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Table of Content

    20 February 2007, Volume 2 Issue 02
    主编手记
    The Stratification Strategies and Case-based Care in the Patients with IschemicStroke
    WANG Yong-Jun
    2007, 2(02):  92-094. 
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    述评
    Stroke Care in 2006, Did We Make Any Progress?
    David Z. Wang;WANG Gui-Hong;QIN Hai-Qiang
    2007, 2(02):  95-101. 
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    论著
    Effects of Androgen on Acute Cerebral Infarction in Elderly Men at High Altitude
    ZHU Ai-qin;CHU Yi-de;LI Ying-lan;et al.
    2007, 2(02):  105-108. 
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    Objective To study the relationship between androgen levels and acute cerebral infarction(ACI) inelderly men at high altitude.Methods Serum levels of testosterone(T) and estradiol (E2)were determined in 60 elderly menwith ACI and 60 healthy elderly men at high altitude (2260 m sea levels above). Serum levels ofinterleukin(IL)-1, IL-6, tumor necrosis factor(TNF)-α and erythropoietin (EPO) were measuredby radioimmunoassay. We also measured the serum levels of triglyeride (TG), total cholesterol(TC), low-density lipoprotein (LDL), high density lipoprotein (HDL), apolipoprotein (Apo)-A1 andApo-B by colorimetry.Results (1) T was significantly lower in patients than in control subjects at high altitude (P <0.001).There was no statistical difference between patients and control subjects in E2, TC, HDL andApo-A1 levels. Compared with control subjects, the levels of TG, LDL and Apo-B in patientswere significantly higher (P <0.05). (2) Serum levels of IL-1β, IL-6 and TNF-α were increasedsignificantly in patients when compared with control subjects. EPO remained no significantdifference in two subjects at high altitude. (3) T was significantly negatively correlated with TG,LDL, Apo-B, TNF-α, IL-1 and IL-6. However, there was no correlated between E2, TC, HDL,Apo-A1, EPO and T.Conclusion These results support the idea that low T level is a risk factor of acute cerebralinfarction in men at high altitude, maybe by influencing upon lipid metabolism and inflammation.
    Expression of Hypoxia Inducible Factor-1α and Erythropoietin in the Rat Model of Brain Ischemic Tolerance
    ZHAO Ren-liang;DONG Rui-jian.
    2007, 2(02):  109-114. 
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    Objective To investigate the expression of hypoxia inducible factor-1α(HIF-lα) and its targetgene erythropoietin(EPO)in the rat model of brain ischemic tolerance induced by ischemicpreconditioning(IP).Methods Eighty-four healthy Wistar rats were enrolled randomly into three groups for differentpretreatments, the sham surgery group(SS+SS,n=4), the sham and middle cerebral arteryocclusion(MCAO) group(SS+MCAO, n=40) and the IP and MCAO group(IP+MCAO, n=40).The latter two groups were further divided into five subgroups due to different IP. The rats weregiven MCAO for 10 minutes for IP. At 1, 3, 7, 14 and 21d after IP, the rats were given the secondMCAO(or sham surgery) for 2 hours followed by 22 hours reperfusion. The infarct volume wasmeasured by triphenyl tetrazolinm chloride(TTC) staining and we detected the protein of HIF-1αand EPO by immunohistochemistry.Results ⑴The infarct volumes in the 1 d, 3 d and 7 d subgroups of IP+MCAO were significantlysmaller than those of the SS+MCAO subgroups(P <0.05). ⑵The expressions of HIF-1α protein inthe 1 d, 3 d and 7 d subgroups of IP+MCAO were significantly higher than those of the SS+MCAOsubgroups(P <0.05), while the expressions of EPO protein in the 3 d and 7 d subgroups ofIP+MCAO were significantly higher than those of the SS+MCAO subgroups(P <0.05).Conclusion Ischemic preconditioning for 10 minutes induces relative tolerance to subsequentMCAO as evidenced by reduction of infarct volumes. Endogenously produced HIF-lα and EPOmay be essential mediators of cerebral ischemic tolerance.
    Relationship between Angiotensin II Type I Receptor (AT1R)-A1166C GenePolymorphisms and Cerebral Infarction
    HE Ji-ling;SUN Hong-ying;YANG Yue-ming;etal.
    2007, 2(02):  115-118. 
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    Objective To explore the relationship between angiotensin II type I receptor (AT1R) A1166C genepolymorphisms and cerebral infarction(CI).Methods The study population was comprised of 77 patients with cerebral infarction and 98healthy individuals. The AT1R-A1166C genotypes were determined by restriction fragment lengthpolymorphism.Results CC genotype was not found both in CI and control group. In CI group, genotypicfrequencies of AA and AC were 38.9% and 61.1%, respectively. The allele frequency of A was 0.695and C was 0.305. In control group, genotypic frequencies of AA and AC were 91.8% and 8.2%,respectively. The allele frequency of A was 0.959 and C was 0.041. AT1R-A1166C polymorphismrevealed significant difference of genotype and allelic distribution between CI patients and controls.In CI group, patients with AC genotype showed significantly higher blood pressure than those withAA genotype. The systolic blood pressure in patients with AA genotype, as well as the systolic anddiastolic blood pressure in patients with AC genotype in CI group were statistically higher thanthose in control group.Conclusion The polymorphism of AT1R-A1166C is related to the incidence of cerebral infarctionand contributes to the development of hypertension, especially for the diastolic blood pressure.
