脑出血患者血小板CD62p、CD42b表达及血浆血栓素B2、6-酮前列腺素-F1a和血管性假血友病因子水平的变化及其意义

目的 研究脑出血患者血小板CD62p、CD42b表达及血浆血栓素B2(TXB2)、6-酮前列腺素-F1a(6-keto-PGF1a)和血管性假血友病因子(vWF)水平的变化及其意义.方法 对46例高血压脑出血患者(脑出血组)发病后＜3 d、1周、2周及20例高血压患者(对照组),用流式细胞仪检测血小板CD62p、CD42b表达,酶联免疫吸附法检测血浆TXB2、6-keto-PGF1a和vWF的水平,并分析脑出血患者血小板CD62p、CD42b表达与血浆vWF水平的相关性.结果 在发病后＜3 d、1周及2周,脑出血组血小板CD62p表达和血浆TXB2、vWF水平及TXB2/6-keto-PGF1a(T/K)比值均明显高于对照组(均P＜0.01).血小板CD42b表达和血浆6-keto-PGF1a水平均明显低于对照组(均P＜0.01).脑出血患者血小板CD62p表达与血浆vWF水平呈正相关(r=0.56,P＜0.01),血小板CD42b表达与血浆vWF水平呈负相关(r=-0.60,P＜0.01).结论 脑出血患者出现血小板CD62p表达和血浆TXB2、vWF水平升高,血小板CD42b表达和血浆6-keto-PGF1a水平降低.提示脑出血后有明显血管内皮功能障碍及血小板活化.     

缺血性脑血管病患者趋化因子受体CX3CR1基因T280M多态性的研究

目的探讨缺血性脑血管病(ICVD)患者趋化因子受体CX3CR1基因T280M的多态性及其频率。方法采用聚合酶链反应和限制性片段长度多态性方法检测165例ICVD患者(脑梗死85例,腔隙性脑梗死40例,短暂性脑缺血发作40例)与150名健康对照者(正常对照组)CX3CR1基因T280M的多态性,比较两组及ICVD亚组的基因频率。结果正常对照组CX3CR1基因T280M只有TT和TM基因型,ICVD组有TT、TM和MM3种基因型,两组间基因型的差异有统计学意义(P<0.05);ICVD组M等位基因频率(8.7%)明显高于正常对照组(2.3%)(P<0.01);不同ICVD亚组之间基因型及M等位基因频率的差异无统计学意义(均P>0.05)。结论ICVD患者趋化因子受体CX3CR1基因T280M有MM基因型,并且M等位基因的频率明显增高,提示CX3CR1基因T280M多态性可能与ICVD有关。     

巴曲酶对血小板膜蛋白GPⅡb/Ⅲa受体的影响及应用研究

目的:1.明确巴曲酶有无血小板膜蛋白GPⅡb/Ⅲa受体拮抗作用。2.探讨巴曲酶与阿司匹林联合治疗急性缺血性脑梗死的协同作用。方法:采用随机、开放及疗程平行组进行临床研究。将102例急性缺血性脑梗死患者随机分成单用阿司匹林组(n=23)、单用DF-521组(n=35)及两者联合治疗组(n=44),观察治疗前后血小板聚集率、GPⅡb/Ⅲa受体表达、纤维蛋白原水平、TXB2、影像学变化、生活自理能力(HBI)及3个月时功能随访。结果:3种治疗方案均有抗血小板聚集作用,联合治疗组作用最明显(P<0.05)。单用阿司匹林及联合治疗组TXB2水平明显降低,单用巴曲酶及联合治疗组治疗后GPⅡb/Ⅲa、纤维蛋白原水平降低差异有统计学意义。3个月生活自理能力随访显示联合治疗组(70.45%)优于单用巴曲酶组(45.71%)优于单用阿司匹林组(17.399%)。结论:DF-521有GPⅡb/Ⅲa受体拮抗作用,与ASA合用后从不同的作用机制发挥抗栓作用。     

北方汉族人PLA2R1基因多态性与脑梗死关系的研究

目的探讨中国北方汉族人群PLA2R1基因多态性与脑梗死的关系。方法选取年龄、性别匹配的中国北方汉族脑梗死患者212人,健康对照组179人,采用PCR技术和限制性内切酶片段长度多态性(RFLP)的方法检测基因型。结果PLA2R1基因SNP的等位基因和基因型在脑梗死组和对照组的频数分布差异无显著性(P>0.05)。结论中国北方汉族人群中PLA2R1基因多态性与脑梗死的发病可能无关。     

花生四烯酸代谢、血小板激活因子、血小板膜蛋白与脑缺血

花生四烯酸(AA)代谢产物,如血栓素A_2(TXA_2)、前列环素(PGI_2)、白三烯(LTs)具有高度生物活性,是启动血小板活化的一个途径。PGI_2—TXA_2平衡失调与脑缺血发生有关;血小板激活因子(PAF)参与脑缺血病理过程,可能影响循环和代谢;已证实纤维蛋白原与血小板膜蛋白GPⅡb/Ⅲa复合物结合是血小板聚集必不可少的条件,并需要钙离子的存在。     

