OBJECTIVE: The most potent vasoconstrictor, endothelin-1 and its receptors, endothelin receptor A (EDNRA) and endothelin receptor B (EDNRB) are involved in hypertension. Hypertension is a major risk factor of intracerebral hemorrhage (ICH). Recent studies have demonstrated increased plasma endothelin-1 level in ICH patients and relationships between EDNRA and EDNRB genetic variants and ischemic stroke. The aim of the current study was to investigate whether EDNRA and EDNRB polymorphisms are associated with ICH by interacting with blood pressure levels. METHODS: Five EDNRA and EDNRB polymorphisms were genotyped in this case-control study. RESULTS: We identified that EDNRA rs5333 T allele might be a protective factor of ICH (adjusted odds ratio [OR] [0.638, 95% CI: 0.417-0.977, P = 0.038), while EDNRB rs5351 A allele could be a risk factor of ICH (adjusted OR = 1.476, 95% CI: 1.042-2.089, P = 0.028). Moreover, we only found that the GG genotype of EDNRA rs5335 had higher diastolic blood pressure than the GC D CC genotypes in ICH patients (91.69 +/- 18.77 vs. 84.71 +/- 21.48, P = 0.004). CONCLUSIONS: These findings support the important role of EDNRA and EDNRB polymorphisms in ICH, and suggest that they do not interact with blood pressure levels on altering ICH risk.

Factor XII (F12) plays a complex role in the coagulation system. T allele of F12 C46T polymorphism was shown to lead to reduced F12 plasma levels in an allele-dose-dependent manner. This functional F12 C46T polymorphism was probably a risk factor for ischemic stroke. We tested whether this genetic variant is associated with the risk for cerebral hemorrhage (CH). We performed a case-control study including 195 patients with CH and 116 healthy population controls, which were all of southern Han-Chinese origin. The F12 C46T genotype was assessed using Touchdown PCR and Multiplex SNaPshot analysis. No statistically significant differences were found in the allele or genotype distributions of the F12 C46T polymorphism among CH patients and control subjects, even after adjusting for different confounding variables (P > 0.05). Our results demonstrated that the F12 C46T polymorphism has no major role in genetic susceptibility to cerebral hemorrhage. The highest T allele distribution in our population among different populations increased the reliability of this conclusion.

OBJECTIVE:To determine whether endothelin converting enzyme-1 (ECE1) gene polymorphisms contribute to susceptibility to intracerebral haemorrhage (ICH) by influencing blood pressure. METHODS:This case-control study enrolled patients with ICH and healthy control subjects from a Southern Han Chinese population. The ECE1 gene polymorphisms rs212528 and rs213045 were genotyped. The association between the genotypes and the risk of ICH was assessed. The effects of these two ECE1 gene polymorphisms on blood pressure were also analysed. RESULTS:A total of 389 patients with ICH and 404 healthy control subjects participated in the study. There was no significant association between the ECE1 rs212528 and rs213045 polymorphisms and ICH even after adjusting for different confounding variables. In patients with ICH, the systolic blood pressure of patients with the rs212528 AA genotype was significantly lower than that of patients with the AG/GG genotypes. CONCLUSIONS:These results indicated that the ECE1 rs212528 and rs213045 polymorphisms had no major role to play in the genetic susceptibility to ICH, although rs212528 might influence blood pressure in patients with ICH.

Protein Z (PZ) and factor (F) VII are two important factors in the clotting pathway which have similar structure, linked function and nearby gene sites. The aims of this study were to investigate whether the common variants of PZ and FVII genes are associated with the risk of cerebral hemorrhage (CH) and to explore the combined effects of PZ and FVII polymorphisms for CH risk. We performed genotyping analysis for two single-nucleotide polymorphisms (SNPs) of FVII (rs510317 and rs6046) and three SNPs of PZ (rs2273971, rs3024718 and rs3024731) both in a population-based case–control study and in a family-based association study. Case–control analysis found no evidence of significant association. But family-based association study revealed that the G allele of PZ rs2273971, and three haplotypes carrying the ‘G’ allele of PZ rs2273971: haplotype GA, CG and CGA of PZ and FVII genes, all had a significant effect on CH susceptibility (Z = 1.882, P = 0.049; Z = 1.922, P = 0.044; Z = 1.826, P = 0.047; Z = 1.977, P = 0.048, respectively). While, the A allele of PZ rs2273971, and four haplotypes carrying or crossing the ‘A’ allele of PZ rs2273971: haplotypes CA, ACAA, ACAT and ACAAT of PZ and FVII genes, may confer protection against CH (Z =−1.882, P = 0.049; Z =−2.000, P = 0.045; Z =−2.319, P = 0.020; Z =−2.002, P = 0.045; Z =−2.015, P = 0.043, respectively). This is a first family-based association study providing genetic evidences that PZ and FVII genes, especially PZ rs2273971 are involved in the development of CH in Han-Chinese families.

