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 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.

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 identify the association between fatigue and depression in Parkinson's disease(PD).Methods 56 PD patients were enrolled in this study.The degree of fatigue was measured by Fatigue Severity Scale (FSS).Hamilton Depression Scale (24 items) was used to evaluate the degree of depression.PD Quality of Life Questionnaire (PDQL) were tested to evaluate the quality of life in PD patients.While other clinical information such as Unified Parkinson's Disease Rating Scale (UPDRS) Ⅲ,Hoehn-Yahr Scale and modified Webster Scale were investigated.Results The incidence of fatigue in this group is 71.4％ (40/56).Score of HAMD and PDQL exhibited a significant correlation to patients' fatigue,coefficient of partial correlation was 0.451 (P ＜ 0.01),-0.346 (P ＜ 0.05).The incidence of fatigue in non-depressive patients was low,27.3 ％.While in depressive patients,the incidence of fatigue is relatively high,for mild depression 75％,moderate depression 100％,severe depression 100％ respectively.Conclusions Fatigue is a prominent symptom of depression in PD patients,sometimes independent of depression also influencing the patients' quality of life.

Objective To investigate the risk factors for intracranial atherosclerosis in patients with ischemic stroke.Methods The demographic data and vascular risk factors in patients with ischemic stroke who performed digital subtraction angiography were analyzed retrospectively.According to the lesion locations,the patients with moderate to severe intracranial arterial stenosis were divided into intracranial internal carotid artery,middle cerebral artery,intracranial vertebral artery,and basilar artery.The démographic data and vascular risk factors among all groups were compared.Results A total of 344 patients with ischemic stroke were recruited,147 (42.7％ ) of them were moderate to severe intracranial arterial stenosis and 197 (57.3％ ) were mild intracranial arterial stenosis.Univariate analysis showed that the proportion of diabetes (34.0％ vs.20.8％,x2 =7.541,P=0.006) or hyperlipidemia (78.9％ vs.66.0％,x2 =6.900,P=0.009) in the moderate to severe intracranial arterial stenosis groups was significantly higher than that in the mild intracranial arterial stenosis group.The levels of total cholesterol (4.656 ±0.955 mmol/L vs.4.401 ±0.882 mmol/L,t =-2.543,P =0.011),low-density lipoprotein cholesterol (3.015 ± 0.817 mmol/L vs.2.741 ± 0.786 mmol/L,t =-3.113,P =0.002),fasting blood glucose (FBG) (6.184 ± 2.127 mmol/L vs.5.568 ±1.772 mmol/L,t =-2.869,P =0.004),and the National Institutes of Health Stroke Scale score (5.48 ± 4.980 vs.4.33 ± 4.094,t =-2.332,P =0.020) were significantly higher.Multivariable logistic regression analysis showed that diabetes (odds ratio [ OR ] 1.907,95％confidence interval [ CI] 1.164-3.124; P =0.010) and low-density lipoprotein cholesterol (OR 1.500,95％ CI 1.133-1.986; P =0.005) were the independent risk factors for moderate to severe intracranial arterial stenosis.Among the patients with different locations of intracranial arteries,there were significant differences in the distribution of the risk factors,such as male (P =0.017),coronary artery disease (P =0.002),and smoking (P =0.026).Conclusion Diabetes and the increased level of low-density lipoprotein cholesterol were the independent risk factors for moderate to severe stenosis of intracranial arteries.The distribution of risk factors for intracranial atherosderosis had location specificity.

Sleep apnea syndrome (SAS) is an independent risk factor for atherosclerosis and stroke. Studies have shown that the incidence of SAS increases significantly after stroke.This article reviews the mechanism of atherosclerosis caused by SAS and the characteristics and research progress of sleep apnea after stroke.

In recent years, here are many new understandings in the definition, etiology, diagnosis and treatment of transient ischemic attack (TLA).The latest viewpoint considers that TIA is a transient episode of neurological dysfunction caused by brain, spinal cord or focal retinal ischemia, without the evidence of acute infarction. The duration of TIA is no longer the key factor, whether the existence of infarction or not is the key factor in the differentiation of TIA and ischemic stroke. Therefore ,it should emphasize the importance of neuroimaging in the diagnosis of TIA. As a neurological emergency, the risk level of TIA should be stratified and evaluated, and the active interventions should be performed.

The article introduces the advances in the evaluation of transient ischemic stroke (TLA) and reviews them from four aspects, including identifying whether the symptoms accord with the diagnosis of TLA, which blood supply area the ischemia is located in, evaluating the pathogenesis of TIA, and predicting its prognosis.