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The Relationship Betweent Prothrombin G20210A Mutation And Pulmonary Thromboembolism

Posted on:2015-03-15Degree:MasterType:Thesis
Country:ChinaCandidate:J ZhangFull Text:PDF
GTID:2254330428998807Subject:Clinical Medicine
Abstract/Summary:PDF Full Text Request
Pulmonary thromboembolism is a dangerous clinical emergency, it hashigh mortality and morbidity.And it seriously threats to people’slife and health. However,it is difficult to diagnose and treat PTEbecause it has not typical clinical symptoms. Earlydiagnosis,prevention and treatment of pulmonary thromboembolismbecomes a hot spot. At present, the studies of the pathogenesis ofPTE is less, especially the molecular genetic mechanism research.In recent years, Europe and the United States scholars put forward,prothrombin gene G20210A mutation is one of the important geneticmechanisms of pulmonary thromboembolism. However, at present mostof the research object is white people in Europe and North America,in our country and other regional is less,especially in northeastChinese. In this paper, the PCR-RFLP technology is taken tounderstand whether patients with pulmonary thromboembolism haveprothrombin gene G20210A mutation, and this paper will study therelationship between the prothrombin gene G20210A mutation and thePTE in northeast Chinese.Objective:To understand whether patients with pulmonary thromboembolism have prothrombin gene G20210A mutation, and to study therelationship between the prothrombin gene G20210A mutation and thePTE in northeast Chinese..Methods:Forty two PTE patients and eighty health controls were recruited.Allpatients were diagnosed by lung ventilation/perfusion scan ormulti-slice CT pulmonary angiography(CTPA). The diagnosis of PTEare formulated on the basis of The Diagnosis And Treatment OfPulmonary Thromboembolism Guidelines (draft), Diagnosis AndTreatment Of Acute Pulmonary Embolism Guide. The experimental groupand control group were extracted venous blood2ml, put in EDTAanticoagulant tube. Then we extracted DNA and used PCR amplificationfrom Eppendorf company to amplify segments of prothrombin gene PCR.PCR products were digestived by HindIII enzyme. Finally by gelimaging analysis system for photographic analysised of enzymeproducts.Results:PCR amplification results:the size of the PCR amplification productfor Prothrombin G20210gene in the patients group and control groupwas506bp.Hind III restriction enzyme digestion results:the PCR amplificationproduct for Prothrombin G20210gene in the patients group andcontrol group was cut with Hind III retriction enzyme.The resultsshowed that the size of the fragment was407bp and99bp, there wasno other size of the fragment. This suggests that all samples of the PCR amplification products did not have other HindIII enzymesites from gene mutations, only one enzyme loci.Prothrombin G20210Amutation was not found in both PTE patients and controls.Conclusion:Prothrombin G20210A gene homozygous and heterozygous mutations inthe experimental group and control group did not appear, HindIIIenzyme electrophoresis has not found the DNA fragments caused bygene mutation.These results prompted that in northeast Chinese,there may not be prothrombin gene G20210A mutation, the genemutation is different in racial and regional. For northeast Chinese.,the gene mutation may not be the main risk factors for PTE.In thefuture,we can find other factors what lead to high risk of pulmonarythromboembolism.
Keywords/Search Tags:Pulmonary thromboembolism, G20210A mutation, gene
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