The ast ( anthocyanin spotted testa) mutant, which was induced by carbon ion radiation, was a single recessive gene mutant of Arabidopsis thaliana (L.) Heynh. with spotted pigment in seed coats, and involved in the an...The ast ( anthocyanin spotted testa) mutant, which was induced by carbon ion radiation, was a single recessive gene mutant of Arabidopsis thaliana (L.) Heynh. with spotted pigment in seed coats, and involved in the anthocyanin biosynthesis. To clone the AST gene by map-based cloning strategy, a series of molecular markers were designed according to the SNPs (single nucleotide polymophisms) and insertion/deletion polymophisms in the Arabidopsis database. With these molecular markers, the fine-structure mapping of the AST gene was finished, the AST locus was located in BAC clone T13M11. It was suggested that the AST candidate gene was T13M11. 8 in the T13M11 This gene was 1432 bp long with 6 exons and 5 introns. The putative protein of T13M11. 8 gene was similar to dihydroflavonol 4-reductase (DFR), which was an important enzyme in the anthocyanin biosynthesis pathway.展开更多
AIM: To identify the prevalence of pre-S2 start codon mutations and to assess their association with liver disease progression. METHODS: The mutations were identified by direct sequencing from 73 asymptomatic carriers...AIM: To identify the prevalence of pre-S2 start codon mutations and to assess their association with liver disease progression. METHODS: The mutations were identified by direct sequencing from 73 asymptomatic carriers, 66 chronic hepatitis (CH), 66 liver cirrhosis (LC) and 63 hepatocellular carcinoma (HCC) patients. Statistical significances were determined using Fisher's exact test, χ 2 test, and t -test analyses whenever appropriate. Pre-S mutation as a risk factor for advanced liver disease was estimated by unconditional logistic regression model adjusted with age, sex, and hepatitis B e antigen (HBeAg). P < 0.05 was considered significant. RESULTS: Mutation of the hepatitis B virus (HBV) pre-S2 start codon was found in 59 samples from 268 subjects (22.0%), with higher prevalence in patients with cirrhosis 27/66 (40.9%) followed by HCC 18/63 (28.6%), chronic hepatitis 12/66 (18.2%) and asymptomatic carriers 2/73 (2.7%) (P < 0.001). Logistic regression analysis showed that pre-S2 start codon mutation was an independent factor for progressive liver disease. Other mutations, at T130, Q132, and A138, were also associated with LC and HCC, although this was not statistically significant when adjusted for age, sex, and HBeAg. The prevalence of pre-S2 start codon mutation was higher in HBV/B than in HBV/C (23.0% vs 19.1%), whilst the prevalence of T130, Q132, and A138 mutation was higher in HBV/C than in HBV/B. The prevalence of pre-S2 start codon mutation was higher in LC (38.9%) and HCC (40.0%) than CH (5.6%) in HBeAg(+) group, but it was similar between CH, LC and HCC in HBeAg(-) group. CONCLUSION: Pre-S2 start codon mutation was higher in Indonesian patients compared to other Asian countries, and its prevalence was associated with advanced liver disease, particularly in HBeAg(+) patients.展开更多
文摘The ast ( anthocyanin spotted testa) mutant, which was induced by carbon ion radiation, was a single recessive gene mutant of Arabidopsis thaliana (L.) Heynh. with spotted pigment in seed coats, and involved in the anthocyanin biosynthesis. To clone the AST gene by map-based cloning strategy, a series of molecular markers were designed according to the SNPs (single nucleotide polymophisms) and insertion/deletion polymophisms in the Arabidopsis database. With these molecular markers, the fine-structure mapping of the AST gene was finished, the AST locus was located in BAC clone T13M11. It was suggested that the AST candidate gene was T13M11. 8 in the T13M11 This gene was 1432 bp long with 6 exons and 5 introns. The putative protein of T13M11. 8 gene was similar to dihydroflavonol 4-reductase (DFR), which was an important enzyme in the anthocyanin biosynthesis pathway.
基金Supported by MRIN Funding, Budget, No. cc041/2010
文摘AIM: To identify the prevalence of pre-S2 start codon mutations and to assess their association with liver disease progression. METHODS: The mutations were identified by direct sequencing from 73 asymptomatic carriers, 66 chronic hepatitis (CH), 66 liver cirrhosis (LC) and 63 hepatocellular carcinoma (HCC) patients. Statistical significances were determined using Fisher's exact test, χ 2 test, and t -test analyses whenever appropriate. Pre-S mutation as a risk factor for advanced liver disease was estimated by unconditional logistic regression model adjusted with age, sex, and hepatitis B e antigen (HBeAg). P < 0.05 was considered significant. RESULTS: Mutation of the hepatitis B virus (HBV) pre-S2 start codon was found in 59 samples from 268 subjects (22.0%), with higher prevalence in patients with cirrhosis 27/66 (40.9%) followed by HCC 18/63 (28.6%), chronic hepatitis 12/66 (18.2%) and asymptomatic carriers 2/73 (2.7%) (P < 0.001). Logistic regression analysis showed that pre-S2 start codon mutation was an independent factor for progressive liver disease. Other mutations, at T130, Q132, and A138, were also associated with LC and HCC, although this was not statistically significant when adjusted for age, sex, and HBeAg. The prevalence of pre-S2 start codon mutation was higher in HBV/B than in HBV/C (23.0% vs 19.1%), whilst the prevalence of T130, Q132, and A138 mutation was higher in HBV/C than in HBV/B. The prevalence of pre-S2 start codon mutation was higher in LC (38.9%) and HCC (40.0%) than CH (5.6%) in HBeAg(+) group, but it was similar between CH, LC and HCC in HBeAg(-) group. CONCLUSION: Pre-S2 start codon mutation was higher in Indonesian patients compared to other Asian countries, and its prevalence was associated with advanced liver disease, particularly in HBeAg(+) patients.
