In this paper,we report the results of a HF/6-31G** and B3LYP/6-31+G** computational investigation of the title reaction for the peptide bond synthesis catalyzed by a single adenine,guanine or uracil.Thus,the analysis...In this paper,we report the results of a HF/6-31G** and B3LYP/6-31+G** computational investigation of the title reaction for the peptide bond synthesis catalyzed by a single adenine,guanine or uracil.Thus,the analysis of the geometry and energetics of the critical structures involved in this title reaction yields insight into the catalytic mode of action of RNA molecules.The imino form of adenine should not be considered as a prerequisite for A2451 to have function as a general acid-base catalyst.The other nucletides of RNA,guanine,cytosine,and uracil,have the similar general acid-base catalytic function and mechanism with those of adenine.展开更多
AIM: To clarify the influence of genetic polymorphisms on colorectal cancer. METHODS: The results of 42 related studies from 1990 to 2001 were analyzed by meta-analysis. Mantel-Haenzel fixed-effect model or Dersimonia...AIM: To clarify the influence of genetic polymorphisms on colorectal cancer. METHODS: The results of 42 related studies from 1990 to 2001 were analyzed by meta-analysis. Mantel-Haenzel fixed-effect model or Dersimonian-Laird random-effect model and ReviewManager 4.1 statistical program were applied in processing the data. RESULTS: Meta analysis of these studies showed that GSTT1 deletion (pooled OR= 1.42), N-acetyltransferase 2 (NAT2)-rapid acetylator phenotype and genotye (pooled OR = 1.08) and NAT2-rapid acetylator phenotype (pooled OR = 1.15) had a significantly increased risk for colorectal cancer (P<0.05), other genotypes like GSTM1 deletion, GSTP1 1le105Val, NAT1*10, NAT2-rapid acetylator genotype CYP1A1 Lle462Val, CYP1A1 MspI*C, MTHFR C677T and MTR A2759G had no significant relationship with colorectal cancer (P>0.05). CONCLUSION: Risks for colorectal cancer are significantly associated with the genetic polymorphisms of GSTT1 deletion, NAT2-rapid acetylator phenotype and genotye and NAT2-rapid acetylator phenotype.展开更多
文摘In this paper,we report the results of a HF/6-31G** and B3LYP/6-31+G** computational investigation of the title reaction for the peptide bond synthesis catalyzed by a single adenine,guanine or uracil.Thus,the analysis of the geometry and energetics of the critical structures involved in this title reaction yields insight into the catalytic mode of action of RNA molecules.The imino form of adenine should not be considered as a prerequisite for A2451 to have function as a general acid-base catalyst.The other nucletides of RNA,guanine,cytosine,and uracil,have the similar general acid-base catalytic function and mechanism with those of adenine.
基金Supported by the National Natural Science Foundation of China, No. 30170828
文摘AIM: To clarify the influence of genetic polymorphisms on colorectal cancer. METHODS: The results of 42 related studies from 1990 to 2001 were analyzed by meta-analysis. Mantel-Haenzel fixed-effect model or Dersimonian-Laird random-effect model and ReviewManager 4.1 statistical program were applied in processing the data. RESULTS: Meta analysis of these studies showed that GSTT1 deletion (pooled OR= 1.42), N-acetyltransferase 2 (NAT2)-rapid acetylator phenotype and genotye (pooled OR = 1.08) and NAT2-rapid acetylator phenotype (pooled OR = 1.15) had a significantly increased risk for colorectal cancer (P<0.05), other genotypes like GSTM1 deletion, GSTP1 1le105Val, NAT1*10, NAT2-rapid acetylator genotype CYP1A1 Lle462Val, CYP1A1 MspI*C, MTHFR C677T and MTR A2759G had no significant relationship with colorectal cancer (P>0.05). CONCLUSION: Risks for colorectal cancer are significantly associated with the genetic polymorphisms of GSTT1 deletion, NAT2-rapid acetylator phenotype and genotye and NAT2-rapid acetylator phenotype.
