Biomedical subjects

Qin Su

Publications and source records attributed to Qin Su.

40 records · Page 3Linked to original sources

PubMed2002

[Sero-and molecular epidemiology of the gene of different ORF of transfusion transmitted virus (TTV) in different population of China].

BACKGROUND: To investigate the distribution of anti-TTV antibody and the different ORF gene in different populations of China. METHODS: The antibody to TTV in sera collected from different population were detected by using ELISA and the different ORF genes were amplified with PCR. RESULTS: The positive rates of TTV ORF1 DNA, ORF2 DNA and the antibody in various populations were as follows: 16.0% (12/75), 10.7% (8/75) and 25.3% (19/75) in paid blood donors; 10.0 (3/30), 16.7% (5/30) and 16.7% (5/30) in patients with hepatitis A, 47.5% (19/40), 42.5% (17/40) and 22.5% (9/40) in patients with hepatitis B; 42.9% (15/35), 37.1% (13/35) and 28.6% (10/35) in patients with hepatitis C; 20.0% (3/15), 26.7% (4/15) and 13.3% (2/15)in patients with hepatitis D; 16.7% (2/12),16.7% (2/12) and 33.3% (4/12)in patients with hepatitis E; 23.8% (5/21), 38.1% (8/21) and 23.8% (5/21) in patients with hepatitis G; 61.1% (11/18), 50.0% (9/18) and 44.4% (8/18) in patients with non A-G hepatitis, respectively. The positive rate of different ORF DNA had no significant difference. Significant differences were found in the positive rates of TTV DNA in various populations. There was no relationship between the TTV DNA and the antibody to TTV. CONCLUSIONS: The antibody to TTV and TTV DNA were found in every population of China. There was no significant difference in the positive rates of TTV DNA between ORF1 and ORF2. The positive rate in patients with non A-G hepatitis was higher than those in the other populations.

Adolescent↗

PubMed2002

Clonality of multiple uterine leiomyomas.

OBJECTIVE: To study the clonality of uterine leiomyomas, especially the relationship between different nodules in multinodular cases. METHODS: Genomic DNA was extracted from fresh tissue samples and digested through incubation with Hpa II and amplified through nested polymerase chain reaction for phosphoglycerate kinase (PGK) gene. The products were treated with Bst XI and resolved on agarose gels. RESULTS: Among the 103 cases examined, 32 (31%) carried the polymorphic Bst XI site at the PGK locus. Eighty-nine tumors from the 29 cases were subjected to the cloning assay. Loss of polymorphism at the PGK locus was found in all tumor nodules, indicating the monoclonality of the tumor. The relationship between multiple tumors was also assessed by comparing their inactivated alleles. Seven nodules from a leiomyosarcoma were found to have originated from a single cell. However, the relationship was found to be more complicated, as demonstrated in 15 cases of multiple leiomyomas. The same inactivated allele was found in all nodules of 8 cases and in most nodules in 2 cases, while totally different inactivation patterns were observed in 5 cases. The difference was not associated with cell proliferation. CONCLUSIONS: Clonality analysis can be applied to define the clonality of focal or nodular lesions. Uterine leiomyomas are of clonal origin. Multiple uterine leiomyomas may be subtyped into fully independent and aggressive types as well as a mixed type of both.

Base Sequence↗

PubMedDate not supplied

Relevance of hepatic preneoplasia for human hepatocarcinogenesis.

Different lesions have been suggested to represent preneoplastic conditions in human liver. They include liver cell dysplasia, separated in large-cell change (LCC) and small-cell change (SCC), adenomatoid hyperplasia, and the more recently identified foci of altered hepatocytes (FAH) and nodules of altered hepatocytes (NAH). FAH have been demonstrated to represent preneoplastic lesions in various animal models of hepatocarcinogenesis. To demonstrate prevalence and significance of FAH in the human liver, the cellular composition, size distribution, and proliferation kinetics of these lesions were studied in 163 explanted and resected human livers with or without hepatocellular carcinoma (HCC). FAH including glycogen-storing foci (GSF), mixed cell foci (MCF), and basophilic cell foci were found in 84 of 111 cirrhotic livers, demonstrating higher incidences in cases with than without HCC. MCF, predominant in cirrhotic livers of the high-risk group, were more proliferative, larger and more often involved in formation of NAH than GSF. The results suggest that the FAH are preneoplastic lesions, MCF being more advanced than GSP. We also investigated the relationship of FAH to liver cell dysplasia. Occurrence of SCC, rather than that of LCC, confers FAH an increased proliferation activity and higher risk to nodular transformation, and, hence, should be considered a precancerous condition. Histological detection of FAH and SCC through needle-aspiration liver biopsy can be used for monitoring HCC development in high-risk populations, such as HBV carriers with chronic hepatitis and/or cirrhosis.

Cell Division↗

PubMedDate not supplied

Significance of hepatic preneoplasia in risk identification and early detection of neoplasia.

Among the different types of liver tumor, hepatocellular neoplasms predominate by far in both animals and man. Consequently, preneoplastic foci of altered hepatocytes (FAH), preceding both hepatocellular adenomas and carcinomas, represent the most prevalent form of hepatic preneoplasia observed in animals for a long time, and identified in human chronic liver diseases associated with, or predisposing to, hepatocellular carcinomas more recently. Morphological, microbiochemical, and molecular biological approaches in situ revealed striking similarities in specific changes of the cellular phenotype of preneoplastic FAH developing in experimental and human hepatocarcinogenesis, irrespective of whether this was elicited by chemicals, hormones, viruses or radiation. The advantage of using FAH for risk identification (aiming at primary cancer prevention) in long-term and medium-term carcinogenesis bioassays has been well documented, but quantitative morphometric approaches appear to be indispensable for an appropriate evaluation of both bioassays. The detection of phenotypically similar FAH in various animal models and in humans prone to develop or bearing hepatocellular carcinomas favors the extrapolation from data obtained in animals to humans. Moreover, the recently reported frequent finding of FAH in fine-needle biopsies of patients suffering from chronic liver diseases opens new perspectives for secondary prevention of human hepatocellular carcinoma.

Animals↗