Moyamoya disease is a cerebrovascular disease that is characterized by the progressive stenosis in the terminal internal carotid artery, the anterior cerebral artery and the origin of the middle cerebral artery, and compensatory enlargement of basal perforating artery. Both the genetic and environmental factors involxe in its pathogenesis. but its exact cause is unknown. Revascularization is the main treatment approach for moyamoya disease. This article reviews the progress in research on epidemiology, etiology, diagnosis and treatment of moyamoya disease.

Experimental studies and clinical practices have found that mild hypothermia has neuroprotective effects. However, its specific mechanism is unclear. Although its efficacy is questioned continuously, mild hypothermia technique is still widely used in the intracranial aneurysm surgery for reducing ischemic injury in recent years. Currently its safety, effectiveness and methods are the focus of studies. The article reviews the recent progress in this field.

Atherosclerosis is the most important pathological basis of ischemic cerebrovascular diseases. As an independent risk factor of atherosclerosis, fibrin(ogen) and its degradation products involve in the processes of the formation and development of atherosclerosis. This article reviews the relationship between fibrin(ogen) and/or its degradation products and atherosclerosis, and also introduces the development and application prospects for some specific motif antagonists of fibrin(ogen) in the treatment of atherosclerosis and ischemic cerebrovascular diseases.

Objective To investigate the expression of NF-?B,TNF-?,ICAM-1 in rat's brain tissue and the sequential changes of serum IL-1?,IL-6,IL-10 after focal cerebral ischemia-reperfusion,and to observe the influence of the Shenxiong Injection.Methods Fifty-four male rats were randomly divided into control,Ligustrazin-treated and Shenxiong-treated group.Rats models of focal cerebral ischemia-reperfusion(I/R)were made by using suture.Drew back sutures 1 hour after the blood supply were blocked.A series of brain and blood samples were obtained directly 6,12 and 24 hours respectively after reperfusion in three groups.The expression of NF-?B,TNF-? and ICAM-1 in the brain tissue was determined by immuno-histochemical method.Serum levels of IL-1?,IL-6 and IL-10 were measured by enzyme linked immunosorbent assay (ELISA).Results As time of I/R prolonged,the expression of TNF-?,ICAM-1 upregulated,but NF-?B reached the maximum at R12 h in three groups.Compared with control group,expression of NF-?B,TNF-?,ICAM-1 in Shenxiong-treated group decreased significantly(P

Objective To investigate the TCM syndrome of metabolic syndrome. Methods The clinic information of the patients with metabolic syndrome was systematically collected through questionnaire investigation. The information was gathered with EXECL and analyzed by the medical statistic software SPSS14.0. Results Metabolic syndrome was closely related to lung, spleen, and kidney, manifested as spleen deficiency, lung deficiency, kidney deficiency, deficiency of both lung and spleen, deficiency of both lung and kidney, and deficiency of both spleen and kidney. The most frequently seen dyndrome is Qi deficiency, and the syndrome with most serious manifestations is phlegm-dampness. Conelesions Metabolic syndrome has a most closed relationship with the three organs of lung, spleen, and kidney. Qi deficiency, phlegm dampness, and blood stasis are the most frequently seen manifestations.

Autophagy is a process for the degradation of long half-life proteins and organelles via the lysosome system. A large body of evidence indicates that the autophagic phenomena exist in the progressive atherosclerotic plaques. Vascular smooth muscle cells, macrophages, and endothelial cells treated with some stimulants that result in atherosclerosis formation in in vitro experiments, these cells show certain autophagic features, such as myelin-like structures, accumulation of ubiquitinated inclusions in the cytoplasm, and extensive vacuolization. However, although the interests in research on autophagy are increasing, the exact role of autophagy in atherosclerosis remains unclear. Therefore, understanding the underlying cellular and molecular mechanisms of autophagy will provide a new idea for studying the mechanisms and treatment of atherosclerotic disease.

As a major adhesion molecule of endothelial junction, vascular endothelial cadherin (VE-cadherin) plays a very important role for the maintenance of vascular homeostasis. It regulates infiltration of vascular endothelia on contents in plasma such as eukocytes and lipid, as well as cellular proliferation and apoptosis. It plays an important role by involving in angiogenesis in the multiple links of the process of atherosclerosis, This article reviews the recent progress in research on the effects and mechanisms of VE-cadherin in the occurrence and developmaent of atherosclerosis in recent years.

