BACKGROUND: The incidence of cognition disturbance after cerebral infarction is about 20% -30% and effective drugs for its prevention and treatment are anticipated.OBJECTIVE: To investigate the effect of nicergoline on cognition disturbance after cerebral infarction and explore its mechanism.DESIGN: Randomized controlled trial based on patients.SETTING: Neurological department in a medical university.PARTICIPANTS: A total of 60 patients admitted to the Neurological Department of the Second Hospital Affiliated to Chongqing Medical University for cerebral infarction during October 1999 and April 2001 were recruited in this study, and randomly divided into two groups, nicergoline treatment group and control group with 30 in each.METHODS: Mini-mental state examination(MMSE) score was evaluated and cerebral blood flow was determined with transcranial Doppler' s ultrasonography within one week after admission and three months after admission, respectively, and data were analyzed with SPSS software.MAIN OUTCOME MEASURES: MMSE score and velocity of blood flow in treatment and control groups.RESULTS: MMSE score in memory, calculation and recollection decreased significantly[ (1.2 ± 1.3), (2. 2 ± 2. 1) and(1.0 ± 1.7), respectively] in control group but did not change much[ (3.9 ± 1.4), (4. 4 ± 1.9) and(4.0 ± 1.6) ]in treatment group. The velocity of blood flow in control group decreased apparently, while it increased in treatment group[(58.31 ±10. 15) and(65.79 ±9.74) cm/s in the right middle cerebral artery].CONCLUSION: Nicergoline can prevent and treat vascular cognition disturbance, and improvement of blood supply may be one of the mechanisms.

BACKGROUND: Changes of physiological structure, changes of phenotype and first basic excision are all the changes of gene expression. The technique of DNA microarray is a new method to filtrate target genes fleetly and largely by using the theory of base-partnershin, which can holistically and magnificently study the expression and function of organics genes. OBJECTIVE: To study early differential expression genes of rats with cerebral hemorrhage with DNA microarray and establish academic foundation for exploring mechanism of cerebral hemorrhage.DESIGN: Randomized controlled research.SETTING: Department of Neurology, Affiliated Hospital of North Sichuan Medical College. MATERIALS: The experiment was conducted at the Affiliated Hospital of North Sichuan Medical College from October 2002 to December 2003. Twenty Wistar rats, of either gender, with body mass of 220-260 g, without special pathogen, provided by Experimental Animal Center of Chongqing University of Medical Sciences, were selected and randomly divided into control group and cerebral hemorrhage group, with 10 in each group. METHODS: Animal models with cute cerebral hemorrhage of rats were established with type Ⅶ collagenase tridimensional localization method,and 4 hours later tissues around hematom and normal cerebral tissue at the same part were detected with gene chip. Fluorescent signal was scanned with scanning apparatus and analyzed with computer. Result of genic expressive pattern was researched with reverse transcriptase-polymerase chain reaction (RT-PCR). MAIN OUTCOME MEASURES: Result of gene chip in cerebral tissue of rats and result of RT-PCR.RESULTS: Four hours after acute cerebral hemorrhage, 129 differential expression genes were screened out, in which there were 114 up-regnlation genes and 15 down-regulation genes. Those genes were mostly related to the following aspects: stress, immunological response, apoptosis, energy metabolism and signal transmitting. Genes related with inflammatory impairment were mostly obvious. The result of RT-PCR suggested that the level of genic expression was as the same as the result of Cdna chip, which indicated that genic expressive pattern based on gene chip had great reliability.CONCLUSION: Early cerebral hemorrhage has many differential expression genes, which can play an important role in hemorrhagic brain damage.

There are a number of serum biomarkers related with the process of the pathogenesis,destabilization and rupture of the atherosclerotic plaque.And thus,it is fairly important in clinical practice to identify vulnerable plaque and predict plaque rupture by detecting the expression of the serum biomarkers.This review aims at giving an overview on recent emerging biomarkers that are related to vulnerable plaque.

Subarachnoid hemorrhage (SAH) is a disease with high disability and mortality rate.It is still lack of effective treatment means in clinical practice.Studies in recent years have found that early brain injury may be the primary causes that result in higher mortality and poor prognosis in patients with SAH.This article mainly reviews the animal models and pathogenesis of early brain injury after SAH.

BACKGROUND:Heparinase can induce syndecan-1 shedding from tumor cells and macrophage motion may correlate with biosynthesis regulation of heparan sulfate proteoglycan.OBJECTIVE:To investigate the effects of heparinase Ⅰ on syndecan-1 and extracelluar signal regulated kinase 2(ERK2)in human umbilical vein endothelial cells(HUVECS)with hypoxia/reoxygenation injury.METHODS:heparinase Ⅰ-precultured HUVECS were treated with hypoxia/reoxygenation.Immunohistochemistry staining,RT-PCR and western blot were applied to detect HUVECS syndecan-1 and ERK2 expression.RESULTS AND CONCLUSION:Expression of syndecan-1 and ERK2 was increased in HUVECS following hypoxia/reoxygenation treatment.Heparinase Ⅰ significantly upregulated the expression of syndecan-1 and ERK2 in HUVECS with hypoxia/reoxygenatiOn treatment.Syndecan-1 and ERK2 expression was positively related.Results show that syndecan-1 and ERK2 participate the pathophysiology of HUVECs hypoxia/reoxygenation injury Heparinase Ⅰ influences ERK2 expression by regulating syndecan-1.

