住院精神分裂症患者伴发代谢综合征的临床分析

目的调查住院精神分裂症患者代谢综合征的发生率,分析与代谢综合征有关的危险因素。方法将符合CCMD-3诊断标准的住院精神分裂症患者为研究对象,以2004年中华医学会糖尿病分会代谢综合征为标准,了解精神分裂症患者伴发代谢综合征的发生率,并用Logistic回归分析其相关因素。结果符合入组条件者共726例,精神分裂症患者伴发代谢综合征患病率为32.3%。代谢综合征患病相关的危险因素为年龄、氯氮平及精神分裂症的病程（P〈0.05）。Logistis回归分析结果显示,精神分裂症患者伴发代谢综合征的危险因素是高龄,病程。结论与普通人群相比,精神分裂症患者具有较高伴发代谢综合征患病风险,可能的危险因素为高龄,病程长和服用氯氮平等。     

精神药物的不良反应（三） 长期住院精神分裂症患者伴发代谢综合征情况

目的：了解长期住院精神分裂症患者伴发代谢综合征（MS）的情况。方法：抽样调查住院至少2年以上的长期住院精神分裂症患者,测定患者身高、腰围、体质量及代谢指标,依据世界糖尿病联盟（IDF）规定的诊断标准甄别出MS患者;同时调查与之相关的抗精神病药使用情况。结果：MS发生率为43.4%,女性52.0%高于男性34.9%（χ2=7.420,P〈0.01）;Logistic回归分析发现MS与性别、体质量指数有关;抗精神病药种类与MS发生无显著相关。结论：长期住院接受抗精神病药治疗的精神分裂症患者伴发MS较高。     

慢性精神分裂症患者血糖、血脂及甲状腺激素水平分析

目的调查长期服用氯氮平治疗的慢性精神分裂症患者糖、脂代谢异常的发生率及与血清甲状腺素水平的关系。方法对100例住院的慢性精神分裂症患者采用全自动生化分析仪检测血糖(FPG)、胆固醇(TC)和甘油脂(TG),采用放免法测定甲状腺相关激素水平;比较血糖、血脂异常者和正常者的甲状腺相关激素水平,并进行相关分析。结果100例慢性精神分裂症患者中,血糖异常者26%;血甘油三脂异常者37%;血糖、甘油三脂均异常者占20%;无胆固醇异常者。所有患者血清甲状腺素水平均在正常范围以内。血糖异常组血清FT3水平显著低于血糖正常组(P<0.01);甘油三脂异常组血清FT3水平显著低于甘油三脂正常组(P<0.01);血糖与血清FT3和T3水平均呈显著负相关;甘油三脂与FT3水平呈显著负相关。结论长期服用氯氮平治疗的慢性精神分裂症患者血糖、血脂代谢异常的发生率高,而且可能与甲状腺功能状态有关联。     

精神分裂症患者伴发糖尿病的相关因素分析

目的 为了解住院精神分裂症患者伴发糖尿病的相关因素。方法 回顾性调查住院精神分裂症患者发生糖尿病与精神药物、体重、血糖及血脂等的相关性。结果 在1472例精神分裂症患者中伴发糖尿病者共162例(11．0％)，其发生与患者的年龄、病程、体重、甘油三酯、胆固醇及服用抗精神病药有相关性，而与性别无关。结论 患者年龄越大、病程越长糖尿病的发生率越高，长期使用抗精神病药可能会导致糖尿病，尤以氯氮平为甚。     

氯氮平治疗精神分裂症引发代谢综合征危险因素研究

目的 探讨氯氮平治疗的精神分裂症患者发生代谢综合征（metabolic syndrome,MS）的危险因素.方法 入组单一使用氯氮平治疗的精神分裂症患者108例,收集患者的年龄、性别、吸烟情况、代谢疾病家族史、服药时间、服药剂量、体质量指数（BMI）、腰围、血压、阳性和阴性综合征量表（PANSS）评分、空腹血糖、甘油三酯（TG）、胆固醇（TC）、高密度脂蛋白、低密度脂蛋白.以是否发生MS分为两组,分析组间代谢相关因素的差异,并进行Logostic回归分析.结果 MS组的腰围、TG、空腹血糖、收缩压、舒张压高于非MS组（P＜0.05）;MS组的年龄、吸烟史、TC、服用氯氮平时间、BMI高于非MS组（P＜0.05）.而MS组的PANSS量表总分低于非MS组（P＜0.05）;经Logistic回归分析筛选,年龄（P=0.008）、腰围（P =0.002）及PANSS总分（P=0.011）进入回归方程.结论 氯氮平治疗发生MS的精神分裂症患者,具有更高的年龄、吸烟比率、腰围、服药时间、BMI、空腹血糖、血压、甘油三酯及胆固醇水平,但精神症状评分较低.发生MS的独立危险因素为：高龄、腰围增加、精神症状评分较轻.     

