精神分裂症血清补体C3、C4、超敏C-反应蛋白及尿酸水平变化

目的探讨精神分裂症(schizophrenia,SZ)患者血清补体C3(complement component 3,C3)、C4(complement component 4,C4)、超敏C-反应蛋白(high sensitivity C reactive protein,hs-CRP)和尿酸(uric acid,UA)的水平变化及其临床意义。方法选择144例SZ患者为SZ组,并根据4周内有无服用抗精神病药物分为治疗组(77例)和停药组(67例),另选择同期来湘雅二医院的健康体检者147例为健康对照组。采用免疫散射比浊法、胶乳增强免疫比浊法、尿酸氧化酶法分别测定各组血清补体C3、C4、hs-CRP和UA浓度,并比较分析。结果 SZ组患者血清补体C3、C4水平低于对照组[(0.99±0.17)g/L vs.(1.03±0.17)g/L、(0.21±0.05)g/L vs.(0.23±0.05)g/L],UA水平高于对照组[(351.61±95.90)μmol/L vs.(300.28±39.57)μmol/L],差异有统计学意义(分别P0.05,P0.05,P0.001)。治疗组患者血清补体C3、C4、hs-CRP和UA水平较停药组均升高[(1.04±0.19)g/L vs.(0.95±0.15)g/L、(0.22±0.06)g/L vs.(0.20±0.05)g/L、1.08(0.33,5.04)mg/L vs.0.47(0.28,1.29)mg/L、(374.54±108.33)μmol/L vs.(331.61±79.03)μmol/L],差异均有统计学意义(P0.01)。治疗组患者血清hs-CRP和UA浓度较对照组均升高[1.08(0.33,5.04)mg/L vs.0.61(0.33,1.26)mg/L、(374.54±108.33)μmol/L vs.(300.28±39.57)μmol/L],差异有统计学意义(P0.001)。结论 SZ患者血清C3、C4、hs-CRP和UA的水平变化对SZ临床诊断和抗精神病药物疗效评估有一定指导意义。     

双相Ⅰ型障碍抑郁发作患者血清尿酸水平及其影响因素

目的调查双相I型障碍抑郁发作患者血清尿酸(UA)水平及其影响因素。方法采用横断面研究,选取双相I型障碍抑郁发作患者(患者组)68例和健康人群(对照组)68例。采用全自动生化仪检测血清UA水平,采用汉密尔顿抑郁量表(HAMD)评定患者抑郁严重程度。结果患者组高尿酸血症(HUA)检出率高于对照组,差异有统计学意义(20.6%vs.7.4%,P0.05);患者组血清UA水平与对照组比较差异有统计学意义[(310.31±83.35)μmol/L vs.(282.47±78.30)μmol/L,P0.05],患者组男性UA水平高于女性[(344.40±100.45)μmol/L vs.(296.10±71.59)μmol/L,P0.05]。相关分析显示:UA水平与性别和精神病家族史呈负相关(r=-0.28、-0.27,P均0.05);与甘油三酯水平呈正相关(r=0.34,P0.01)。逐步多元回归分析显示,性别、阳性精神疾病家族史对血清UA水平有明显影响(P均0.01)。结论双相I型障碍抑郁发作患者UA水平增高,并与性别、精神疾病家族史相关。     

双相情感障碍血清尿酸水平研究

目的探讨双相情感障碍患者血清尿酸(uric acid,UA)水平变化及其临床意义。方法纳入双相情感障碍患者126例(躁狂发作77例,抑郁发作49例)、首发精神分裂症患者69例和正常对照126名,测定其血清UA水平,并采用杨氏躁狂量表(Young mania rating scale,YMRS)和汉密尔顿抑郁量表(Hamilton depressionscale,HAMD)评定双相情感障碍患者症状。结果双相情感障碍组血清UA水平[(349.34±107.21)μmol/L]高于精神分裂症组[(319.71±84.48)μmol/L]和对照组[(280.94±71.90)μmol/L],差异有统计学意义(P0.01);躁狂发作患者UA水平高于抑郁发作患者[(366.45±104.01)μmol/L vs.(322.45±107.69)μmol/L],且二者均高于对照组(P0.01);双相情感障碍患者中是否使用精神科药物的亚组间UA水平无统计学差异(P0.05)。双相情感障碍患者血清UA水平与YMRS、HAMD分数线性相关均无统计学意义(P0.05)。结论双相情感障碍患者血清UA水平升高,血清UA水平升高可能是双相情感障碍的一个生物标记物。     

