急性缺血性脑卒中患者CYP2C 19基因分型与临床预后的相关性分析

目的探讨急性缺血性脑卒中患者CYP2C 19基因分型与临床预后的相关性。方法选取本院收治的156例应用氯吡格雷治疗的急性缺血性脑卒中患者作为研究对象,对患者进行CYP2C19*2和CYP2C19*3基因型检测,根据检测结果分为野生型组(GG)和突变型组(GA/AA)。对比两组的血小板抑制率、氯吡格雷疗效及临床预后情况。结果野生型组患者的平均血小板抑制率为(42. 42±2. 74)%,突变型组为(32. 41±2. 69)%,突变型组的平均血小板抑制率显著低于野生型组(P <0. 05)。突变型组的氯吡格雷抵抗发生率为26. 32%,显著高于野生型组的1. 25%(P <0. 05)。突变型组的预后不良发生率显著高于野生型组,卒中复发率及心脑血管不良事件总发生率也显著高于野生型组(P <0. 05)。与野生型组相比,突变型组患者随访期间累积无再发心脑血管不良事件的生存率明显更低(P <0. 05)。结论急性缺血性脑卒中患者的CYP2C 19基因分型与血小板抑制率、临床预后密切相关,携带CYP2C19突变型基因型的患者,血小板抑制率更低,氯吡格雷敏感性越差,预后不良风险越高。     

多学科团队协作模式在MRI指导下脑卒中静脉溶栓诊疗中的应用

目的探讨多学科团队协助模式在脑卒中静脉溶栓诊疗中的应用,为急性脑梗死的诊疗提供参考。方法选取2017年1～12月行rt-PA静脉溶栓治疗的113例急性缺血性脑卒中患者为对照组,另选取流程改进后(2018年1～12月)行rt-PA静脉溶栓治疗的120例急性缺血性脑卒中患者为观察组,分析就诊至完善影像学检查时间、就诊至溶栓开始时间(DNT)时间、静脉溶栓治疗前后美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin量表(mRS)评分、Barthel指数变化、有无出血并发症等影响因素。结果观察组CT至完成头颅MRI时间、MR至静脉溶栓时间、DNT时间均较对照组缩短(P 0. 05);两组溶栓后24 h NIHSS评分改善差异无统计学意义(P 0. 05),观察组溶栓后7、30和90 d NIHSS评分、mRS评分、Barthel指数改善均优于对照组(P 0. 05);静脉溶栓过程中牙龈出血及症状性颅内出血两组比较差异无统计学意义(P 0. 05)。结论多学科团队协助模式可有效缩短急性缺血性脑卒中患者的就诊时间、检查时间及DNT时间,促进患者的神经功能恢复。     

CYP2C19基因多态性与急性脑梗死患者氯吡格雷疗效的相关性研究

目的探讨急性脑梗死患者CYP2C19基因多态性与氯吡格雷疗效的相关性。方法采用限制性片段长度多态性PCR法对171例急性脑梗死患者进行CYP2C19基因多态性检测。所有患者给予氯吡格雷治疗2周。分别于治疗前及治疗后第1 d、第5 d进行血小板聚集率检测,于治疗前及治疗后第1周、第2周进行NIHSS和日常生活活动能力评价(ADL)评分。计算血小板聚集抑制率并进行分析。结果本组171例患者中野生型纯合子(A组)79例,均为CYP2C19*1/*1;野生型基因与突变基因杂合子(B组)71例,包括55例CYP2C19*1/*2及16例CYP2C19*1/*3;突变基因纯合子或杂合子(C组)21例,包括11例CYP2C19*2/*2、9例CYP2C19*3/*3及1例CYP2C19*2/*3。治疗后第1 d及第5 d时,3组间血小板聚集抑制率的比较差异均有统计学意义(均P0.05)。与治疗前比较,3组治疗后第1周、第2周NIHSS评分均显著降低,ADL评分均显著升高(均P0.05)。与A组比较,B组及C组治疗后第1周、第2周NIHSS评分均明显升高,ADL评分均明显降低(均P0.05)。多因素Logistic回归分析显示,吸烟(OR=1.584,95%CI:1.079~2.136,P=0.004)及CYP2C19基因多态性(OR=1.837,95%CI:1.106~2.540,P=0.002)均与急性脑梗死患者血小板聚集抑制率独立相关。结论 CYP2C19基因多态性可影响急性脑梗死患者氯吡格雷治疗的疗效。     

华法林治疗椎基底动脉延长扩张症并缺血性脑卒中患者的临床疗效

目的观察华法林抗凝治疗在椎基底动脉延长扩张症并脑梗死或短暂性脑缺血发作患者二级预防中的疗效及安全性。方法36例确诊为椎基底动脉延长扩张症并发缺血性脑卒中患者随机分为华法林组与对照组,分别给予华法林、阿司匹林或氯吡格雷治疗,通过随访比较2组患者再发脑梗死、短暂性脑缺血发作和出血等不良事件的发生率。结果华法林组再发脑梗死或短暂性脑缺血发作的发生率低于对照组,且差异有统计学意义(P<0.05)。2组出血等不良事件发生率经统计学检验差异无统计学意义(P>0.05)。结论在椎基底动脉延长扩张症并发缺血性脑卒中患者的二级预防中,华法林抗凝治疗的疗效优于抗血小板聚集治疗,且出血等不良反应无明显差异。     

缺血性脑血管病患者 CYP2 C19 基因多态性的相关性研究

目的探讨缺血性脑血管病(ischemic cerebrovascular disease,ICVD)患者CYP2C19基因单核苷酸多态性(single nucleotide polymorphism,SNP)与临床特征、治疗效果之间的关系。为脑血管疾病患者服用抗血小板药物的个体化治疗提供参考依据。方法昆明医科大学第一附属医院神经外科2015年1月—2017年4月间完善CYP2C19(*2、*3、*17)基因检测的153例患者作为研究对象。将所有患者分别按每个基因位点基因检测的结果分为突变组及非突变组,分析CYP2C19基因各位点突变与患者临床特征、缺血性脑血管病发病及服药后发生缺血事件的关系。结果本组153例患者中,男70例(45. 8%),女83例(54. 2%),平均年龄(53. 2±11. 6)岁; CYP2C19(*2、*3、*17)各位点基因型突变的频率分别为53. 6%、9. 2%及2. 0%。CYP2C19*2位点突变与非突变组患者的吸烟、饮酒比率及血胆固醇(TC)、低密度脂蛋白胆固醇含量比较,差异均有统计学意义(P 0. 05-0. 01); CYP2C19*3位点突变与非突变组患者的血高密度脂蛋白胆固醇含量的差异有统计学意义(P 0. 005)。CYP2C19 3个位点突变与与非突变组患者发生ICVD的差异均无统计学意义(均P 0. 05)。CYP2C19*2位点突变患者服药后的缺血事件发生率比非突变患者明显增加(P 0. 05)。结论患者是否患有ICVD与CYP2C19(*2、*3、*17)基因位点多态性无明显关系;抗血小板治疗后是否发生缺血性事件与CYP2C19*2基因位点突变有关。因CYP2C19*2基因的突变率较高(本组患者达53. 6%),建议患者服抗血小板药前先行基因检测,以避免可能预后不佳。     

血清脂蛋白相关磷脂酶A2水平与急性缺血性脑卒中患者病情及预后的关系

目的探讨血清脂蛋白相关磷脂酶A2(Lp-PLA2)水平与急性缺血性脑卒中患者病情及预后的关系。方法收集120例急性缺血性脑卒中者和92例健康体检者的一般资料,采用酶联免疫吸附法检测血清LpPLA2水平,于患者入院时采用NIHSS量表评估病情严重程度,于患者出院后3个月采用mRS量表评估预后,分析血清Lp-PLA2水平与患者病情严重程度的相关性,并分析影响患者预后的危险因素。结果急性缺血性脑卒中组患者的高血压比例、血清Lp-PLA2水平明显高于对照组,差异均具有统计学意义(P 0. 05)。120例急性缺血性脑卒中患者中轻度47例、中度38例、重度35例,3组患者的血清Lp-PLA2水平相比差异有统计学意义(P 0. 05)。Pearson相关分析结果显示,血清Lp-PLA2水平与患者NIHSS评分呈正相关(P 0. 05)。120例急性缺血性脑卒中患者中预后良好81例、预后不良39例,预后不良组患者的年龄显著大于预后良好组(P 0. 05)、发病至入院时间显著长于预后良好组(P 0. 05),血清Lp-PLA2水平显著高于预后良好组(P 0. 05)。多因素Logistic回归分析结果显示,年龄、Lp-PLA2是急性缺血性脑卒中患者预后的危险因素(P 0. 05)。结论急性缺血性脑卒中患者血清Lp-PLA2水平越高,则患者的病情严重程度越重,Lp-PLA2是急性缺血性脑卒中患者预后的危险因素。     

急性缺血性脑卒中发病后不同时期降压控制的预后分析

目的探讨不同时期降压控制对急性缺血性脑卒中患者预后的影响。方法选取急性缺血性脑卒中患者90例,随机分为A组、B组、C组,分别于入院后第4、7、10天行降压治疗,行神经功能缺损评分(NIHSS),观察治疗后血压变化,记录缺血性事件发生率。结果 3组治疗后收缩压和舒张压均明显低于治疗前,差异具有统计学意义(P0.05);A组治疗2个月后NIHSS评分为(9.65±3.52)分明显高于B组(3.28±4.05)分、C组(2.57±1.54)分,差异具有统计学意义(P0.05),B、C组差异无统计学意义(P0.05)。A组缺血事件和复发率分别为13.33%、10.0%均高于B组(3.33%、3.33%)、C组(0、0),但差异无统计学意义(P0.05)。结论急性缺血性卒脑中患者入院后于第7天行降压治疗,可有效改善神经功能受损情况。     

急性脑梗死患者基因多态性对氯吡格雷疗效及终点事件的影响

目的探讨急性脑梗死患者基因多态性对氯吡格雷疗效及终点事件的影响。方法选取2016-06—2017-06新乡市第一人民医院神经内科收治的急性脑梗死患者418例。口服氯吡格雷5 d后抽取外周肘静脉血,血栓弹力图仪测定血小板抑制率。采用改良多重高温连接酶检测反应技术(iMLDR)对患者CYP2C19与ABCBl基因多态性进行分型。出院后进行24个月的随访,记录主要终点事件发生类别及时间。结果根据CYP2C19*2/*3快速代谢型、中间代谢型、慢代谢型的血小板抑制率之间,以及ABCBl C3435T不同基因型之间差异均有统计学意义(P0.01);而ABCBlT(-620)C不同基因型的血小板抑制率之间差异无统计学意义(P0.05)。校正可能的混杂因素后,进行多元线性回归分析显示,CYP2C19*2/*3、ABCBl C3435T是血小板抑制率的独立影响因素;同时还发现体重指数(BMI)26 kg/m~2也是血小板抑制率的独立影响因素。共382例患者完成随访研究,终点事件发生率为13.61%(52/382),其中缺血性脑卒中复发36例(9.42%),心肌梗死4例(1.05%),血管性死亡12例(3.14%)。根据是否携带CYP2C19*2/*3基因分为2组,生存分析Log-Rank检验显示差异有统计意义(P0.05);而ABCBlT(-620)C、ABCBl C3435T基因的显性与阴性患者生存曲线间差异无统计学意义(P0.05)。多因素Cox回归分析显示,CYP2C19*2/*3基因携带是临床终点时间的独立危险因素;同时年龄也是临床终点时间的独立危险因素。结论携带CYP2C19*2/*3、ABCBl C3435T等位基因的急性脑梗死患者氯吡格雷疗效降低,其中携带CYP2C19*2/*3等位基因的患者终点事件风险增高。     

rt-PA溶栓时机对急性缺血性脑卒中伴心房颤动患者的溶栓效果及安全性的影响

目的 探讨rt-PA溶栓时机对急性缺血性脑卒中伴心房颤动患者的溶栓效果及安全性的影响。方法 选取本院2015年4月-2017年8月收治急性缺血性脑卒中伴心房颤动患者共124例,其中发病后3～4.5 h行rt-PA溶栓共64例设为对照组,发病后3 h内行rt-PA溶栓共60例设为观察组; 比较2组患者溶栓有效率、治疗前后NIHSS评分、随访mRS评分及严重出血事件发生率。结果 观察组患者溶栓有效率显著高于对照组(P<0.05); 2组患者治疗后1和7d NIHSS评分均显著低于治疗前(P<0.05); 观察组患者治疗后1 d NIHSS评分显著低于对照组(P<0.05); 2组患者治疗后7d NIHSS评分比较差异无显著性(P>0.05); 2组患者随访mRS评分分级情况比较差异无显著性(P>0.05); 2组患者出血性脑梗死和脑部症状性出血发生率比较差异无显著性(P>0.05); 观察组患者治疗后脑实质出血发生率显著低于对照组(P<0.05)。结论 急性缺血性脑卒中伴心房颤动患者在发病后3 h内行rt-PA溶栓在可提高溶栓效果和促进受损神经功能恢复方面较发病后3～4.5 h溶栓具有明显优势,但在远期疗效和严重出血事件发生风险方面两者接近。     

尤瑞克林针治疗急性缺血性脑卒中的疗效观察

目的探讨尤瑞克林针治疗急性缺血性脑卒中的治疗效果。方法收集我院2015-02-2016-01收治的43例急性缺血性脑卒中患者为观察组,给予尤瑞克林针治疗,并选取同时期的42例常规治疗的急性缺血性脑卒中患者为对照组,治疗3周后观察2组NIHSS、MBI、FM-B评分变化,观察患者治疗后的出血情况。结果观察组治疗后NIHSS评分显著降低,MBI评分、FM-B评分显著上升,与对照组相比差异有统计学意义(P0.05),2组脑出血发生率差异无统计学意义(P0.05)。结论尤瑞克林针应用于急性缺血性脑卒中显著效果,可对脑神经元形成明显保护,改善患者神经功能缺损症状,值得临床应用推广。     

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.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

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.