The total RNA was extracted from Microtus fortis liver tissue which before being infected and after being infected 10 d and 15 d by the Schistosoma japonicum cercariae. Using rattus norvegicus CD72 gene probes were us...The total RNA was extracted from Microtus fortis liver tissue which before being infected and after being infected 10 d and 15 d by the Schistosoma japonicum cercariae. Using rattus norvegicus CD72 gene probes were used to hybridize analysis of CD72 difference expression in the Microtus fortis liver tissues which were infected with Schistosoma japonicum before and after being infected. At the same time, the cDNA sequence and encoded amino acid sequence of the rattus norvegicus CD72 gene and CD72 protein structural domains were analyzed by using bioinformatics. The results showed that the CD72 expression levels in the liver tissue of Microtus fortis after being infected was significantly higher than before being infected. The rattus norvegicus CD72 cDNA sequence of a total length is 1479 bp and encode 364 amino acid residues and rattus norvegicus CD72 protein containing a CD72 superfamily domain.展开更多
Aim： To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk. We focus on allele variants of low-penetrance genes associated with cell control, ...Aim： To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk. We focus on allele variants of low-penetrance genes associated with cell control, the detoxification processes and smoking. Methods： In a case-control study we compared people carrying p53cd72 Pro allele, CYP1A1 M1 allele and GSTM1 null genotypes with their prostate cancer risk. Results： The joint risk for smokers carrying Pro^＊ and MI^＊, Pro^＊ and GSTM1null or GSTM1 null and CYP1A1 MI^＊ variants was significantly higher （odds ratio [OR]： 13.13, 95% confidence interval [CI]： 2.41-71.36; OR： 3.97, 95% CI： 1.13-13.95 and OR： 6.87, 95% CI： 1.68-27.97, respectively） compared with that for the reference group, and for non-smokers was not significant. OR for combinations among p53cd72, GSTM1 and CYP1A1 M1 in smokers were positively and significantly associated with prostate cancer risk compared with non-smokers and compared with the putative lowest risk group （OR： 8.87, 95% CI： 1.25-62.71）. Conclusion： Our results suggest that a combination of p53cd72, CYP1A1, GSTM1 alleles and smoking plays a significant role in modified prostate cancer risk on the study population, which means that smokers carrying susceptible genotypes might have a significantly higher risk than those carrying non-susceptible genotypes.展开更多
Aim:To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk.We focus on allele variants of low-penetrance genes associated with cell control,the ...Aim:To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk.We focus on allele variants of low-penetrance genes associated with cell control,the detoxifica- tion processes and smoking.Methods:In a case-control study we compared people carrying p53cd72 Pro allele, CYP1A1 M1 allele and GSTM1 null genotypes with their prostate cancer risk.Results:The joint risk for smokers carrying Pro* and Ml*,Pro* and GSTMlnull or GSTM1 null and CYP1A1 Ml* variants was significantly higher (odds ratio [OR]:13.13.95% confidence interval [CI]:2.41-71.36;OR:3.97,95% CI:1.13-13.95 and OR:6.87. 95% CI:1.68-27.97,respectively)compared with that for the reference group,and for non-smokers was not significant. OR for combinations among p53cd72,GSTM1 and CYP1A1 M1 in smokers were positively and significantly associated with prostate cancer risk compared with non-smokers and compared with the putative lowest risk group(OR:8.87,95% CI:1.25-62.71).Conclusion:Our results suggest that a combination of p53cd72,CYP1A1,GSTM1 alleles and smoking plays a significant role in modified prostate cancer risk on the study population,which means that smokers carrying susceptible genotypes might have a significantly higher risk than those carrying non-susceptible genotypes.展开更多
文摘The total RNA was extracted from Microtus fortis liver tissue which before being infected and after being infected 10 d and 15 d by the Schistosoma japonicum cercariae. Using rattus norvegicus CD72 gene probes were used to hybridize analysis of CD72 difference expression in the Microtus fortis liver tissues which were infected with Schistosoma japonicum before and after being infected. At the same time, the cDNA sequence and encoded amino acid sequence of the rattus norvegicus CD72 gene and CD72 protein structural domains were analyzed by using bioinformatics. The results showed that the CD72 expression levels in the liver tissue of Microtus fortis after being infected was significantly higher than before being infected. The rattus norvegicus CD72 cDNA sequence of a total length is 1479 bp and encode 364 amino acid residues and rattus norvegicus CD72 protein containing a CD72 superfamily domain.
文摘Aim： To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk. We focus on allele variants of low-penetrance genes associated with cell control, the detoxification processes and smoking. Methods： In a case-control study we compared people carrying p53cd72 Pro allele, CYP1A1 M1 allele and GSTM1 null genotypes with their prostate cancer risk. Results： The joint risk for smokers carrying Pro^＊ and MI^＊, Pro^＊ and GSTM1null or GSTM1 null and CYP1A1 MI^＊ variants was significantly higher （odds ratio [OR]： 13.13, 95% confidence interval [CI]： 2.41-71.36; OR： 3.97, 95% CI： 1.13-13.95 and OR： 6.87, 95% CI： 1.68-27.97, respectively） compared with that for the reference group, and for non-smokers was not significant. OR for combinations among p53cd72, GSTM1 and CYP1A1 M1 in smokers were positively and significantly associated with prostate cancer risk compared with non-smokers and compared with the putative lowest risk group （OR： 8.87, 95% CI： 1.25-62.71）. Conclusion： Our results suggest that a combination of p53cd72, CYP1A1, GSTM1 alleles and smoking plays a significant role in modified prostate cancer risk on the study population, which means that smokers carrying susceptible genotypes might have a significantly higher risk than those carrying non-susceptible genotypes.
文摘Aim:To assess the role of several genetic factors in combination with an environmental factor as modulators of prostate cancer risk.We focus on allele variants of low-penetrance genes associated with cell control,the detoxifica- tion processes and smoking.Methods:In a case-control study we compared people carrying p53cd72 Pro allele, CYP1A1 M1 allele and GSTM1 null genotypes with their prostate cancer risk.Results:The joint risk for smokers carrying Pro* and Ml*,Pro* and GSTMlnull or GSTM1 null and CYP1A1 Ml* variants was significantly higher (odds ratio [OR]:13.13.95% confidence interval [CI]:2.41-71.36;OR:3.97,95% CI:1.13-13.95 and OR:6.87. 95% CI:1.68-27.97,respectively)compared with that for the reference group,and for non-smokers was not significant. OR for combinations among p53cd72,GSTM1 and CYP1A1 M1 in smokers were positively and significantly associated with prostate cancer risk compared with non-smokers and compared with the putative lowest risk group(OR:8.87,95% CI:1.25-62.71).Conclusion:Our results suggest that a combination of p53cd72,CYP1A1,GSTM1 alleles and smoking plays a significant role in modified prostate cancer risk on the study population,which means that smokers carrying susceptible genotypes might have a significantly higher risk than those carrying non-susceptible genotypes.
