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1.
目的观察电针对阿尔茨海默病(AD)患者血清白细胞介素-1β(IL-1β)、干扰素-γ(IFN-γ)、S100B水平的影响。方法选取63例AD患者,采用随机数表法分为2组,观察组32例患者在运动锻炼、饮食控制、心理治疗、营养脑神经治疗基础上加电针治疗,对照组31例患者未加用,采用ELISA测定治疗前、治疗70 d后血清IL-1β、IFN-γ、S100B水平,同时应用简明智力状态检查量表(MMSE)及日常生活活动能力量表(ADL)评估患者的智能状况及日常生活能力。结果 2组IL-1β、IFN-γ、S100B、MMSE、ADL治疗前比较无明显差异(P0.05),治疗70 d后上述指标较治疗前降低或升高(P0.01),但观察较对照组降低或升高更显著(P0.05或P0.01)。结论电针刺激可显著抑制AD患者外周血IL-1β、IFN-γ、S100B的表达,改善AD患者的认知功能,提高其日常生活质量。  相似文献   

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目的研究首发精神分裂症患者血清白细胞介素(IL)4、IL-10、IL-12及干扰素-γ(IFN-γ)水平与病程及精神症状严重程度的相关性.方法患者组为30例符合入组标准的首发精神分裂症患者,对照组为58名符合入组标准的正常人.应用夹心酶联免疫吸附测定法测定血清中IL-4,IL-10,IL-12及IFN-γ浓度水平.应用简明精神病评定量表、阳性和阴性症状量表对患者进行精神症状评定.结果患者组IL-4[ (68±29) ng/L]、IL-10为[(61±25) ng/L]均明显高于对照组 [(50±23) ng/L,(32±18) ng/L],差异有非常显著性(P=0.01,P=0.00);IL-12 [(35±15) ng/L]明显低于对照组[(53±27) ng/L],差异有显著性(P=0.01); IFN-γ [(41±17) ng/L]与对照组 [(51±23) ng/L]的差异无显著性(P=0.09).首发精神分裂症患者血清IL-4、IL-10、IL-12及IFN-γ浓度水平与病程无相关(r=0.09,0.07,-0.20,-0.21;P=0.63,0.71,0.30 , 0.27), IL-4、IL-10、IL-12及IFN-γ浓度水平均与精神症状评定无显著相关(P>0.05).患者组IL-4 浓度水平与IL-10的浓度水平正相关(r=0.52,P=0.03),IL-12与IFN-γ浓度水平也存在正相关关系(r=1.00,P=0.00).对照组4种细胞因子间均无相关(P>0.05).结论首发精神分裂症患者IL-4、IL-10、IL-12及IFN-γ浓度水平存在紊乱,但与精神症状严重程度及病程长短无相关性.  相似文献   

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目的研究白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、白细胞介素10(IL-10)在焦虑症患者血清变化及意义。方法选取2017年11月~2018年11月我院收治的42例慢性焦虑症患者和42例抑郁症患者分别作为焦虑组和抑郁组,选择同期42例健康体检者作为健康组。患者均采用选择性5-羟色胺再摄取抑制剂连续治疗8周。比较治疗前后两组患者和对照组的血清IL-1β、IL-6、IL-10水平。结果焦虑组患者IL-6水平显著低于健康组和抑郁组(P0.05);抑郁组患者IL-6水平与健康组比较差异无统计学意义(P0.05)。焦虑组和抑郁组患者IL-10水平均显著高于健康组(P0.05);焦虑组患者IL-10水平与抑郁组比较差异无统计学意义(P0.05)。治疗后两组患者的IL-1β、IL-6、IL-10水平均有显著改善(P0.05),两组患者IL-1β、IL-6、IL-10水平无明显差异(P0.05)。结论焦虑症和抑郁症与健康者可能具有不同免疫机制,可通过血清IL-10和IL-6来鉴别。  相似文献   

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目的 通过检测重症肌无力 ( MG)患者乙酰胆碱受体 ( ACh R)特异性 IFN-γ、IL-1 0分泌细胞水平 ,观察大剂量甲基强的松龙 ( MP)与硫唑嘌呤 ( AZ)联合治疗对 MG患者 Th1及 Th2类细胞因子 ( CK)的影响。方法 用酶联免疫斑点 ( ELISPOT)技术检测 2 1例 MG患者免疫治疗前后外周血 ACh R特异性 IFN-γ、IL-1 0分泌细胞的数目。同时进行临床绝对评分。结果  MP与 AZ联合治疗可使 MG患者外周血 ACh R特异性 IFN-γ分泌细胞的数目减少 ,对 IL-1 0分泌细胞影响不大。IFN-γ分泌细胞水平与临床绝对评分呈明显正相关 ( r=0 .5 1 2 ,P <0 .0 1 )。结论  MP与 AZ联合治疗可抑制 MG患者 Th1类 CK的产生 ,恢复 Th1和 Th2类细胞因子之间的平衡 ,继而改善临床症状。 IFN-γ分泌细胞水平可作为反映肌无力严重程度的指标。  相似文献   