Objective To investigate the localization coexpression in situ of matrix metalloproteinase(MMP)-2,-8 and vascular endothelial growth factor(VEGF)in human atherosclerotic unstable plaques with monocytes,smooth muscle cells(SMCs)and endothelial cells(ECs).Methods The histopathologic changes of unstable human atherosclerotic plaques were observed by hematoxylin and eosin(HE)staining,and the localization coexpression of MMP-2,MMP-8 and VEGF in the unstable human atherosclerotic plaques were observed by double fluorescent immunochemistry technology and confocal microscopy.Results The human atherosclerotic plaques in 6 cases had typical histopathologic instability,which was classified as super-Ⅳ type unstable plaques.The MMP-2 coexpression was the most obvious in the smooth muscle cells of fibrous cap infiltrated by monocyts,and in the monocytes of shoulder of plaques,and more expression of MMP-2 in the microvascular endothelial cells at the edge of shoulder and lipid necrosis;MMP-8 coexpressed obviously with the monocytes in the fibrous cap and lipid cores of plaques,and next to coexpressing in the smooth muscle cells of fibrous cap,while coexpression in endothelial cells was very little;VEGF coexpression was significant in the proliferative microvascular endothelial cells of plaques;The fibrous cap,which consisted of the smooth muscle cells mainly,and the edge of lipid necrosis infiltrated by more monocyts,were over-expression areas of VEGF.Conclnsions MMP-2,-8 and VEGF can coexpress with monocytes,SMCs and ECs in unstable plaques,and the major expression areas are in the fibrous cap,shoulder and micro-vessel at the edge of lipid necrosis,which are infiltrated by monocytes.Moreover,the outer membrane of vessel is involved in the pathogenesis of atherosclerosis.

Objective The study consisted of two parts: in part Ⅰ the effects of propofol or/and procaine on CD18, CD62L expression and superoxide anion (SOA) release of phorbol 12-myristal 13-acetate(PMA) stimulated human neutrophils (PMNs) were studied in vitro; in part Ⅱ the effects of propofol or/and procaine on IL-6 and TNF-?production in endotoxin-stimulated human whole blood were studied. Methods PMNs were separated from the whole blood obtained from healthy 20-40yr old subjects. Part Ⅰ consisted of 9 groups: in group 1 (control) phosphate buffer solution was added to PMNs; in group 2 PMNs were stimulated by PMA 100mg?ml-1 ; in group 3-5 different concentrations of propofol (0.4, 4.0,40?g?ml-1) were added to PMA stimulated PMNs; in group 6-8 different concentrations of procaine (1.5,15,150?g?ml-1 ) were added to PMA stimulated PMNs; in group 9 propofol 2?g?ml-1 and procaine 8?g?ml-1 were added to PMA stimulated PMNs. Part II also consisted of 9 groups: in groupl whole blood was mixed with normal saline; in group2 lipopolysaccharide (LPS) l?g?ml-1 was added to whole blood; in group 3-5 different concentrations of propofol (0.4,4.0,40?g?ml-1) were added to LPS stimulated whole blood; in group 6-8 different concentrations of procaine (1.5, 15, 150?g?ml-1 ) were added to LPS stimulated whole blood; in group 9 propofol 2?g?ml-1 and procaine 8?g?ml-1 were added to LPS stimulated whole blood. CD18, CD62L expressions were measured by flow cytometry. SOA release was determined by cytochrome C reduction in the presence or absence of superoxide dismutase (SOD) . IL-6 and TNF-? production were measured by using radioimmunoassay. Results Propofol or/and procaine depressed CD18 up-regulation, CD62L shedding and SOA release of PMA-stimulated PMNs and propofol was more effective than procaine. Propofol enhanced but procaine inhibited the increased production of TNF-? and IL-6 in the LPS stimulated whole blood but when propofol and procaine were used in combination. The effectof procaine predominated. Conclusions Propofol or/and procaine can attenuate tissue damage induced by neutrophils by inhibiting the function of neutrophils.

Objective To investigate the relationship between carotid atheromatous plaque and its related biochemical indexes and cerebral infarction.Methods 65 cases with cerebral infarction served as cerebral infarction(CI) group and 35 cases of non-cerebral infarction as control group. In both groups,the location,number and nature of carotid atheromatous plaque and diamete of carotid artery were assessed by Doppler ultrasonography,and the related biochemical indexes such as blood lipid,blood glucose and fibrinogen were evaluated.Results Significant differences of the detectable rate of carotid atheromatous plaque and the diameter of common carotid artery were found between CI group[81.54%,( 7.43? 0.07)mm of left side,(7.52?0.60)mm of right side] and control group[28.57%,(7.75?0.10)mm of left side,( 7.97? 0.75)mm of right side]( P