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Changes in lipid metabolism or the supply of fatty acids to the developing fetus have also been reported in other models of fetal programming such as high fat (Williams et al. 2014) or folate-deficient ...doi:10.14814/phy2.12908 pmid:27905292 pmcid:PMC5112487 fatcat:c3ajzglb35beheybeeoxd2xmau
Croden, 4 Daniel J Owens, 5 Jonathan Tang, 6 Alastair Miller, 3 Clare Lawton, 4 Louise Dye, 4 Graeme L Close, 5 William D Fraser, 6 Anne McArdle, 1 Michael B J Beadsworth 1,3 ► Prepublication history ... Analysis of vitamin D Vitamin D metabolites 25(OH)D 2 and 25(OH)D 3 were analysed as previously described. 8 25(OH)D 2 and 25(OH)D 3 were extracted from serum samples, following zinc sulfate protein ...doi:10.1136/bmjopen-2016-015296 pmid:29118054 pmcid:PMC5695299 fatcat:po6rzhxmjbdxrmib3vc4p5wdwe
Annual Pressure Ulcer Prevention Consensus Meeting, Idaho Pressure Ulcer Prevention Coalition, Boise Idaho, 2007. (4) Baumgarten M, Hawkes WG, Langenberg P, Magaziner J, Margolis D, Orwig D, Palmer MH, ... University of Maryland General Clinical Research Center Grant, General Clinical Research Centers Program, National Center for Research Resources (M01 RR 16500); and National Institute on Aging Claude D. ...doi:10.1111/j.1532-5415.2009.02245.x pmid:19484841 pmcid:PMC3382012 fatcat:ddvl43m7lrd63o4fl5izi2t5wy
Background-The etiology of cardiovascular disease (CVD) is multifactorial. Efforts to identify genes influencing CVD risk have met with limited success to date, likely due to the small effect sizes of common CVD risk alleles and the presence of gene by gene and gene by environment interactions. Methods-The Heredity and Phenotype Intervention (HAPI) Heart Study was initiated in 2002 to measure the cardiovascular response to four short-term interventions affecting cardiovascular risk factors anddoi:10.1016/j.ahj.2008.01.019 pmid:18440328 pmcid:PMC2443415 fatcat:eka4q5wmcjgvnfz5a7vq7t7a7y
more »... r risk factors and to identify the genetic and environmental determinants of these responses. The measurements included blood pressure responses to the cold pressor stress test and to a high salt diet, triglyceride excursion in response to a high fat challenge, and response in platelet aggregation to aspirin therapy. Results- The interventions were carried out in 868 relatively healthy Amish adults from large families. The heritabilities of selected response traits for each intervention ranged from 8-38%, suggesting that some of the variation associated with response to each intervention can be attributed to the additive effects of genes. Conclusions-Identifying these response genes may identify new mechanisms influencing CVD and may lead to individualized preventive strategies and improved early detection of high-risk individuals.
We then tested 68-1.2 vectors with genetic modifications that affect PRC function without complete abrogation of both Rh157.5 or Rh157.4 expression, including deletion (D) of Rh157.5 alone, Rh157.4 alone ... that the MHC-II-restricted CD8 + T cell priming of the former vector was more efficient (88% of total epitopes) than the latter vectors (57% of total epitopes; p<0.001 by binomial exact test) (Figs. 1C,D) ...doi:10.1101/2020.09.30.321349 fatcat:dpd72nkibnbmjcto2xpjkej2p4
These authors were joint principal investigators and contributed equally to this work Author Contributions Statement LF and DAvH analysed UK GWAS data, selected SNPs and designed assays for golden gate genotyping. Substantial contributions to sample collections were made by DAvH, LD, GKTH, PH, JRFW, DSS (UK2 cases); DPS, WLMcA (1958 cohort controls); CJM, WV, MLM (DUTCH samples); VT, FMS, COM, NPK, DK (IRISH samples). UKGWAS genotyping was performed as described in PD lab 2 . KAH extracteddoi:10.1038/ng.102 pmid:18311140 pmcid:PMC2673512 fatcat:xhted6743zay3kepw4fvbvge64
more »... KAH extracted UKGWAS and UK2 celiac DNA samples and performed UK2 sample golden gate genotyping. GrahamT and AWR prepared Irish DNA samples. GrahamT, AWR and KAH performed Irish sample golden gate genotyping. UK2 and IRISH genotyping was performed in CAM lab, DP performed quality control steps. AZ prepared DUTCH celiac and control DNA samples, and AZ and JR performed DUTCH sample golden gate genotyping in CW lab. DVH and KAH performed final golden gate genotype clustering on all samples, with assistance from RG. LD and DAvH collected Paxgene RNA celiac blood samples, GH extracted Paxgene RNA, GH and MB performed expression chips in CW lab, GH and LF analysed expression data. GosiaT performed IL18RAP re-sequencing. MCW processed intestinal biopsies, MB and MCW performed expression chips in CW lab, MCW and GH analysed expression data. DJP performed analysis of genes in intestinal T cell subsets. KAH and GH performed bioinformatics and annotation of celiac risk variant regions DAvH, RMM, CW were Principal Investigators and directed respectively the UK, IRISH and DUTCH sample collections and with RJP designed overall strategy and obtained funding for the study. DAvH directed the entire study, performed statistical analysis and generated the figures. DAvH and CW wrote the paper. RMcG, FT and WMMcL performed additional statistical analysis.
