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Regulating Effect Of ICOS-ICOSL On The Immunomechanism Of Atherosclerosis And Its Being Interferentialed By Statin

Posted on:2007-03-18Degree:DoctorType:Dissertation
Country:ChinaCandidate:L XuFull Text:PDF
GTID:1104360185988545Subject:Department of Cardiology
Abstract/Summary:PDF Full Text Request
Atherosclerosis (AS) is presently one of the most harmful human diseases with highest morbidity. It has been proved that AS has complex factors at multiple levels. The famous Framingham tests founded it was the various injury factors for AS, such as smoking, hypertention, high blood fat and high blood sugar. While three doctrines, the first is Fatty infiltration, the second is Thrombogenesis, and the last is Response to injury hypothesis have then been put forward. But, however, the above theories still cannot entirely explain the cause of formation and the seriousness of AS, and new researches involving the etiopathogenesis and the pathologic alteration of AS have therefore been widely put into attention. Based on numbers of basic and clinical researches, it is found that pyloric spirillum, cytomegalic virus, and pneumonic chlamydia can be detected in AS plaque. Although, up to now, the pathologic model of the above three major types of pathogen have not been able to be duplicated, yet the view point that the related bacteria, virus, and chlamydia should be the dangerous factors which cause the AS disease have been accepted by numerous scholars. Under infection, the estrogen, hemicystine, and C-reaction protein, etc., will promote the formation of AS, that is to say the inflammation medium does participate the formation and development of AS and should be one of the most important etiopathogenesis of this disease. Recently, some researchers have further found that nearly 40% of patients who have suffered from myocardial infraction or cerebrovascular disease used to be under the condition of being immune from chronic disease, and so they hold that: since AS matches the following conditions...
Keywords/Search Tags:Inducible co-stimulator, Inducible co-stimulator ligand, immunity, Atherosclerosis, Simvastatin
PDF Full Text Request
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