急性脑梗死患者血清YKL-40、hs-CRP水平与颈动脉粥样硬化斑块的相关性研究

目的 探讨急性脑梗死患者颈动脉粥样硬化性斑块与人类软骨糖蛋白-39(YKL-40)、超敏C-反应蛋白(hs-CRP)含量的关系.方法 选取130例急性脑梗死患者和30例正常对照者检测血清YKL40、hs-CRP水平.对急性脑梗死患者结合颈动脉超声检查结果,分为颈动脉IMT正常组30例、颈动脉IMT增厚组30例、颈动脉斑块组70例,其中稳定斑块37例,不稳定斑块33例,测定并比较各组血清YKL40、hs-CRP水平.结果 急性脑梗死组血清YKL40、hs-CRP水平显著高于正常对照组(P＜0.01);在急性脑梗死患者中,有颈动脉粥样硬化组血清YKL-40、hs-CRP水平较颈动脉IMT正常组明显升高(P＜0.01),颈动脉IMT斑块形成组血清YKL-40、hs-CRP水平较颈动脉IMT增厚组明显升高(P＜0.01),颈动脉粥样硬化不稳定斑块组血清YKL-40、hs-CRP水平显著高于稳定斑块组;线性相关分析表明YKL-40水平和hs-CRP水平无明显相关性(r=0.04,P＞0.05);Logistic回归分析结果显示:YKL-40、hs-CRP是发生颈动脉粥样硬化的危险因素(OR=1.128,95％C1 1.21～1.87;OR=2.62,95％ CI1.76 ～4.47).结论 YKL-40、hs-CRP可能反映急性脑梗死患者颈动脉粥样硬化斑块的炎症程度以及斑块的不稳定程度,病变越重,斑块越不稳定,YKL-40、hs-CRP水平越高,且YKL-40水平独立于hs-CRP水平.     

亲环素A及脑梗死相关血液指标与颈动脉粥样硬化斑块形成和稳定性及脑梗死的相关性研究

目的探究亲环素A(Cyclophilin A,CyPA)及脑梗死相关血液指标与颈动脉粥样硬化斑块形成和稳定性之间的关系,从而探究其与脑梗死的相关性。方法收集河北医科大学第二医院神经内科2017年12月～2018年12月就诊的患者脑梗死组56例,斑块组(无梗死,仅有斑块)患者72例,无斑块组40例;各组中斑块的稳定程度用斑块评分来表示,斑块评分越高斑块越不稳定;应用酶联免疫吸附测定法(Enzyme-linked immune sorbent assay,ELISA)测定CyPA含量,并收集一些常见血液指标数据;应用颈动脉超声检测颈动脉斑块并根据超声中颈动脉斑块的形态确定斑块评分。结果无斑块组和斑块组CyPA水平差异有统计学意义(P<0.05),CyPA是颈动脉斑块形成的危险因素(OR=1.002,95%CI 0.824～1.219);脑梗死组和斑块组中CyPA水平与颈动脉斑块评分(颈动脉斑块稳定性)之间无相关性(P>0.05);斑块组与脑梗死组的斑块评分差异有统计学意义(P<0.05)。脑梗死组中纤维蛋白原、糖化血红蛋白与斑块评分呈正相关,血红蛋白与斑块评分之间呈负相关,且有统计学意义(P<0.05)。经Logistics回归后,纤维蛋白原是动脉粥样硬化斑块发展的独立危险因素(OR=8.988,95%CI 3.017～3.422)。血红蛋白是动脉粥样硬化斑块发展的保护因素(OR=0.936,95%CI 134.031～144.583);斑块组,中高密度脂蛋白与斑块评分呈负相关,差异有统计学意义。经Logistic回归分析后,高密度脂蛋白是动脉粥样硬化斑块发展的保护因素(OR=0.052,95%CI 1.237～1.364)。结论血清中CyPA水平是颈动脉粥样硬化斑块形成的危险因素,但与斑块的稳定性不相关;脑梗死患者中的斑块不稳定程度较非脑梗死患者斑块不稳定程度明显增加;对于急性脑梗死的患者纤维蛋白原、糖化血红蛋白都与颈动脉斑块的稳定程度呈负相关,血红蛋白含量与斑块稳定性呈正相关,其中纤维蛋白原是动脉粥样硬化斑块发展的独立危险因素,血红蛋白是动脉粥样硬化斑块发展的保护因素;在非脑梗死患者中,高密度脂蛋白与斑块的稳定程度呈正相关且是斑块发展的保护因素。     

