Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Approximately half of the patients with type C hepatitis do not have a history of parenteral exposure. The route of nonparenteral infection remains unknown. To evaluate the possible role of body fluids, the existence of hepatitis C virus (HCV) RNA in saliva, urine, seminal fluid, and ascites was examined by "nested" polymerase chain reaction (PCR). Amplification of the HCV 5' noncoding sequences was carried out. The amplified product was confirmed by Southern blot hybridization and restriction endonuclease digestion. Among 34 patients with chronic liver disease who were positive for anti-HCV and serum HCV RNA, the prevalence of HCV RNA in body fluids was 100% (7/7) in ascites, 48% (15/31) in saliva, 24% (4/17) in seminal fluid, and 7% (2/29) in urine. The body fluids collected from 3 healthy subjects and 5 patients with chronic liver disease who were positive for anti-HCV but negative for serum HCV RNA were all negative for HCV RNA. Hence, the potential infectivity of body fluids in patients testing negative for serum HCV RNA can probably be discounted. Conversely, the presence of HCV RNA in saliva and seminal fluid of patients positive for serum HCV RNA suggests sexual and household contact as likely modes of nonparenteral transmission of type C hepatitis. Furthermore, the high prevalence of HCV RNA in ascites and saliva may have important implications in medical and dental practice.
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PMID:Detection of HCV RNA in saliva, urine, seminal fluid, and ascites. 133 8

In order to investigate how chronic liver diseases, including liver cirrhosis and chronic hepatitis, are associate with hepatocarcinogenesis in terms of gene alteration, the methylation states of the c-myc and c-Ki-ras genes were examined in 34 liver tissues from patients with chronic liver disease without hepatocellular carcinoma (HCC), 34 non-tumor liver tissues from patients with HCC, 18 HCC tissues and 31 control liver tissues. The methylation states were analyzed by the Southern hybridization method using the restriction endonuclease isoschizomers MspI and HpaII. The CCGG sites at the second exon of the c-myc gene tended to be more extensively hypomethylated both in chronic liver disease and in non-tumor tissues than in control livers. Whereas the CCGG sites of the c-Ki-ras, and the third exon of the c-myc gene tended to be hypomethylated only in HCC tissues in comparison with other tissue groups. These results suggest that chronic liver disease may be situated between normal liver and HCC based on the state of DNA methylation and associated with the development of HCC through hypomethylation of the c-myc and/or c-Ki-ras gene.
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PMID:Hypomethylation of the c-myc oncogene in liver cirrhosis and chronic hepatitis. 254 2

Little is known about the replicative forms of hepatitis B virus (HBV) in the liver in chronic liver disease. We therefore analyzed HBV DNA and the changes in DNA signals after endonuclease digestion in liver tissues taken from 64 patients with hepatitis B surface antigen-positive chronic liver disease. The "active" replication pattern, which included various replicative intermediates, was seen in 36 of 38 (95%) hepatitis B e antigen-seropositive patients. This pattern was also found in 5 of 26 (19%) hepatitis B e antigen-seronegative patients who showed the highest mean serum alanine aminotransferase level (403 +/- 184 mU/ml). Most of them had advanced liver disease. Episomal viral DNA of an "inactive" type having only the supercoiled form was found in 3 patients; they showed the lowest mean serum alanine aminotransferase level (27 +/- 7 mU/ml) and only mild liver disease. As with duck HBV infection, episomal replicative forms of human HBV could be resolved by Southern blot analysis and seem to have clinical implications in human HBV infection.
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PMID:Active and inactive replication of hepatitis B virus deoxyribonucleic acid in chronic liver disease. 401 3

We used PCR for hepatitis C virus (HCV) genotyping with type-specific primers from the core and NS5 genes. Type I was predominant in the general population (58% in blood donors) as well as in different risk groups, such as intravenous drug abusers (58%), blood transfusion recipients (64%), hemophiliacs (62%), and patients with HCV chronic liver disease (76%). Types II, III, and IV were less prevalent in Canada, being found in 10.92, 6.72, and 5.88% of the population, respectively. The type II core primer was not type specific and reacted with the majority of our type I HCV samples, suggesting a false-positive dual infection with two different genotypes (I and II). Digestion of these amplified type I and type II products with restriction endonuclease AccI proved to be very useful in the exclusion of false-positive dual type I and type II infections.
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PMID:Genotyping of Canadian hepatitis C virus isolates by PCR. 798 65