Platelet glycoprotein (GP) mediated the role of platelet in coagulation. Platelet GP Ia 807C/T is the only GP polymorphism associated with the expression levels of GP Ia/IIa (the platelet collagen receptor). Recently, the GP Ia 807C/T polymorphism has been reported to have no association with cerebral hemorrhage (CH) in two studies pertained to Caucasian populations. The purpose of this study is to evaluate the association between platelet GP Ia 807C/T polymorphism and CH in a Han Chinese population. We performed genotype analysis for platelet GP Ia 807C/T polymorphism in a case-control study involving 195 patients with CH and 116 age- and sex-matched controls. In contrast to previous reports, we found that the frequencies of GP Ia 807C/T T allele, CT and TT genotype were much higher in CH patients than in controls (33.9% vs. 22.8%, p = 0.004; 45.5% and 11.1% vs. 40.4% and 2.6%, p = 0.022). Logistic regression analysis revealed that the presence of GP Ia 807C/T C allele and CC genotype were both associated with a decreased risk of CH compared with T allele, CT and TT genotypes, respectively (adjusted odds ratio [OR] = 0.565, 95% CI: 0.384-0.887, p = 0.005; adjusted OR = 0.172, 95% CI: 0.043-0.639, p = 0.009; adjusted OR = 0.254, 95% CI: 0.085-0.961, p = 0.041, respectively). These findings indicated that platelet GP Ia 807C/T polymorphism could be a protective factor of CH in the Chinese population.

Objective: To explore the influence of nano-manganese dioxide on the rat spatial learning and memory function and its injury for rat ventral midbrain. Methods: Under cerebral stereotaxis, the physiological saline was injected into the brains of rats in the control group, while nano-manganese dioxide was injected into the brains of rats in the experimental groups. Morris water maze tests were performed one, two, three and four weeks after the injection, respectively. The ventral brain tissues of rats in each group were separated, and RT-PCR and Western blot were used to detect the expression changes of tyrosine hydroxylase, glial fibrillary acidic protein and inducible nitric oxide synthase in the tissues. Results: Intracerebral injection of nano-manganese dioxide made the rats swim slower in Morris water maze test. Two and three weeks after the injection, the time of finding the platform for rats and the latent period became significantly longer. The search platform strategy changed from tendency type and stochastic type to tendency type and edge type. The analysis results of RT-PCR and Western blot showed that the tyrosine hydroxylase expression level in the rat ventral brain tissues decreased and the expression levels of glial fibrillary acidic protein and inducible nitric oxide synthase increased obviously (P < 0.05). Conclusion: Intracerebral injection of nano-manganese dioxide can affect the rat spatial learning and memory function, cause the destruction of dopaminergic neuron in the rat midbrain, the decrease of tyrosine hydroxylase expression level and the increase of the expression levels of glial fibrillary acidic protein and inducible nitric oxide synthase, and have certain injury for ventral midbrain.

目的 研究部分汉族人群IGF-1 rs972936的单核苷酸多态性与阿尔茨海默病的相关性.方法 本研究于2009年4月～2011年12月期间,筛选170例湖南汉族AD患者与147例性别、年龄匹配的健康人群,其IGF-1rs972936位点的基因型、等位基因采用聚合酶链式反应-限制性内切酶片段长度多态性(PCR-RFLP)方法检测并分析.结果 IGF-1 rs972936 GG、AG和AA在两组间的分布频率:AD组48.82％、38.23％、12.94％,对照组20.41％、40.82％、38.78％;等位基因G、A分布频率为:AD组67.94％、32.06％,对照组40.82％、59.18％,以上各频率分布差异均有统计学意义(P＜0.05).结论 IGF-1 rs972936的GG基因型、G等位基因可能为湖南汉族人群AD发病的危险因素.

