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)




    Secretory Phospholipase A2-IIA and Cardiovascular Disease: A Mendelian Randomization Study.
  • Author:"Holmes, Michael V;Simon, Tabassome;Exeter, Holly J;Folkersen, Lasse;Asselbergs, Folkert W;Guardiola, Montse;Cooper, Jackie A;Palmen, Jutta;Hubacek, Jaroslav A;Carruthers, Kathryn F;Horne, Benjamin D;Brunisholz, Kimberly D;Mega, Jessica L;van Iperen, Erik P A;Li, Mingyao;Leusink, Maarten;Trompet, Stella;Verschuren, Jeffrey J W;Hovingh, G Kees;Dehghan, Abbas;Nelson, Christopher P;Kotti, Salma;Danchin, Nicolas;Scholz, Markus;Haase, Christiane L;Rothenbacher, Dietrich;Swerdlow, Daniel I;Kuchenbaecker, Karoline B;Staines-Urias, Eleonora;Goel, Anuj;van 't Hooft, Ferdinand;Gertow, Karl;de Faire, Ulf;Panayiotou, Andrie G;Tremoli, Elena;Baldassarre, Damiano;Veglia, Fabrizio;Holdt, Lesca M;Beutner, Frank;Gansevoort, Ron T;Navis, Gerjan J;Mateo Leach, Irene;Breitling, Lutz P;Brenner, Hermann;Thiery, Joachim;Dallmeier, Dhayana;Franco-Cereceda, Anders;Boer, Jolanda M A;Stephens, Jeffrey W;Hofker, Marten H;Tedgui, Alain;Hofman, Albert;Uitterlinden, Andre G;Adamkova, Vera;Pitha, Jan;Onland-Moret, N Charlotte;Cramer, Maarten J;Nathoe, Hendrik M;Spiering, Wilko;Klungel, Olaf H;Kumari, Meena;Whincup, Peter H;Morrow, David A;Braund, Peter S;Hall, Alistair S;Olsson, Anders G;Doevendans, Pieter A;Trip, Mieke D;Tobin, Martin D;Hamsten, Anders;Watkins, Hugh;Koenig, Wolfgang;Nicolaides, Andrew N;Teupser, Daniel;Day, Ian N M;Carlquist, John F;Gaunt, Tom R;Ford, Ian;Sattar, Naveed;Tsimikas, Sotirios;Schwartz, Gregory G;Lawlor, Debbie A;Morris, Richard W;Sandhu, Manjinder S;Poledne, Rudolf;Maitland-van der Zee, Anke H;Khaw, Kay-Tee;Keating, Brendan J;van der Harst, Pim;Price, Jackie F;Mehta, Shamir R;Yusuf, Salim;Witteman, Jaqueline C M;Franco, Oscar H;Jukema, J Wouter;de Knijff, Peter;Tybjaerg-Hansen, Anne;Rader, Daniel J;Farrall, Martin;Samani, Nilesh J;Kivimaki, Mika;Fox, Keith A A;Humphries, Steve E;Anderson, Jeffrey L;Boekholdt, S Matthijs;Palmer, Tom M;Eriksson, Per;Pare, Guillaume;Hingorani, Aroon D;Sabatine, Marc S;Mallat, Ziad;Casas, Juan P;Talmud, Philippa J"

  • Published Year:2013

  • Journal:Journal of the American College of Cardiology

  • Abstract:"OBJECTIVES: This study sought to investigate the role of secretory phospholipase A2 (sPLA2)-IIA in cardiovascular disease. BACKGROUND: Higher circulating levels of sPLA2-IIA mass or sPLA2 enzyme activity have been associated with increased risk of cardiovascular events. However, it is not clear if this association is causal. A recent phase III clinical trial of an sPLA2 inhibitor (varespladib) was stopped prematurely for lack of efficacy. METHODS: We conducted a Mendelian randomization meta-analysis of 19 general population studies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acute coronary syndrome (ACS) cohorts (2,520 recurrent MVE in 18,355 individuals) using rs11573156, a variant in PLA2G2A encoding the sPLA2-IIA isoenzyme, as an instrumental variable. RESULTS: PLA2G2A rs11573156 C allele associated with lower circulating sPLA2-IIA mass (38% to 44%) and sPLA2 enzyme activity (3% to 23%) per C allele. The odds ratio (OR) for MVE per rs11573156 C allele was 1.02 (95% confidence interval [CI]: 0.98 to 1.06) in general populations and 0.96 (95% CI: 0.90 to 1.03) in ACS cohorts. In the general population studies, the OR derived from the genetic instrumental variable analysis for MVE for a 1-log unit lower sPLA2-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and differed from the non-genetic observational estimate (OR: 0.69; 95% CI: 0.61 to 0.79). In the ACS cohorts, both the genetic instrumental variable and observational ORs showed a null association with MVE. Instrumental variable analysis failed to show associations between sPLA2 enzyme activity and MVE. CONCLUSIONS: Reducing sPLA2-IIA mass is unlikely to be a useful therapeutic goal for preventing cardiovascular events."

  • 10.1016/j.jacc.2013.06.044

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