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目的 探讨蛛网膜下腔出血(Subarachnoid hemorrhage,SAH)中凝血酶(Thrombin,TH)诱导脑积水形成时肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素-1β(Interleukin-1β,IL-1β)在脑积水病理发展过程中对水孔蛋白1(Aquaporin 1,AQP1)和水孔蛋白4(Aquaporin 4,AQP4)表达水平的调控作用。方法 选用健康雄性远交群(Sprague Dawley,SD)大鼠40只,随机分成4组(n=10):假手术组、凝血酶(Thrombin,TH)组、TH/TNF-α抑制剂组、TH/IL-1β抑制剂组; 假手术组大鼠枕大池注入0.3 mL生理盐水; TH组大鼠枕大池注入0.3 mL(10 U/mL)凝血酶; TH/TNF-α抑制剂组大鼠枕大池注入0.3 mL(10 U/mL)凝血酶+(0.25 μM)TNF-α抑制剂Simponi,TH/IL-1β抑制剂组大鼠枕大池注入0.3 mL(10 U/mL)凝血酶+(0.25 μM)TH/IL-1β抑制剂GIBH-130; 每组大鼠至少5只以上,按照缺失补足以保证充足的样本量; 建模后的第1、3 d对大鼠行神经功能评分; 第3 d将大鼠处死,计算相对侧脑室面积,免疫组织化学染色评价大鼠TNF-α,IL-1β,AQP1及AQP4的阳性表达水平。结果(1)第3 d假手术组、TH组、TH/TNF-α抑制剂组、TH/IL-1β抑制剂组大鼠侧脑室面积分别为(3.58±0.40)、(6.09±0.82)、(5.06±0.53)、(5.25±0.68)%; 与假手术组比较,TH组、TH/TNF-α抑制剂组、TH/ IL-1β抑制剂组相对侧脑室面积增大(P<0.01); 与TH组比较,TNF-α抑制剂组与IL-1β抑制剂组相对侧脑室面积减少(P<0.01);(2)免疫组织化学染色检测:1)大鼠TNF-α与IL-1β的免疫阳性表达主要分布于胞浆内,TNF-α主要位于侧脑室周围组织的星形胶质细胞及神经元,IL-1β主要位于侧脑室周围组织的小胶质细胞及星形细胞; 与假手术组比较,TH组、TH/TNF-α抑制剂组、TH/IL-1β抑制剂组TNF-α与IL-1β的阳性表达增加(P<0.01); 与TH组比较,TH/TNF-α抑制剂及TH/IL-1β抑制剂组TNF-α与IL-1β的阳性表达减少(P<0.01); 2)AQP1与AQP4的免疫阳性表达主要分布于胞膜,其中AQP1主要位于脉络丛上皮细胞,AQP4主要位于侧脑室周围组织的室管膜细胞; 与假手术组比较,TH组、TH/TNF-α抑制剂组及TH/IL-1β抑制剂组AQP1,AQP4的阳性表达增加(P<0.01); 与TH组比较,TH/TNF-α抑制剂及TH/IL-1β抑制剂组AQP1,AQP4的阳性表达减少(P<0.01)。结论(1)在TH诱发的SAH脑积水病理发展中TH可诱导TNF-α、IL-1β表达水平上调,从而增加AQP1的表达,促进脉络丛分泌脑脊液; AQP4表达水平升高可能为脑积水后的代偿反应;(2)通过抑制TNF-α,IL-1β表达可以下调AQP1,并引起继发性的AQP4的表达减少,改善大鼠神经功能缺损症状; TNF-α,IL-1β可作为临床治疗脑积水的重要靶点。  相似文献   

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目的 探讨不同病情严重程度阿尔茨海默病(Alzheimer's disease,AD)患者血清白介素-33(Interleukin-33,IL-33)、白介素-1β(Interleukin-1β,Il-1β)的水平变化及其临床意义。方法 选取60例阿尔茨海默病住院患者(AD组)和40例健康老年者(N组)作为研究对象,进行回顾性病例-对照研究; 采用简易精神状态量表(Mini-mental state examination,MMSE)评价标准将AD组分为轻度组、中度组、重度组; 用酶联免疫吸附测定(Enzyme linked immunosorbent assay,ELISA)法检测患者血清IL-33和IL-1β水平。结果 与N组比较,轻度组IL-1β水平升高(P<0.05),IL-33水平降低,但无明显差异(P>0.05); 随病情加重,IL-33水平呈降低趋势,IL-1β水平呈升高趋势(P<0.05)。回归分析显示,IL-33水平与AD的严重程度呈独立负相关(P<0.001); Il-1β水平与AD的发生风险和AD的严重程度呈独立正相关(P<0.001)。采用受试者工作特征曲线(Receiver operating characteristic curve,ROC)分析显示IL-33的曲线下面积(Area Under Curve,AUC)是0.807,敏感性和特异性最好的截断值是30 ng/L(P<0.01); IL-1β的AUC是0.913,敏感性和特异性最好的截断值是1.77 ng/L(P<0.01)。结论 在体内IL-33和IL-1β水平异常变化可能是导致AD发生或程度加重的危险因素之一; 对于已经发生AD的患者,IL-33和IL-1β水平均可以作为评估病情严重程度的指标。  相似文献   

