How to Build CHD@ZJU

CHD related Articles were retrieved from Pubmed, by entering keywords "coronary heart disease" and constrict the publish date from 2000/1/1 to now (2013/1/23). As a result, totally 115898 articles were found and their abstracts were downloaded for text mining. Since some articles didn't contain abstracts, only 88396 abstracts remained.
The text-mining process to get CHD related genes could be divided in to 5 following steps:

  • 1) Extracting all keywords from abstracts and ignoring those keywords start with numbers. 101402 keywords were extracted.

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  • 2) Input these keywords into Gene library in ArrayTrack and find possible related genes. 4674 genes were then found.

  • 3) Put these 4674 genes again into pubmed abstracts to find related aticles. Only genes which offical name or there keyword description (such as prolactin for gene PRL) could be found in the abstract would be remained. As a result, 1247 genes were remained.

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  • 4) Manually examined on the 1247 genes to validate it was acutally related to CHD. Some genes would be filtered if it represents other meanings (such as gene CAD, Entrez ID:790, carbamoyl-phosphate synthetase 2, is mostly meant coronary arterial disease in articles). 681 genes were then validated with at least one reference.

  • 5) All genes was compared with 1078 CHD genes in RGD database, and 370 genes were overlapped. These 370 genes were labels as "RGD_Supported" and the other 293 genes were labels as "REFERED". All 663 genes had supported references in CHD@ZJU which were examined by step 4.

    • How To contact Us

    Collaboration Information: Prof. Xiaohui Fan (fanxh@zju.edu.cn)

    Website using assistance : Leihong Wu (11019004@zju.edu.cn)




    Common genetic loci influencing plasma homocysteine concentrations and their effect on risk of coronary artery disease.
  • Author:"van Meurs, Joyce B J;Pare, Guillaume;Schwartz, Stephen M;Hazra, Aditi;Tanaka, Toshiko;Vermeulen, Sita H;Cotlarciuc, Ioana;Yuan, Xin;Malarstig, Anders;Bandinelli, Stefania;Bis, Joshua C;Blom, Henk;Brown, Morris J;Chen, Constance;Chen, Yii-Der;Clarke, Robert J;Dehghan, Abbas;Erdmann, Jeanette;Ferrucci, Luigi;Hamsten, Anders;Hofman, Albert;Hunter, David J;Goel, Anuj;Johnson, Andrew D;Kathiresan, Sekar;Kampman, Ellen;Kiel, Douglas P;Kiemeney, Lambertus A L M;Chambers, John C;Kraft, Peter;Lindemans, Jan;McKnight, Barbara;Nelson, Christopher P;O'Donnell, Christopher J;Psaty, Bruce M;Ridker, Paul M;Rivadeneira, Fernando;Rose, Lynda M;Seedorf, Udo;Siscovick, David S;Schunkert, Heribert;Selhub, Jacob;Ueland, Per M;Vollenweider, Peter;Waeber, Gerard;Waterworth, Dawn M;Watkins, Hugh;Witteman, Jacqueline C M;den Heijer, Martin;Jacques, Paul;Uitterlinden, Andre G;Kooner, Jaspal S;Rader, Dan J;Reilly, Muredach P;Mooser, Vincent;Chasman, Daniel I;Samani, Nilesh J;Ahmadi, Kourosh R"

  • Published Year:2013

  • Journal:The American journal of clinical nutrition

  • Abstract:"BACKGROUND: The strong observational association between total homocysteine (tHcy) concentrations and risk of coronary artery disease (CAD) and the null associations in the homocysteine-lowering trials have prompted the need to identify genetic variants associated with homocysteine concentrations and risk of CAD. OBJECTIVE: We tested whether common genetic polymorphisms associated with variation in tHcy are also associated with CAD. DESIGN: We conducted a meta-analysis of genome-wide association studies (GWAS) on tHcy concentrations in 44,147 individuals of European descent. Polymorphisms associated with tHcy (P < 10((-)(8)) were tested for association with CAD in 31,400 cases and 92,927 controls. RESULTS: Common variants at 13 loci, explaining 5.9% of the variation in tHcy, were associated with tHcy concentrations, including 6 novel loci in or near MMACHC (2.1 x 10(-)(9)), SLC17A3 (1.0 x 10(-)(8)), GTPB10 (1.7 x 10(-)(8)), CUBN (7.5 x 10(-)(1)(0)), HNF1A (1.2 x 10(-)(1)(2))), and FUT2 (6.6 x 10(-)(9)), and variants previously reported at or near the MTHFR, MTR, CPS1, MUT, NOX4, DPEP1, and CBS genes. Individuals within the highest 10% of the genotype risk score (GRS) had 3-mumol/L higher mean tHcy concentrations than did those within the lowest 10% of the GRS (P = 1 x 10(-)(3)(6)). The GRS was not associated with risk of CAD (OR: 1.01; 95% CI: 0.98, 1.04; P = 0.49). CONCLUSIONS: We identified several novel loci that influence plasma tHcy concentrations. Overall, common genetic variants that influence plasma tHcy concentrations are not associated with risk of CAD in white populations, which further refutes the causal relevance of moderately elevated tHcy concentrations and tHcy-related pathways for CAD."

  • 10.3945/ajcn.112.044545

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