双相障碍抑郁发作患者血清谷氨酸系统代谢紊乱特征及相关因素

目的探讨双相障碍抑郁发作患者外周血清中谷氨酸系统各指标变化的特点及其相关因素。方法选取50例双相障碍抑郁发作患者及48名正常对照,以汉密尔顿抑郁量表(Hamilton depression scale-17,HAMD-17)和汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)评估患者抑郁和焦虑症状,以酶联免疫吸附法测定被试血清谷胺酰胺(glutamine,Gln)、谷氨酸(glutamate,Glu)、γ-氨基丁酸(γ-aminobutyric acid,GABA)及谷氨酸脱羧酶(glutamic acid dehydrogenase,GAD)水平,计算Glu/GABA比值。结果双相障碍抑郁发作组较之对照组,血清Glu水平[(35.80±6.34)mg/L vs.(28.69±5.73)mg/L,t=4.68,P0.01]及Glu/GABA[(6.18±1.40)vs.(5.06±1.29),t=3.44,P0.01]增高,血清GABA水平[(5.09±0.71)μmol/L vs.(5.83±1.17)μmol/L,t=3.10,P=0.01]、GAD水平[(28.72±5.39)U/L vs.(35.78±7.22)U/L,t=4.46,P0.01]降低。双相障碍抑郁发作组血清Glu水平与HAMD总分呈正相关(r=0.52,P=0.03),血清GABA水平与HAMD睡眠障碍因子分呈负相关(r=-0.38,P=0.04)。结论双相障碍抑郁发作患者存在Glu能神经元活性增强,GABA能神经元活性降低,兴奋性神经元与抑制性神经元功能失平衡。     

首发精神分裂症血清脂联素及代谢指标与第二代抗精神病药引发肥胖相关性研究

目的通过检测首发精神分裂症患者(first-episode schizophrenic patients,FEP)服用第二代抗精神病药物(second generation antipsychotics,SGAs)8周前后的血清脂联素(adiponectin,APN)及代谢相关指标水平,探讨SGAs对首发精神分裂症患者APN的影响以及APN在SGAs引发肥胖中的作用。方法选取86例首发未服药的精神分裂症患者,及88名性别年龄相匹配的正常对照,患者组使用单一SGAs治疗8周,测定患者组治疗前、治疗8周末及对照组的体重、体质指数(body mass index,BMI)、腰臀比(waist-to-hip ratio,WHR)及空腹血糖(fasting plasma glucose,FPG)、甘油三酯(triglyceride,TG)、APN、空腹胰岛素(fasting insulin,FINS)等指标。结果患者组在治疗前APN水平低于对照组[(9.32±0.76)μg/m L vs.(10.9±0.66)μg/m L],FINS水平高于对照组[(12.68±11.70)μIU/m L vs.(6.47±2.87)μIU/m L],差异有统计学意义(P0.05)。与治疗前相比,患者组SGAs治疗8周后体重[(59.01±10.56)kg vs.(63.80±9.78)kg]、BMI[(21.74±3.57)kg/m2vs.(23.49±3.44)kg/m2]、WHR[(0.88±0.07)vs.(0.92±0.05)]、TG[(0.94±0.92)mmol/L vs.(1.63±1.08)mmol/L]和FINS水平[(12.68±11.70)μIU/m L vs.(20.27±15.02)μIU/m L]增加,差异均有统计学意义(P0.01),而患者组治疗后APN[(9.32±0.76)μg/m L vs.(8.03±0.68)μg/m L]及FPG[(5.04±1.01)mmol/L vs.(4.46±0.57)mmol/L]水平降低,差异均有统计学意义(P0.05)。在男性患者组中,基线APN水平与治疗后体重增加值呈正相关(r=0.548,P=0.005),女性患者组中该相关无统计学意义(P0.05)。结论首发精神分裂症患者在治疗前APN水平降低,SGAs可进一步降低患者APN水平;在男性患者中,基线APN水平对服药后的体重增加有预测作用。     

首次躁狂发作未服药患者血清尿酸水平的研究

目的:探讨首次躁狂发作未用药患者血清尿酸(UA)水平及其临床影响因素。方法:检测105例首次躁狂发作未用药患者(患者组)和105名健康对照者(对照组)血清UA水平,同时采用杨氏躁狂量表(YMRS)评估躁狂症状严重程度。结果:患者组血清UA水平[(371.17±103.63)μmol/L]显著高于对照组[(301.10±78.40)μmol/L](P0.01);高尿酸血症(HUA)发生率(35.2%,37例)显著高于对照组(8.5%,9例)(P0.01);患者组男性[(399.20±99.35)μmol/L]和对照组男性[(329.62±76.34)μmol/L]之间、患者组女性[(333.80±100.71)μmol/L]与对照组女性[(263.06±64.23)μmol/L]之间血清UA水平差异有统计学意义(均P0.01)。相关分析显示血清UA水平与YMRS评分无相关(P0.05)。结论:首次躁狂发作未用药患者血清UA水平升高,但其与躁狂病情无关。     