Objective To explore the mechanism of early-onset sub-clinical seizures following acute cerebral infarction. Methods Right middle cerebral artery occlusion (MCAO) rats models were made by threads methods. Sub-clinical seizures were detected with recording apparatus at the same time. Glial glutamate transporter-1 (GLT-1) were detected by immunohistochemical method in rats hippocampus. Results Sub-clinical seizures occurred in 27.4% rats following MCAO. The GLT-1 expressions in CA_1 and CA_3 regions were lower in sub-clinical seizure group[(344.5?35.0)?m~2 and (360.4?13.5)?m~2 respectively] than those in the controls[(447.0?22.8)?m~2 in CA_1 region and (402.3?28.5)?m~2 in CA_3 region]. But there were not significant differences of GLT-1 immunoreactivities in dentate gyrus between the two groups above. Conclusion Early-onset sub-clinical seizures occur following the acute MCAO in rats, which should be related to the decreased expression of GLT-1 in CA_1 and CA_3 of hippocampus.

AIM: To investigate the effect of hirudo and earthworm liquor extract on the expression of syndecan-1 in focal cerebral ischemia reperfusion rats and the relationship between syndecan-1 expression and cellists underlying antiinflammatory mechanism. METHODS: The MCAO models of rats were built with the intraluminal filament occlusion. Rats' brains were cut at the levels of the hippocampus as the templates. Immunohistochemistry staining and HE staining were used to facilitate the observation of the distribution and the quantities of cells with expression of syndecan-1 and the pathological change of MCAO ischemia 2 h reperfusion 4, 24, 72 h and 7 d with hirudo and earthworm liquor extract or saline treatment, respectively. RESULTS: Hirudo and earthworm liquor extract could upregulate the expression of syndecan-1 on ischemia/ reperfusion in rats' brains, especially at 72 h. The numbers of syndecan-1 cells got peak, hirudo and earthworm extract liquor could downregulate polynucleation inflammatory cells at 24 and 72 h. The expression of inflammatory cells in both hirudo and earthworm liquor extract group and saline group at 4 h was not significant. Hirudo and earthworm extract liquor downregulated the monocytic inflammation cells infiltration at 7 d. CONCLUSION: Hirudo and earthworm liquor extract can upregulate the expression of syndecan-1 on ischemia reperfusion in rats' brains. The upregulation of syndecan-1 can decrease inflammatory cell infiltrate.

Objective To evaluate the effect of late course accelerated hyperfractionation radiotherapy(LCAHR) for esophageal carcinoma. Methods Six clinical trials on LCAHR for esophageal carcinoma were reviewed by means of Meta analysis . Results The 1 and 3 year survival rates in the LCAHR group derived from the fixed effect model were 2.39 (1.58～3.62) and 3.05(1.96～4.74) times higher than the conventional fractionation group. With the random effect model,the 1 and 3 year survival rates in the LCAHR group were 2.43(1.54～3.82) and 2.99(2.08～4.30) times higher than the conventional fractionation group.Conclusion For esophageal carcinoma,the better outcome of LCAHR makes it advisable in extensive clinical practice.

Objective To explore the expression of syndecan-1 in different intervals following focal cerebral ischemia/reperfusion in rat and the relationship between syndecan-1 and inflammatory cells in the rat brain.Methods The rat model of middle cerebral artery occlusion(MACO) was performed by using the intraluminal filament occlusion for 2 h,then released.The rat brain were cut in the coronal planes at the levels of the hippocampus as the templates.The immunohistochemical staining and HE staining were used to observe the distribution and the quantity of syndecan-1 and inflammatory cell expression in the normal control group,sham operation group and the MCAO groups at 4,24,72 h and 7 d after reperfusion.Results The expression of syndecan-1 was mainly in the cortex and the subcortex in the rats of normal control group and sham operation group.The immunoreactivity of syndecan-1 in the infarcted core and perilesional infarcted zone started decreasing at 4 h after ischemia/reperfusion,reached the lowest at 24 h.The expression of syndecan-1 in the perilesional infarcted zone was up-regulated at 72 h and recovered at 7 d.The relationship between syndecan-1 and inflammatory cells was of negative correlation.Conclusion The decreasing of syndecan-1 may contribute to inflammatory response in the cerebral infarction region after focal cerebral ischemia/reperfusion.

Objective To study the effects of hirudo extract liquor(HEL) on the expressions of HSP70 and TGF?-1 in intracerebral perihematoma tissues of rats.Methods We established the experimental ICH models in Wistar rats by stereotaxical injecting quantitative collagenase(0.7 U collagenaseⅦ) into their left caudate nuclei.The rats continued to be treated with HEL(treatment group) or normal saline(control group) through intravenous injection by vena caudalis and the scores of neurologic impairment in two groups were evaluated every day.The slices of these samples at 3rd,6th and 10th day were stained by immunohistochemistry and the positive cells of HSP70 and TGF?-1 were counted by image analysis system,respectively.Results The scores of neurologic impairment in two groups were remarkably reduced with time going((P