in liver cell cytoplasm, partially in nucleus. There presented the phenomenon of cell fuse. SEN-V positive cells accounted for about 3%～10% of total cells.Conclusions SEN-V can be found in liver tissue of patients with non A to E hepatitis in south China. Maybe it can cause liver damage.
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98%. In the pDOR-myb infected HSCs, c-myb expression levels, the cell proliferation, and ? 1-Ⅰ collagen mRNA expression were repressed significantly. CONCLUSIONS: c-myb plays a key role in the activation and proliferation of HSC. c-myb antisense RNA can inhibit cell proliferation and ? 1-Ⅰ collagen mRNA expression in the infected HSC. These data suggest that inhibition of c-myb gene expression would be a potential way for the treatment of liver fibrosis.