Remodeling of extracellular matrix (ECM) and breakdown of blood–brain barrier (BBB) are crucial events in the pathogenesis of intracerebral hemorrhage (ICH). Matrix metalloproteinases (MMPs), particularly MMP-9 and MMP-2, are the most important degrading enzymes in the ECM and BBB. These proteolytic effects are controlled predominantly by tissue inhibitors of metalloproteinases (TIMPs). TIMP-1 is the main endogenous inhibitor of MMP-9. Two polymorphisms in the TIMP-1 gene (rs4898 and rs2070584) were selected through a literature review and successfully genotyped in a study sample of 410 ICH patients and 305 controls. Differences in genotype and allele frequencies of identified polymorphisms were determined. Furthermore, the serum levels of TIMP-1 were measured in a subgroup of 96 ICH patients on days 1 after ICH onset and 76 controls. Analyses showed that C allele of rs2070584 was significantly associated with the development of ICH in male subjects (p = 0.037, OR = 1.535, 95%CI 1.025–2.300). Multiple logistic regression analysis under three genetic models demonstrated both rs4898 and rs2070584 were not risk factors for ICH in female subjects. Furthermore, serum levels of TIMP-1 were significantly higher in ICH patients than those in normal controls. However, the serum levels of TIMP-1 showed a nonsignificant decrease, depending on the alleles and genotypes of rs2070584 both in male and female cases. In conclusion, this is the first association study of the TIMP-1 gene variants with ICH. Our data suggest that C allele of rs2070584 is a risk factor for ICH development in the Chinese male population. However, the precise function of this variant needs further investigation.

The present study examined the effects of Gouqi (Lycium barbarum) on the learning and memory abilities of an APP/PS1 double transgenic mouse model of Alzheimer's disease. We employed a Morris water maze to examine the spatial memory in this mice line with or without Gouqi extracts treatment. We identified that 2 weeks of oral administration of Gouqi extracts at 10 mg/kg improved the performance of the APP/PS1 mice in the learning and the memory retrieval phases of the Morris maze. In correlation with this, the levels of Aβ(1-42) in hippocampal tissue were reduced by the Gouqi treatment. We conclude that pharmacological treatment with Gouqi extracts is beneficial at the later stages of Alzheimer's disease.

[目的]探讨DDAH2C-449G基因多态性与脑卒中及其危险因素的关系.[方法]本研究共纳入388例脑卒中患者和181例对照人群,其中动脉粥样硬化性脑梗死236例、脑出血152例,以DDAH2C-449G基因为遗传标记,采用聚合酶链式反应(PCR)和限制性片段长度多态性技术(RFLP)检测DDAH2基因多态性.[结果]动脉粥样硬化性脑梗死组GG基因型、G等位基因频率较对照组高,差别具有统计学意义(P＜0.05)；脑出血组三种基因型频率及G和C等位基因频率较对照组无显著性差异(P＞0.05).[结论]DDAH2基因C-449G多态性可能与动脉粥样硬化性脑梗死发病有关,G等位基因可能是动脉粥样硬化性脑梗死易感基因；DDAH2基因C-449G多态性可能与脑出血发病无关.

报道1例以中枢性睡眠呼吸暂停综合征为表现的Arnold-Chiari畸形合并脊髓空洞症的病例.

临床资料 患者男性,37岁,湖南湘阴县人,屠夫.因"腰痛4d,头痛、意识障碍2d伴发热"于2011年12月10日入院.患者于12月6日下午4点无诱因出现腰痛,行走困难,7日在当地医院行腰椎X线检查未见异常.8日腰痛剧烈并出现头痛,当时未测体温.9日患者病情加重,上午9点出现意识障碍,呼之不应,小便失禁,伴发热,体温达39℃,为求进一步诊治收入我科.发病以来,患者精神睡眠差,食欲下降.发病前3d患者曾宰杀病猪和死猪各1头.