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目的探讨精神分裂症患者血清可溶性白细胞介素-2受体(SIL-2R)水平及其临床意义.方法用酶联免疫试验检测42例首发精神分裂症患者治疗前后及正常人SIL-2R含量,并进行有关量表评定.结果精神分裂症患者治疗前SIL-2R明显高于正常组(P<0.05),男女患者间无差异;Ⅰ型精神分裂症血清SIL-2R浓度显著高于Ⅱ型和混合型(P<0.05),后两者之间无显著性差异治疗前,SIL-2R浓度与起病年龄呈负相关(r=-0.469,P<0.05),与阴性和阳性症状量表(PANSS)总分呈正相关(r=0446,P<0.05);氯氮平和利培酮能显著升高血清SIL-2R浓度(P<0.01,P<0.05);此外,治疗后血清SIL-2R水平升高与病程,治疗前的SIL-2R和PANSS总分显著相关.结论血清SIL-2R升高可能与精神分裂症发病有关,亦可能成为其临床亚型分布和早期病情严重程度评价的新指标.非典型抗精神病药(尤其是氯氮平)可能通过升高SIL-2R血清浓度达到免疫抑制作用.  相似文献   

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目的 探讨血清白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-18(interleukin-18,IL-18)在急性脑梗死(acute cerebral infarction,ACI)中的动态变化,并分析两者与ACI病情严重性之间的关系.方法 83例ACI患者在发病24 h内入院,分别在入院后第1、3、7d抽血,采用酶联免疫吸附法动态监测血清IL-1β、IL- 18的水平,采用欧洲卒中神经功能缺损评分(European Stroke Scale,ESS)评价ACI的严重程度.同时监测32例健康成人的血清IL-1β、IL- 18的水平作为对照.结果 ACI组IL- 1β、IL- 18水平在发病后第1、3d明显高于对照组,差异有统计学意义(P<0.05),第7d呈下降趋势. ESS与IL-1β,IL-18值呈负相关.结论 在ACI发病后血清IL- 1β、IL-18水平升高,说明炎性免疫因素可能参与ACI发生、发展过程,血清IL- 18水平能反映ACI病情及严重程度.  相似文献   

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目的观察重组组织型纤溶酶原激活剂(rt-PA)溶栓治疗对急性脑梗死患者血清白介素-17(IL-17)的影响,探讨IL-17在脑梗死发病机制中的作用。方法 采用酶联免疫吸附法(ELISA)检测急性脑梗死患者rt-PA溶栓治疗前后血清IL-17浓度值,并与常规治疗组、正常对照组比较。结果 两治疗组治疗前血清IL-17浓度明显高于对照组(P〈0.001)。治疗前及治疗后12h,溶栓组和常规治疗组血清IL-17浓度无明显差异(P〉0.05)。治疗后12h溶栓组血清IL-17浓度明显下降(P〈0.001),而常规治疗组IL-17浓度继续增高,3d后血清IL-17浓度下降(P〈0.05)。治疗14d溶栓组血清IL-17浓度与对照组无明显差异(P〉0.05),常规治疗组则明显高于对照组(P〈0.001)。结论 急性脑梗死患者血清IL-17水平明显升高,rt-PA溶栓治疗能显著降低急性脑梗死患者血清IL-17的水平。  相似文献   

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目的探讨精神分裂症中核转录因子-κB(NF-κB)活性与白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)mRNA表达及其血清蛋白水平的关系。方法应用酶联免疫吸附法(ELISA)测定83例首发精神分裂症患者和65名健康对照外周血单个核细胞(PBMC)中NF-κB的活性,同时采用ELISA和逆转录-聚合酶链反应(RT-PCR)方法检测血清细胞因子IL-1β、IL-6、TNF-α的蛋白水平和PBMC中IL-1β、IL-6、TNF-α的mRNA表达。结果患者组的NF-κB活性及血清IL-1β、IL-6、TNF-α的水平均明显高于对照组,差异有统计学意义(P<0.05)。患者组PBMC中IL-1β、IL-6、TNF-α的mRNA表达明显高于对照组,差异有统计学意义(P<0.05)。患者组中NF-κB的活性与血清IL-1β、TNF-α水平及二者的mRNA表达水平均呈正相关(r分别为0.578、0.532、0.536、0.454,P均小于0.05),而对照组中NF-κB的活性与血清IL-1β、TNF-α水平及二者的mRNA表达水平均呈正相关(r分别为0.456、0.549、0.519、0.513,P均小于0.05)。两组中NF-κB的活性与血清IL-6及其mRNA均无明显相关(P均大于0.05)。结论精神分裂症患者存在免疫激活,激活状态的PBMC是细胞因子的主要来源之一;精神分裂症中活化的NF-κB对IL-1β、TNF-α的基因转录起了重要的调控作用。  相似文献   

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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.  相似文献   

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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.  相似文献   

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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  相似文献   

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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.  相似文献   

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