帕金森病患者血尿酸水平的变化及其与血清铁和血红蛋白的相关性

目的 研究帕金森病(PD)患者血尿酸水平的变化及其与血清铁和血红蛋白的相关性.方法 测定65例PD患者和65名正常人的血尿酸、血清铁和血红蛋白水平,分析PD患者血尿酸与血清铁、血红蛋白水平之间的相关性.结果 PD组血尿酸水平[(271.88±7.20)μmol/L]比正常对照组[(313.46±5.52)μmol/L]明显降低(P<0.01);PD组的血尿酸与血清铁、血红蛋白水平均无相关性.结论 PD患者的血尿酸水平明显降低,其与血清铁和血红蛋白的水平无相关性.提示低血尿酸水平可能导致PD的发生.     

帕金森病患者血浆同型半胱氨酸和尿酸水平的变化及意义

目的探讨帕金森病(PD)患者血浆同型半胱氨酸(Hcy)和尿酸(UA)水平的变化及临床意义。方法 150例PD患者和80例健康对照者纳入研究对象,并将PD患者按HoehnYahr分期进一步分组。抽取所有患者空腹静脉血分别测定UA和Hcy含量,分别对PD与UA、Hcy的相关性进行分析。结果与对照组比较,PD组UA水平降低[(253.2±32.6)μmol/L vs(337.6±49.2)μmol/L,P0.05],且随着HoehnYahr分期的增加,UA水平逐渐降低(P0.05)。而与对照组比较,PD组Hcy水平升高[(15.28±6.05)μmol/L vs(9.29±3.97)μmol/L,P0.05],且随着HoehnYahr分期的增加,Hcy水平逐渐升高(P0.05)。结论血浆中低浓度的UA和高浓度的Hcy与PD的发病及临床分期可能密切相关。     

双相Ⅰ型障碍躁狂发作患者高尿酸血症发生率及其影响因素的研究

目的:探讨双相I型躁狂发作患者高尿酸血症(HUA)的发生率及其影响因素。方法:检测77例双相I型躁狂发作住院患者(患者组)和77名健康对照者(正常对照组)血清尿酸水平,同时检测体质量、腰臀比、血压及三酰甘油(TG)水平。结果:患者组HUA的发生率28.6%(22例)显著高于正常对照组7.8%(6例)(χ2=11.18,P0.01)。平均血清尿酸水平患者组(365.19±103.45)μmol/L显著高于正常对照组(301.77±76.04)μmol/L,差异有统计学意义(F=25.70,P0.01);男性血清尿酸水平高于女性[(381.43±99.02)vs(291.38±70.33)]μmol/L(F=50.08,P0.01)。相关分析显示,患者组中性别与血清尿酸水平呈负相关(r=-0.56,P0.01);TG水平与血清尿酸水平呈正相关(r=0.419,P0.01)。结论:双相I型障碍躁狂发作患者HUA发生率增加并与性别、血清TG水平相关。     

首发未服药精神分裂症患者血浆非酶抗氧化物浓度分析

目的探讨首发未服药精神分裂症患者血浆非酶抗氧化物水平及其与临床特征间的关系。方法测定55例首发未服用抗精神病药精神分裂症患者和42名正常对照的血浆非酶抗氧化物水平,包括白蛋白、总胆红素浓度和尿酸浓度;采用阳性和阴性症状量表(positive and negative symptoms scale,PANSS)评定精神症状。结果患者组血浆白蛋白和尿酸浓度明显低于对照组[(44.72±3.42)g/Lvs(46.70±3.43)g/L,(3.11±1.00)×102μmoL/Lvs(5.00±1.01)×102μmoL/L,P均小于0.05];以阳性症状为主的患者血浆总胆红素浓度明显高于以阴性症状为主的患者[(12.48±3.86)μmoL/L vs(10.27±1.78)μmoL/L,P=0.04];男性患者尿酸浓度明显高于女性患者[(3.54±1.21)×102μmoL/L vs(2.88±0.76)×102μmoL/L,P=0.01];对照组男女性之间上述3个指标的差异均无统计学意义(P>0.05);相关分析仅发现对照组血浆白蛋白、尿酸与年龄相关(r=-0.39,P=0.01;r=-0.40,P=0.01)...     

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.