The aim of this study was to evaluate the protective effects of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component extracted from Polygonum multiflorum, on learning/memory deficits in Alzheimer's disease (AD). We randomly divided 24 male Sprague-Dawley rats among 4 groups: (i) the sham-operated group (control); (ii) sham-operated group also treated with TSG (sham+TSG); (iii) beta amyloid treated group (Aβ); and (iv) Aβ treatment group also treated with TSG (Aβ+TSG). Rats in the Aβ and Aβ+TSG groups were treated with Aβ₁₋₄₂ intracerebroventricularly, whereas the control and sham+TSG groups were given phosphate-buffered saline. Rats in the sham+TSG and Aβ+TSG groups were then treated intragastrically with TSG (50 mg·(kg body mass)⁻¹·day⁻¹) for 4 weeks, and rats in the Aβ and control groups were treated with saline. The results from Morris water maze tests, electron microscopy, real-time polymerase chain reaction, and Western blotting demonstrated that Aβ₁₋₄₂ induced impairment in learning and memory, degeneration in synaptic structures, and downregulation of Src and NR2B at the gene and protein level, respectively. These alterations were reversed by the administration of TSG, suggesting that TSG exerts anti-AD properties by protecting synaptic structure and function. TSG-induced upregulation of Src and NR2B may be responsible for this process.

Fibrinogen plays an important role in the intrinsic and extrinsic pathways of blood coagulation. This study investigated the association between common variants in the fibrinogen gene and the risk of developing sporadic cerebral hemorrhage (CH). We performed genotyping analyses for three single nucleotide polymorphisms (SNP) in the fibrinogen gene in a case-controlled study involving 195 patients with CH and 116 control participants; both groups were of southern Han-Chinese origin. Logistic regression analysis indicated that haplotypes ATA (rs1800790+rs1800787+rs6050), AA (rs1800790+rs6050) and TA (rs1800787+rs6050) could nearly double the risk of sporadic CH (odds ratio [OR]=1.738, 95% confidence interval [CI]: 1.103–2.740, p=0.017; adjusted OR=1.762, 95% CI: 1.042–2.982, p=0.035), although the three SNP were not associated with sporadic CH when analyzed separately. These findings indicate that rs1800790, rs1800787 and rs6050 polymorphisms may contribute to the etiology of sporadic CH in the Chinese population.

Aim: Little is known about the potential role of genes in the pathogenesis of most intracerebral hemorrhagic stroke. Kininogens (KNG1) are the precursor of potent vasoactive kinin peptides and also function as cysteine proteinase inhibitors which are involved in hypertension and aneurysm. The purpose of this study is to investigate whether KNG1 gene polymorphisms are associated with intracerebral hemorrhage (ICH) in a Chinese Han population. Materials and methods: A hospital based case-control study was conducted and we investigated the rs1656922 and rs2304456 polymorphisms of KNG1 gene from 351 ICH patients and 312 unrelated ageand gender-matched controls by using the multiplex SNaPshot reaction. Results: The results showed that the T allele of rs1656922 was significantly over represented in the ICH patients. However, multiple logistic regression analysis both under recessive and dominant model were failed to confirm the two variants as risk factors for ICH. Furthermore, no gender or hematoma site specific associations were discovered between the two variants of KNG1 gene and ICH. However, the prevalence of the rs2304456 GG genotype (p=0.014) and the frequency of the G allele (p=0.012) were significantly increased among hypertensive patients when compared with normotensive patients. Conclusion: In conclusion, these findings represent an important negative result indicating that rs1656922C/T and rs2304456G/T polymorphisms of KNG1 gene are not associated with ICH while rs2304456 GG genotype may be a risk factor for hypertension in a Chinese Han population. Conflict of interest: There are no any actual or potential conflicts of interest including any financial, personal or other relationships with other people or organizations.

The aim of this study is to evaluate the protective effects of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) on learning and (or) memory deficit in aged rats, as well as to explore the possible connection between TSG and the β-amyloid precursor protein (APP) pathway. Sprague-Dawley rats were randomly divided into a young control group (age, 4 months), an aged control group (age, 22 months), and a TSG-treated group (age, 22 months). TSG at doses of 50 mg·kg(-1)·day(-1) was intragastrically administered to 22-month-old rats for 4 weeks. The learning and (or) memory ability was measured using the Morris water maze (MWM) test, and the mRNA and protein expression of APP pathway proteins was measured by real-time polymerase chain reaction (RT-PCR) and Western blot, respectively. The aged rats exhibited obvious learning and (or) memory deficit when compared with the young rats, but TSG treatment significantly improved the learning and (or) memory ability in the aged rats, as noted from the MWM test. RT-PCR and Western blot analysis showed an increase in the expression of beta-site APP cleaving enzyme 1 (BACE1) and A Disintegrin And Metalloproteinase 17 (ADAM17) in aged rats, and a decrease in ADAM10; however, TSG treatment significantly increased the mRNA and protein expression of ADAM10 (p < 0.01, compared with aged control rats). These results provide solid evidence for the therapeutic effect of TSG on age-related cognitive impairment, especially spatial learning and memory deficit. TSG might exert this effect through the APP pathway, although further studies on the topic are required.