Manhattan plot showing the significance of association of all SNPs (n=532,694) across chromosomes 1-22 and × in the meta-analysis with BMI in asthmatic adults (n=3,242 individuals). d. ...doi:10.1111/cea.12054 pmid:23517042 pmcid:PMC3608930 fatcat:lmcyuomk75aongowqisrr6b5ky
(TIFF) Figure S2 Regional association plots of the most significant lung function-associated loci among ever-smokers in SpiroMeta (A-D). ...doi:10.1371/journal.pone.0019382 pmid:21625484 pmcid:PMC3098839 fatcat:7mvshs3fxnam7beunpkqcm7yai
D. S. Postma has consultant arrangements with AstraZe- neca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Takeda, and TEVA; has TABLE I . ... D. M. Evans has received a grant in the form of the MRC New Investigator Award G0600705. K. Berhane has received research support from the NIH. W. J. ...doi:10.1016/j.jaci.2013.08.053 pmid:24315451 pmcid:PMC4334587 fatcat:j632xhhfibebvdb3wvf2ed7boy
Birth Cohort 2742 1952 POBI - 2866 a Data available for 80% (GWAS) 86% (Replication), b Data available for 84% (GWAS) 81% (Replication), c Data available for 64% (GWAS) 79% (Replication), d ... 897) Extensive 43.3% (864) 37.4% (707) Smoking at diagnosis c Ex-smoker 36.7% (556) 30.3% (553) Current smoker 10.8% (163) 16.4% (300) Never smoked 52.5% (794) 53.2% (971) Colectomy d ...doi:10.1038/ng.483 pmid:19915572 pmcid:PMC2812019 fatcat:yrbzqv4ssfbbhjvbd27o2kxxaq
Williams MD, Rosemary A. ... McArdle MD, *D. EckhoffMD, *S. Bynon MD. ...doi:10.1007/bf03022274 fatcat:u6oy7phwtbed7by3xfzgysfeuq
Brunson, Assistant Professor William E. ... ' No t to be offere d in 1 972-73. "Not to be offered in 19 72-73 . ...fatcat:l3foge4e4vff5f762ejnn2cbm4
A randomized, controlled clinical trial established the efficacy and safety of short-term use of hydroxyurea in adult sickle cell anemia. To examine the risks and benefits of long-term hydroxyurea usage, patients in this trial were followed for 17.5 years during which they could start or stop hydroxyurea. The purpose of this follow-up was to search for adverse outcomes and estimate mortality. For each outcome and for mortality, exact 95% confidence intervals were calculated, or tests weredoi:10.17615/y997-wd39 fatcat:lbwmexmm4vemtd5a6q3oocir5a
more »... or tests were conducted at α = 0.05 level (p-value <0.05 for statistical significance). Although the death rate in the overall study cohort was high (43.1%; 4.4 per 100 person-years), mortality was reduced in individuals with long-term exposure to hydroxyurea. Survival curves demonstrated a significant reduction in deaths with long-term exposure. Twenty-four percent of deaths were due to pulmonary complications; 87.1% occurred in patients who never took hydroxyurea or took it for <5 years. Stroke, organ dysfunction, infection and malignancy were similar in all groups. Our results, while no longer the product of a randomized study because of the ethical concerns of withholding an efficacious treatment, suggest that long-term use of hydroxyurea is safe and might decrease mortality.
We also discuss that it is implausible that the observed effect of the FTO SNP on variance is due to its strong linkage disequilibrium (D′ = 1) with a causal variant that has a large effect on the mean ... and the non-centrality parameter (NCP v0 ) of the χ 2 test under the null hypothesis of no effect on variance is: 4 , in which n is the sample size, p is the frequency of the coded allele, and a and d ...doi:10.1038/nature11401 pmid:22982992 pmcid:PMC3564953 fatcat:wod3qf2i7fgjvgtzmtq7gxumeq
SNPs in 12 regions showed genome-wide significant association (P < 5 × 10 −8 ) with either PP or MAP in our discovery data (stage 1) (Supplementary Fig. 1c,d) , including two previously unidentified regions ...doi:10.1038/ng.922 pmid:21909110 pmcid:PMC3445021 fatcat:6gkmrs4r3va5pcgtfwf3qbmpeu
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