    Treatment of Acute Ischemic Stroke with Intra-arterial Thrombolysis Using Urokinase Seven Case Reports
    HUANG Yan;LI Zhan-peng;ZHOU Yi-xing;et al.
    2007, 2(02):  119-122. 
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    Objective To evaluate the safety and clinical efficacy of intra-arterial thrombolysis using urokinasein patients with acute ischemic stroke.Methods Total 7 patients of acute ischemic stroke in 6h were treated with intra-arterialthrombolysis using urokinase. They were assessed by neurologists using National Institutes ofHealth Stroke Scale(NIHSS) score at admittance to the hospital, after the treatment and 14d afterthe treatment.Results Seven patients achieved complete recanalization. It was improved obviously of theneurologic function defect of the 7 patients after 14d. None of cerebral hemorrhage was observed.Conclusion Intra-artery thrombolysis therapy using urokinase for acute ischemic stroke might besafe and effective, but we need a large sample, randomized and control study to confirm.
    Risk Factors and Preventive Strategies of Pneumonia in Stroke Patients in Hospital
    HE Hong;WANG Shao-chun;JIANG Zhong-xin.
    2007, 2(02):  123-125. 
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    Objective To investigate the risk factors and preventive measurement for pneumonia in strokepatients.Methods A total of 255 patients with pneumonia from Jan 2003 to Dec 2005 were retrospectivelyanalyzed, and the risk factors of pneumonia were summarized.Results The rate of hospital pneumonia in stroke patients was 33.4%, and risk factors prone tohospital pneumonia were aging, long hospitalization, respiratory machine application, respiratorytract incision and underlying diseases.Conclusion Effective measurement against different risk factors may decrease the rate ofpneumonia in hospital.
    Analysis of Pathogenic Microorganism in Neurological Intensive Care Unit
    XU Xue-xin;ZHANG Wei
    2007, 2(02):  126-128. 
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    Objective To investigate and analyze nosocomial infection incidence and pathogen epidemiologyof neurological intensive care unit(NICU) and propose the nursing strategies to reduce the infectionrate.Methods Total 237 patients admitted in NICU were enrolled in this retrospective study fromMay 2002 to April 2004. We analyzed the pathogenic microorganism of 326 samples for the totalpatients.Results Total 324 bacterium strains were found in 326 samples,including 178 strains of Gramnegativebacillus (54.94%), 107 strains of Gram-positive bacillus (33.02%) and 39 strains offungus(12.04%). Most of Gram-negative bacilli were Escherichia coli, Klebsislla pneumoniae,Pseudomonas pyocyanea, Acinetobacter baumannii and Enterobacter cloacae. And most of Grampositivebacilli were Staphylococcus aureus, Enterococcus and Coagulase-negative staphylococci.Pneumonia and urinary system infection were usually found in this study.Conclusion It is important to monitor bacterium, use antibiotics correctly, detect the pathogenicmicroorganism and prevent risk factors for controlling the infection of NICU.
    综述
    The Relationship between Small Deep Cerebral Infarcts in Anterior CirculationTerritory and Large Extra- or Intra-cranial Artery Disease
    WANG Wei;GAO Shan.
    2007, 2(02):  156-159. 
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    Small deep cerebral infarcts, often referred to lacunes,have been traditionally associated withsmall-vessel disease affecting the deep penetrating arterial system. However, small deep cerebralinfarcts with ipsilateral large cerebral artery disease are often observed. The aim of this articleis to investigate the relationship between the small deep cerebral infarcts and the large arterydisease. This article reviewed 21 pieces of related literatures aboard which discussed the pattern ofcerebral infarcts in stenotic or occluded cerebral arteries of anterior circulation, and the potentialmechanisms of small deep cerebral infarcts caused by large artery disease. Large cerebral arterydisease can also cause the small deep cerebral infarcts like “lacunar infarcts”.
    Advances in the Genetics of Ischemic Cerebrovascular Disease
    SUN Cui-mei;TANG Ke-ren.
    2007, 2(02):  160-165. 
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    Genetics play important roles in the incidence of ischemic cerebrovascular disease. This article reviews the clinical manifestations, mutation feature, gene location and phenotype of different ischemic cerebrovascular disease caused by monogenic disorders, including coagulation disorders,erythrocytic disorders, inherited small vessel disease, metabolic disorders, connective tissue diseases, vasculopathies and disorders of unknown etiology.
    Investigation of Antioxidant and Atherogenesis
    WANG You-ming;WANG Yong-jun.
    2007, 2(02):  166-171. 
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    Atherosclerosis can cause cardiovascular and cerebrovascular diseases and do great harm tohuman health. Recent researches on the mechanisms of atherosclerosis show that oxidized lowdensity lipoprotein(ox-LDL) is one of the most important factors which cause the initiation anddevelopment of atherosclerosis. Researches on the new drugs that can inhibit the oxidation of lowdensity lipoprotein(LDL) will provide a new method to develop new drugs to protect the artery fromdeveloping atherosclerosis.