SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Dai JY) "

Sökning: WFRF:(Dai JY)

  • Resultat 1-10 av 16
  • [1]2Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Tidskriftsartikel (refereegranskat)
  •  
2.
  • Tidskriftsartikel (refereegranskat)
  •  
3.
  • Tidskriftsartikel (refereegranskat)
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  • Neumeyer, Sonja, et al. (författare)
  • Mendelian randomisation study of age at menarche and age at menopause and the risk of colorectal cancer
  • 2018
  • Ingår i: ; 118:12, s. 1639-1647
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Substantial evidence supports an association between use of menopausal hormone therapy and decreased colorectal cancer (CRC) risk, indicating a role of exogenous sex hormones in CRC development. However, findings on endogenous oestrogen exposure and CRC are inconsistent.METHODS: We used a Mendelian randomisation approach to test for a causal effect of age at menarche and age at menopause as surrogates for endogenous oestrogen exposure on CRC risk. Weighted genetic risk scores based on 358 single-nucleotide polymorphisms associated with age at menarche and 51 single-nucleotide polymorphisms associated with age at menopause were used to estimate the association with CRC risk using logistic regression in 12,944 women diagnosed with CRC and 10,741 women without CRC from three consortia. Sensitivity analyses were conducted to address pleiotropy and possible confounding by body mass index.RESULTS: Genetic risk scores for age at menarche (odds ratio per year 0.98, 95% confidence interval: 0.95-1.02) and age at menopause (odds ratio 0.98, 95% confidence interval: 0.94-1.01) were not significantly associated with CRC risk. The sensitivity analyses yielded similar results.CONCLUSIONS: Our study does not support a causal relationship between genetic risk scores for age at menarche and age at menopause and CRC risk.
  •  
8.
  • Wang, Xiaoliang, et al. (författare)
  • Mendelian randomization analysis of C-reactive protein on colorectal cancer risk
  • 2019
  • Ingår i: ; 48:3, s. 767-780
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Chronic inflammation is a risk factor for colorectal cancer (CRC). Circulating C-reactive protein (CRP) is also moderately associated with CRC risk. However, observational studies are susceptible to unmeasured confounding or reverse causality. Using genetic risk variants as instrumental variables, we investigated the causal relationship between genetically elevated CRP concentration and CRC risk, using a Mendelian randomization approach.Methods: Individual-level data from 30 480 CRC cases and 22 844 controls from 33 participating studies in three international consortia were used: the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colorectal Transdisciplinary Study (CORECT) and the Colon Cancer Family Registry (CCFR). As instrumental variables, we included 19 single nucleotide polymorphisms (SNPs) previously associated with CRP concentration. The SNP-CRC associations were estimated using a logistic regression model adjusted for age, sex, principal components and genotyping phases. An inverse-variance weighted method was applied to estimate the causal effect of CRP on CRC risk.Results: Among the 19 CRP-associated SNPs, rs1260326 and rs6734238 were significantly associated with CRC risk (P = 7.5 × 10-4, and P = 0.003, respectively). A genetically predicted one-unit increase in the log-transformed CRP concentrations (mg/l) was not associated with increased risk of CRC [odds ratio (OR) = 1.04; 95% confidence interval (CI): 0.97, 1.12; P = 0.256). No evidence of association was observed in subgroup analyses stratified by other risk factors.Conclusions: In spite of adequate statistical power to detect moderate association, we found genetically elevated CRP concentration was not associated with increased risk of CRC among individuals of European ancestry. Our findings suggested that circulating CRP is unlikely to be a causal factor in CRC development.
  •  
9.
  •  
10.
  • Dai, JY, et al. (författare)
  • Conformational cycling in beta-phosphoglucomutase catalysis: Reorientation of the beta-D-glucose 1,6-(bis) phosphate intermediate
  • 2006
  • Ingår i: Biochemistry. - : The American Chemical Society (ACS). - 0006-2960. ; 45:25, s. 7818-7824
  • Tidskriftsartikel (refereegranskat)abstract
    • Activated Lactococcus lactis beta-phosphoglucomutase (beta PGM) catalyzes the conversion of beta-D-glucose 1-phosphate (beta G1P) derived from maltose to beta-D-glucose 6-phosphate (G6P). Activation requires Mg2+ binding and phosphorylation of the active site residue Asp8. Initial velocity techniques were used to define the steady-state kinetic constants k(cat) = 177 +/- 9 s(-1), K-m = 49 +/- 4 mu M for the substrate, beta G1P and K-m = 6.5 +/- 0.7 mu M for the activator beta-D-glucose 1,6-bisphosphate (beta G1,6bisP). The observed transient accumulation of [C-14]beta G1,6bisP (12% at similar to 0.1 s) in the single turnover reaction carried out with excess beta PGM (40 mu M) and limiting [C-14]beta G1P (5 mu M) and beta G1,6bisP (5 mu M) supported the role of beta G1,6bisP as a reaction intermediate in the conversion of the, G1P to G6P. Single turnover reactions of [C-14]beta G1,6bisP with excess, beta PGM were carried out to demonstrate that phosphoryl transfer rather than ligand binding is rate-limiting and to show that the beta G1,6bisP binds to the active site in two different orientations (one positioning the C(1) phosphoryl group for reaction with Asp8, and the other orientation positioning the C(6) phosphoryl group for reaction with Asp8) with roughly the same efficiency. Single turnover reactions carried out with beta PGM, [C-14]beta G1P, and unlabeled beta G1,6bisP demonstrated complete exchange of label to the beta G1,6bisP during the catalytic cycle. Thus, the reorientation of the beta G1,6bisP intermediate that is required to complete the catalytic cycle occurs by diffusion into solvent followed by binding in the opposite orientation. Published X-ray structures of beta G1P suggest that the reorientation and phosphoryl transfer from beta G1,6bisP occur by conformational cycling of the enzyme between the active site open and closed forms via cap domain movement. Last, the equilibrium ratio of beta G1,6bisP to beta G1P plus G6P was examined to evidence a significant stabilization of beta PGM aspartyl phosphate.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 16
  • [1]2Nästa
 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy