奥扎格雷对进展性脑血栓形成患者血小板活化功能变化的影响

目的：探讨奥扎格雷对进展性脑血栓形成患者血小板活化功能变化的影响。方法：68例颈内动脉系统进展性脑血栓形成患者随机分为奥扎格雷治疗组和丹参治疗组。应用流式细胞仪和单克隆抗体动态测定CD62p、CD63，行血小板活化指标和临床疗效对照观察。结果：进展性脑血栓形成患者发病早期（24h内）CD62p、CD63值较对照组显著增高（P〈0．001）。患者经丹参治疗后，血小板表达CD62p、CD63缓慢下降，14d时其值仍高于健康对照组（P〈0．05）。经奥扎格雷治疗后血小板表达CD62p、CD63快速下降，至14d时已接近健康对照组（P〉0．05）。奥扎格雷组临床疗效明显优于丹参组。结论：进展性脑血栓形成患者中血小板表达CD62p、CD63明显增加，并与病情转归相关。奥扎格雷治疗后可使CD62p、CD63快速下降、提高临床疗效。     

奥扎格雷对急性脑梗死患者血小板CD62p和CD63表达的影响及其疗效

目的观察奥扎格雷对急性脑梗死(ACI)患者血小板CD62p、CD63表达的影响及其疗效。方法将64例ACI患者随机分为奥扎格雷治疗组和血塞通治疗组(对照组),采用流式细胞术检测ACI患者治疗前后及正常人(正常组)血小板CD62p、CD63的表达;观察奥扎格雷治疗组和对照组的临床疗效并进行比较。结果ACI患者血小板CD62p、CD63表达水平明显高于正常组(均P<0.01);奥扎格雷治疗组与对照组治疗后血小板CD62p、CD63表达水平较治疗前均有明显下降(P<0.05～0.01),奥扎格雷治疗组又明显低于对照组,差异有显著性(均P<0.05)。奥扎格雷治疗组的基本痊愈率、显著进步率、总有效率明显高于对照组(均P<0.05)。结论ACI发病后血小板CD62p、CD63表达水平显著增高;奥扎格雷有明显抑制血小板表达CD62p、CD63的作用,对ACI的治疗效果显著。     

氯吡格雷联合奥扎格雷钠治疗急性缺血性卒中疗效评价

研究背景抗血小板治疗已经成为缺血性卒中的常规治疗方法,目前对其作用的肯定主要源于临床应用,迄今尚无一项能够准确评价其有效性的实验室指标。有研究证实,血小板活化程度与动脉粥样硬化和缺血性卒中相关,尤其是血小板α颗粒膜糖蛋白CD62p和溶酶体膜糖蛋白CD63均为血小板活化的重要指标。本研究旨在通过观察急性缺血性卒中患者血小板膜表面CD62p和CD63表达变化,探讨以血小板活化程度反映氯吡格雷(75 mg)、奥扎格雷钠(80 mg)与阿司匹林(0.15 g)的疗效差异。方法采用流式细胞术检测急性缺血性卒中患者氯吡格雷(75 mg)联合奥扎格雷钠(80 mg,联合治疗组)及阿司匹林单药(阿司匹林组)治疗前后血小板CD62p和CD63阳性表达率,美国国立卫生研究院卒中量表(NIHSS)评价神经功能改善程度。结果与正常对照组相比,治疗前急性缺血性卒中组患者血小板CD62p和CD63阳性表达率升高(P=0.001,0.032);治疗后CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000)。与治疗前相比,治疗后联合治疗组和阿司匹林组患者血小板CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000),但组间差异无统计学意义(均P>0.05)。CD62p和CD63阳性表达率在不同观察时间点与治疗分组之间不存在交互作用(F=1.403,P=0.250;F=2.830,P=0.063),但NIHSS评分在不同观察时间点与治疗分组之间存在交互作用(F=4.518,P=0.013)。结论抗血小板药物治疗急性缺血性卒中有效,但氯吡格雷与奥扎格雷钠联合治疗之疗效与阿司匹林单药治疗并无差异。缺血性卒中急性期测定血小板CD62p阳性表达率可以用于评价抗血小板药物的疗效,但CD63表达的临床价值尚待进一步研究。     

氯吡格雷联合奥扎格雷钠对急性缺血性卒中患者血小板CD62p、CD63的影响

目的评价氯吡格雷联合奥扎格雷钠治疗急性缺血性卒中的疗效。方法选取我院神经内科于2012-08—2013-08收治的120例急性缺血性卒中患者为研究对象,随机分为观察组与对照组。观察组60例给予氯吡格雷联合奥扎格雷钠治疗,对照组60例给予阿司匹林治疗。治疗结束后对比2组患者血小板CD62p、CD63表达情况、NIHSS评分及疗效。结果2组患者治疗前后的CD62p、CD63表达阳性率及NIHSS评分均无显著差异(P0.05)。观察组治疗总有效率95.00%,对照组96.67%,2组比较差异无统计学意义(P0.05)。结论抗血小板药物治疗急性缺血性卒中疗效肯定,且与阿司匹林疗效无差异,CD62p、CD63蛋白可以有效反映血小板活化情况。     

奥扎格雷钠治疗急性脑梗死65例疗效观察

目的 观察奥扎格雷钠治疗急性脑梗死的效果.方法 将127例初发急性脑梗死患者随机分为治疗组65例,对照组62例.治疗组应用奥扎格雷钠,对照组应用复方丹参注射液,观察比较2组患者神经功能缺损评分,临床疗效及用药期间不良反应.结果 奥扎格雷钠组治疗总有效率87.7%,对照组总有效率74%,与对照组比较差异有统计学意义(P<0.05).结论 奥扎格雷钠治疗急性脑梗死具有良好疗效.     

氯吡格雷与阿司匹林联合应用在急性脑梗死治疗中的疗效评定

目的观察急性脑梗死患者血小板上α颗粒膜糖蛋白(CD62p)及溶酶体颗粒膜糖蛋白(CD63)的表达,通过血小板活化的变化,探讨阿司匹林与氯吡格雷联合用药与阿司匹林单药治疗的疗效差异。方法将60例脑梗死患者随机分为两个亚组:单药组(阿司匹林0.15 g/d)和联合用药组(阿司匹林0.10 g/d+氯吡格雷75 mg/d),30例健康体检者为对照组。使用流式细胞术检测所有病例CD62p、CD63阳性率,对单药组和联合用药组治疗前后的CD62p、CD63阳性率进行比较,同时进行NIHSS评分。结果脑梗死组血小板CD62p、CD63阳性率显著高于对照组(P<0.01)。单药组和联合用药组在治疗一周和二周后CD62p、CD63阳性率和NIHSS评分均较治疗前显著下降(P<0.01)。联合用药组治疗二周后与单药组比较CD62p、CD63阳性率和NIHSS评分明显降低,差异有统计学意义(P<0.01)。结论抗血小板治疗对脑梗死有效,阿司匹林+氯吡格雷联合治疗的总体疗效明显优于单用阿司匹林,CD62p、CD63可以衡量抗血小板治疗效果。     

奥扎格雷钠联合疏血通治疗急性脑梗死临床观察

目的 了解奥扎格雷钠联合疏血通治疗急性脑梗死的临床疗效.方法 选择急性脑梗死患者240例,随机分为治疗组120例,对照组120例.治疗组给予奥扎格雷钠注射液联合疏血通注射液静滴,1次/d;对照组给予奥扎格雷钠联合丹参静滴,1次/d,治疗2周后进行疗效评定,检测血液流变学及凝血常规.结果 治疗组治疗后血小板聚集率降低、纤维蛋白原含量较治疗前降低,差异有统计学意义（P＜0.05）.治疗组显效率67.5%,对照组为38.3%;治疗组有效率94.2%,对照组为75.0%,2组比较差异有统计学意义（P＜0.01）.结论 奥扎格雷钠联合疏血通治疗急性脑梗死的疗效肯定,值得临床推广.     

奥扎格雷钠和依达拉奉联合治疗急性脑梗死疗效观察

目的探讨奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效。方法将80例急性进展型脑梗死患者随机分为治疗组(40例)和对照组(40例)。对照组应用低分子右旋糖酐、复方丹参液、胞二磷胆碱治疗。治疗组在对照组基础上加用奥扎格雷钠和依达拉奉治疗。2组于治疗前及治疗后3个月时进行神经功能缺损评分、疗效评定和生活能力评定。结果治疗组神经功能缺损评分下降明显优于对照组,总有效率明显高于对照组。治疗组生活能力评定显著优于对照组。结论奥扎格雷钠联合依达拉奉治疗急性脑梗死疗效好,无明显不良反应。     

血小板活化指标与短暂性脑缺血发作的转归

目的探讨短暂性脑缺血发作(TIA)患者疾病转归与血小板活化指标α颗粒膜糖蛋白(CD62p)、溶酶体颗粒膜糖蛋白(CD63)、血小板膜表面糖蛋白(CD41)的关系.方法57例TIA患者随访2个月,分别在服药后1 d、1周、1个月和2个月时采用流式细胞仪检测血小板CD62p、CD63和CD41表达的百分率,同时监测病情发展趋向.结果TIA缓解组、TIA反复发作组与TIA进展为脑梗死组的血小板CD62p、CD63、CD41阳性百分率逐级升高(P＜0.05～＜0.001),尤其以进展为脑梗死组指标升高最为明显(P＜0.01～0.001).结论血小板活化CD62p,CD63及CD41可作为TIA发展演变的估测指标.     

巴曲酶联合奥扎格雷治疗进展性脑梗死疗效观察

目的研究巴曲酶联合奥扎格雷治疗进展性脑梗死的临床疗效及安全性。方法发病72h之内的进展性脑梗死患者96例,随机分为联合组(治疗组)和奥扎格雷组(对照组);对照组采用奥扎格雷80 mg静滴,2次/d,共14 d。治疗组采用巴曲酶10、5、5BU静滴,隔日1次,共3 d。其余时间应用奥扎格雷80 mg静滴,2次/d,共11 d。分别在治疗前及治疗后2周,对2组患者的血小板、凝血四项及临床神经功能缺损评分进行研究。结果治疗组临床总有效率95.8%,明显优于对照组(81.2%);2组均无明显不良反应。结论巴曲酶联合奥扎格雷治疗进展性脑梗死安全有效,值得临床组推广应用。     

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.