P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性与缺血性脑梗死血小板白细胞聚集体的相关性探讨

目的探讨血小板白细胞聚集体在缺血性脑梗死中的变化以及与P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性的关系。方法选取58例缺血性脑梗死患者作为病例组,20例正常人群作为对照组。病例组分为大动脉粥样硬化性脑梗死(LAA)19例,小动脉闭塞性脑梗死(SAO)39例。运用流式细胞技术检测所有受试者的血小板白细胞聚集体(PLA)、血小板单核细胞聚集体(PMA)、血小板淋巴细胞聚集体(PLy A)和血小板中性粒细胞聚集体(PNA)水平。并运用基因测序方法检测P-选择素基因S290N和P-选择素糖蛋白配体-1基因M62I多态性。结果 PMA%在病例组与对照组、LAA与对照组、SAO与对照组间差异有统计学意义(P=0.000,P=0.018,P=0.000)。PNA%在病例组与对照组、LAA与对照组间差异有统计学意义(P=0.045,P=0.002)。PNA%在LAA组SELP基因S290N位点SS和SN基因型间差异有统计学意义(P=0.008)。PLA%在LAA组PSGL-1基因M62I位点MM、MI和Ⅱ基因型间差异有统计学意义(P=0.046)。结论 PMA和PNA与缺血性脑梗死发病有关,SELP基因S290N位点SN基因型以及PSGL-1基因M62I位点MM基因型会增加LAA发生风险。     

氯吡格雷、阿司匹林药物相关基因多态性的临床分析

目的分析CYP2C19、GPⅢa、PTGS1、GP1BA基因多态性。方法收集2017年1月至11月在我院神经内科住院共159例患者基本信息,检测CYP2C19、GPⅢa、PTGS1、GP1BA基因。结果患者平均年龄(65. 32±12. 71)岁,其中男112例(70. 4%),女47例(29. 6%)。CYP2C19*2G681A基因中GG 58例(36. 5%),GA 82例(51. 6%),AA 19例(11. 9%); CYP2C19*3G636A分型:GG 141例(88. 7%),GA 18例(11. 3%); CYP2C19*17C806T分型:CC 155例(97. 5%),CT 4例(2. 5%); GPⅢa基因:TT 157例(98. 7%),TC2例(1. 3%); PTGS1基因:AA 159例(100%); GP1BA基因CC 136例(85. 5%),CT 23例(14. 5%)。除PTGS1外,余基因型的频率没有显著偏离Hardy-Weinberg平衡。表型:氯吡格雷超快代谢者2例(1. 3%),快代谢者47例(29. 6%),中间代谢82例(51. 6%),慢代谢者28例(17. 6%);阿司匹林抵抗型2例(1. 3%),敏感型157例(98. 7%)。结论基因型分型提示氯吡格雷慢代谢者发生率明显高于阿司匹林抵抗型。     

云南白族、汉族人群载脂蛋白E基因多态与缺血性脑血管病的相关性

目前已知,缺血性脑血管病(ICVD)的主要发病原因为动脉粥样硬化,而大量研究表明,ApoE基因型是动脉粥样硬化在个体间发病差异的主要因素.中国云南省白、汉两民族ICVD患者ApoE基因的研究国内外还未见报道,我们采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术和基因测序法同时检测ApoE基因多态,旨在探讨云南白、汉两民族人群中ApoE基因与ICVD的关系.     

紫外线照射充氧自血回输对重型颅脑损伤患者TXB_2及PGI_2作用的研究

观察紫外线照射充氧自血回输疗法 (UBIO)对重型颅脑损伤患者急性期血浆血栓素B2(thromboxaneB2 ,TXB2 )、6 -酮 -前列腺素F1α( 6 -keto prostaglandinF1α,6 -keto-PGF1α)及TXB2 / 6 -keto-PGF1α值 (T/K)的影响 ,探讨UBIO治疗重型颅脑损伤患者的机制。　　方法　将 6 5例重型颅脑损伤患者 (GCS≤ 8分 )随机分为两组 ,其中一组采用常规治疗 ,另一组在常规治疗基础上于伤后 1天、3天、5天、7天加用UBIO。动态检测两组患者伤后 7天内血浆TXB2 、6 -keto -PGF1α、T/K比值 ,并于伤后 1个月进行疗效评定。　　结果　伤后 1天、3天、7天 ,UBIO组TXB2 及T/K比值明显低于对照组 ,UBIO组的意识恢复时间明显短于对照组 ,GOS恢复良好率亦明显高于对照组。　　结论　UBIO能够改善颅脑损伤患者前列腺素代谢失衡状态及预后     

血小板膜糖蛋白I bα基因多态性与脑梗死关系的研究

目的:探讨血小板膜糖蛋白I bα基因HPA2多态性与脑梗死之间的关系。方法:选取按年龄、性别、有无高血压及糖尿病病史相匹配的病例组及对照组各100例,PCR扩增GPI bα基因长为588bp的片段,产物经限制性内切酶Hinl I消化后确定其基因型。结果:在总病例组、大动脉粥样硬化型脑梗死组及小动脉闭塞型脑梗死组(TOAST分型)与相应对照组之间GP I bαHPA2基因型频率的分布差异无显著性;大动脉粥样硬化型中杂合突变型比例(16.1%) 要高于小动脉闭塞型中杂合突变型比例(10.1%),但差异无显著意义。结论:GP I bαHPA2基因杂合突变型可能并非脑梗死的危险因素。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.