长期住院精神分裂症患者伴发代谢综合征的调查

目的 研究长期住院精神分裂症患者的代谢综合征患病情况.方法 以长期住院的精神分裂症患者为研究对象,进行一般资料问卷调查和实验室检查,包括血糖和脂代谢相关指标.结果 资料完整的421例长期住院精神分裂症患者,伴发代谢综合征者131例,占31％,女性高于男性,精神分裂症合并代谢综合征患者生活质量明显下降.结论 长期住院的精神分裂症患者易合并代谢综合征,应重视相关代谢高危因素并及早进行干预.     

慢性精神分裂症伴代谢综合征的认知功能研究

目的 探讨慢性精神分裂症伴发代谢综合征患者的认知功能缺损特征.方法 选择符合中国精神障碍分类与诊断标准第3版(CCMD-3)诊断标准的慢性精神分裂症住院患者205例,其中伴代谢综合征者(MS组)92例,无代谢综合征者(非MS组)113例.收集临床资料,采用阳性和阴性症状量表(PANSS)及治疗中出现的症状量表(TESS)评定临床症状和不良反应;重复性成套神经心理状态测验(RBANS)评定认知功能.结果 MS组与非MS组的PANSS及TESS评分均无显著性差异(P均＞0.05).MS组的RBANS总分、即刻记忆因子分及延时记忆因子分均显著低于非MS组(P＜0.05);两组在注意、视觉广度及言语功能因子分上无显著性差异(P均＞0.05).结论 代谢综合征会加重慢性精神分裂症患者的认知功能缺损,在即刻记忆和延时记忆方面损害更明显.     

精神分裂症患者伴发代谢综合征的调查

目的:研究住院精神分裂症伴发代谢综合征者的患病率及生活质量,并分析其可能的影响因素.方法:对500例住院精神分裂症患者进行问卷调查和实验室检查. 结果:500例精神分裂症患者中代谢综合征者的患病率为37％,与代谢综合征患病风险相关的危险因素中包括年龄、病程(P＜0.05).精神分裂症伴发代谢综合征患者在生活质量方面,心...     

中国汉族人泛醌NADH脱氢酶Fe-S蛋白1基因多态性与氯氮平所致代谢综合征的关联研究

目的:探索中国汉族精神分裂症患者人泛醌NADH脱氢酶Fe-S蛋白1(NDUFS1)基因多态性与长期服用氯氮平所致代谢综合征(MS)的关系。方法:收集388例长期服用氯氮平2年的慢性精神分裂症患者临床资料及代谢指标;分为MS组(159例)和非MS组(299例);对NDUFS1基因rs13024804、rs1044120、rs6435330、rs4147713这4个位点进行多态性检测,并进行组间及性别间分析。结果:NDUFS1基因4个位点各等位基因及基因型分布两组间差异无统计学意义;性别分层后发现,两组女性患者中携带rs1044120 T等位基因(GT+TT vs GG,P=0.002,OR=0.25,95%CI:0.10～0.61)、rs6435330 T等位基因(GT+TT vs GG,P 0.001,OR=0.21,95%CI:0.09～0.50)及rs4147713 G等位基因(TG+GG vs TT P=0.002,OR=0.26,95%CI:0.11～0.61)者患MS的危险性下降。男性患者中rs1044120位点T等位基因携带者血浆高密度脂蛋白水平显著高于非携带者[(1.33±1.26) mmol/L vs(1.09±0.48) mmol/L,P=0.034];女性患者中rs6435330位点T等位基因携带者舒张压显著低于非携带者[(71.43±7.134) mmHg vs (74.47±6.419) mmHg,P=0.032]。结论:在中国汉族精神分裂症患者中,NDUFS1基因多态性与氯氮平相关的MS无关联,女性患者中NDUFS1基因多态性与氯氮平相关的MS存在关联。     

较低剂量氯氮平合并阿立哌唑对精神分裂症患者体质量及糖脂代谢的影响

目的:探讨较低剂量氯氮平合并阿立哌唑对精神分裂症患者体质量及糖脂代谢的影响.方法:选取2008年3月至2010年3月我院住院精神分裂症患者92例,随机分为研究组和对照组,研究组给予较低剂量氯氮平合并阿立哌唑治疗,对照组给予单纯氯氮平治疗.两组观察疗程24周.两组患者分别在治疗前、治疗12周及24周对其体质量、身高、血糖、餐后2h血糖、三酰甘油及胆固醇进行测定,并做统计分析. 结果:与对照组相比,研究组治疗前后体质量及糖脂代谢变化显著较小(P均＜0.01).研究组体质量、血糖及三酰甘油异常率明显低于对照组(P均＜0.01). 结论:较低剂量氯氮平合并阿立哌唑治疗与单用较高剂量氯氮平相比,对精神分裂症患者体质量及糖脂代谢影响较小.     

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.