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.

Lipoprotein-associated phospholipase A2(Lp-PLA2) can rapidly hydrolize and oxidize the oxidized phosphatidylcholine molecules produced in low density lipoprotein and atherogenic lipoprotein (a),generating the soluble proinflammatory and proapoptotic mediatorslyso-phosphatidylcholine and oxidized free fatty acids.It stimulates aggregation and activation of monocyte-macrophage system and induces apoptosis and damages the removal of dead cells.It plays an important role in the development of lipid necrotic core of atherosclerosis.Lp-PLA2 is not an independent risk marker of coronary artery disease and ischemic stroke,but also plays an important role in the development of atherosclerotic plaques.Selective Lp-PLA2 inhibitor reduces the development of necrotic cores.It may play a role in the stabilization of atherosclerotic plaques.At the same time,it may represent a novel target for the treatment of atherosclerosis.

With the improvement of radiation therapy technology and the comprehensive treatment of malignant tumors,the survival time of patients with malignant tumors is gradually extended.In recent years,carotid stenosis and cerebrovascular disease complications after radiation therapy have received increasing attention.Existing studies have shown that carotid stenosis after radiation therapy is not only associated with atherosclerosis,it is likely to be an independent vascular lesion.This article reviews the correlation between head,neck and cerebral ischemic events,characteristics and mechanisms of vascular injury after radiation therapy,as well as the risk factors for carotid stenosis,clinical manifestations,and diagnosis and treatment methods after radiation therapy.

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.

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

Traditional Chinese Medical Culture is rich in content,which contains the humanitarian spirit of respect for life,life-saving,caring and saving,the idea of pursuing equality,fairness,justice,happiness and harmony,and the ecological medical values of promoting harmony between man and nature.The above values provide rich cultural resources for the construction of universal values,and significant ideological platform for the construction of global ethics.

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.