日志
induction promote
|
inflammation stimulate a potential contact. Ault etc (21) reported in acute coronary patients with ischemic events and platelet activation of continuous evidence. Platelet related P choice is sensitive indicators, platelet activation in the ACS clinically stable after a month still can keep rising, this persistent inflammation may be sustained platelet activate the stimulation. The ACS sICAM - 1, the latter moncler sVCAM - 1, soluble E choice and soluble P select element continue to rise. But also have the author thinks platelet activate index and the correlation between serum CRP levels.5 infection factors and ACS in atherosclerosis and began to infection factors in the development of pathogenic role is still controversial. Acute infection can change in ischemic eents hemodynamic and blood moncler jackets coagulation and fibrinolysis system. Chronic infections (e.g. outside blood-vessel gingivitis, prostatitis and bronchitic etc) can increase the blood vessels of proinflammatory cytokines, proinflammatory cytokines can make the distant atherosclerosis. Intravascular infection, inflammation irritants directly aggravating atherosclerosis. The most common pathogens is pneumonic chlamydia and cytomegalovirus (CMV). CMV can hint of restenosis after coronary intervention, 43% of serum reaction (negative only moncler vest 8% for patients with coronary angiography. Restenosis dangerous. With IgG antibody, The ACS is higher in IgE (22). There's a heart transplant patients infected CMV grafted part vulnerable to atherosclerosis. Pneumonia chlamydia positive serum with AMI UA and relevant. Bu rian etc (23) reported to heat shock protein 60 and pneumonia chlamydia antibody concentration of independent risk factors for coronary moncler coats artery disease is both greatly increases the risk exists. So the heat shock protein 60 in atherosclerosis also plays a certain role (24). From atherosclerotic parts can be separated from pneumonia chlamydia and CMV. Despite the large clinical epidemiological data, but still have no problem solving, such as in the ACS, infection factors are the causes of independent existence or Cheap Moncler merger of accidental, not the coexistence of pathogenic role.6 the ACS inflammation mechanism is not only the inflammation may be at increased risk of ACS index (25), also participated in the obstruction. Acute inflammation directly affect thrombosis, inflammation, inhibit endogenous fibrinolysis system to promote thrombosis and blood coagulation. Monocytes exposure to immune source or other stimuli, in its surface express Discount Moncler an induction promote clotting factors that stimulate blood clot formation lymphoid factor. Activated macrophages secretion of IL - 1, IL - 6 to stimulate cell factors as strong smooth muscle cell proliferation and induced liver cells to produce large acute c-reactive protein such as CRP, combined with lipoprotein CRP, the classic way, then can activate the complement system of terminal Moncler Outlet complex and terminal C5b - 9, protein neointimal damaged. Mononuclear cells and neutrophils are contain plenty of CRP CRP receptor, the receptor, the activation, through direct or indirect infiltration, gathered) (produce) cell factors causing vascular injury. Endothelial hemal wall with human existence, the CRP CRP neutrophilic closely, CRP induction complement, with some cell activation of CRP adhesion molecules, the adhesion Moncler Sale molecules in the white wall by endothelial adhesion and cell-extracellar plays an important role in the process of atherosclerosis, this is an important step to. The local exists rupture plaque can produce MMPs macrophages. The ACS patients MMP plasma - 9 and matrix metalloproteinases inhibitors (TIMP - 1) level is higher (26). These MMPs atherosclerotic plaque can cause all fibrous
/1 