[Objective]To explore the effect of apolipoprotein B (apoB) gene G12669A polymorphism on plasma lipid levels of Changsha Han Chinese with cerebral hemorrhage.[Methods]Peripheral blood specimens were collected from 93 cerebral hemorrhage patients and 100 normal control people.The levels of TG,TC,HDL and LDL were examined by oxidase method.The serum levels of LP (a),apoB-100 and apoAI were determined by immune methods.The G12669A polymorphism of apoB was analyzed by polymerase chain reactiun-restriction fragment Changsha Han Chinese with cerebral hemorrhage were significantly higher than those of control group,while the people with G/A genotype were significantly higher than those in the people with G/G genotype,while the level of and the control group were 0.097 and 0.045 respectively.A allele frequency of apeB G12669A in CH patients was significantly higher than that in the control group(P＜0.05).[Conclusion]Lipid levels of cerebral hemorrhage patients in Changsha Han Chinese are significantly higher than in control group(P＜0.05),which may be related with A allele of apoB G12669A polymorphism.

OBJECTIVE To explore the association between single nucleotide polymorphisms (SNPs) of KLK1 gene and cerebral hemorrhage in Changsha Han Chinese. METHODS Two hundred and seventy-three cerebral hemorrhage (CH) patients and 140 healthy controls were collected. The SNPs of rs5516 and rs5517 loci of KLK1 gene were analyzed by SNaPshot methods and direct sequencing. RESULTS (1)Genotype and allele frequencies in rs5516 locus had no difference between the CH patients and controls (P> 0.05). However, the A allele frequency of the rs5517 locus in CH patients was higher than that in the control group (0.419, 0.321 respectively, P< 0.05). (2)In the control group,the levels of diastolic blood pressure (DBP) of the GA and AA genotype carriers of the rs5517 locus were significantly higher than those of the GG genotype (P< 0.05), while the levels of blood pressure were not significantly different among different genotypes of the rs5516 polymorphism in both CH patients and the control group(P> 0.05). CONCLUSION Author's preliminary results suggested that the rs5517 polymorphism was associated with cerebral hemorrhage, while the rs5516 polymorphism was not in Changsha Han Chinese.

线粒体脑肌病伴高乳酸血症和卒中样发作(mitochondrial enceph-alomyopathy with lactic acidosis and stroke-like episodes, MELAS)是线粒体脑肌病的一种临床类型,临床比较少见,症状复杂多样,极易误诊为其他神经系统疾病.本研究收治了1例被反复误诊为"病毒性脑炎"的MELAS综合征患者,现报告如下.

Objective: To identify the relationships between elevated cTnT and stroke severity, location, and prognosis. Methods: Cardiac Troponin T (cTnT) concentrations and 12-lead electrocardiograms were obtained during the first day of admission in 247 patients with acute ischemic stroke but without overt ischemic heart disease. The cut-off value for elevated serum cTnT was set at 0.5ng/ml. Patients were divided into 2 groups: an elevated cTnT group and a normal cTnT group. Results: Serum cTnT was elevated in 10.5% of cases, with elevated cTnT associated with greater stroke severity, as assessed by the NIHSS score. Insular-lobe involvement and abnormalities of ECG were more common in patients with elevated cTnT than in the normal cTnT group. Short-term prognosis was more unfavorable in the elevated cTnT group than in the normal cTnT group. Conclusions: Elevated cTnT in acute ischemic stroke was associated with severe neurological deficits at stroke onset and damages to the insular lobe. The outcome of acute ischemic stroke was worse for patients with elevated cTnT than for those with normal cTnT.