急性脑梗死患者血清视黄醇结合蛋白水平与颈动脉粥样硬化斑块的相关性研究

目的探讨急性脑梗死(ACI)患者颈动脉粥样硬化性斑块与视黄醇结合蛋白(RBP)含量的关系。方法选取96例ACI患者(ACI组)和95例正常对照者(对照组),检测血清RBP水平;同时检测ACI组和对照组患者血清尿酸(UA)和血浆D-二聚体(DD)、纤维蛋白原(FIB)水平。对于ACI患者结合其颈动脉超声检查结果,分为无斑块组(41例)、颈动脉稳定斑块组(28例)和颈动脉不稳定斑块组(27例);比较各组血清RBP水平。结果 ACI组血清RBP水平显著高于正常对照组(P0.05)。在ACI患者中,颈动脉稳定斑块组和不稳定斑块组的血清RBP水平较无斑块组明显升高(均P0.05);颈动脉不稳定斑块组血清RBP水平显著高于稳定斑块组(P0.05)。线性相关分析表明,RBP水平和UA、DD和FIB水平无明显相关性(r=0.192,r=0.088,r=0.096,均P0.05)。Logistic回归分析结果显示,RBP是发生颈动脉粥样斑块的危险因素(OR=2.769,95%CI 0.007-0.722)。结论血清RBP可能是动脉硬化形成的一个重要标志物,并且可能与ACI患者动脉粥样硬化斑块的稳定性密切相关。     

脑梗死患者颈动脉粥样硬化斑块稳定性与血清C反应蛋白水平的关系

目的探讨脑梗死患者颈动脉粥样硬化斑块的稳定性与血清C反应蛋白(CRP)水平的关系。方法对112例颈内动脉系统脑梗死患者进行颈动脉彩色多普勒超声检查,明确粥样硬化斑块类型,同时测定血清CRP水平。结果脑梗死患者中不稳定斑块组、稳定斑块组、无斑块组血清CRP水平比较差异有统计学意义(P<0.01)。结论血清CRP水平可反映脑梗死患者颈动脉粥样硬化斑块的稳定性。     

急性脑梗死患者血清sfgl2、ANGPTL8水平与颈动脉不稳定斑块的关系

目的 探讨急性脑梗死(ACI)患者血清可溶性纤维蛋白原2(sfgl2)、血管生成素样蛋白8(ANGPTL8)水平与颈动脉不稳定斑块的关系.方法 选取2017年1月到2019年12月期间在黄河三门峡医院接受治疗的183例ACI患者,根据患者是否有斑块将其分为斑块组(151例)和非斑块组(32例),斑块组再根据斑块的稳定性...     

急性脑梗死患者血清纤维蛋白原血浆D-二聚体与颈动脉粥样硬化斑块的相关性研究

目的观察和分析急性脑梗死(ACI)患者血清纤维蛋白原(FG)、血浆D-二聚体(D-D)与颈动脉粥样硬化斑块的相关性。方法选取150例ACI患者为病例组,选取100例健康人为对照组。对2组颈动脉粥样硬化斑块及稳定性进行检测和比较,并将病例组分为稳定斑块组、不稳定斑块组2个亚组;检测和比较2组血清FG水平、血浆D-D水平。结果病例组颈动脉粥样硬化斑块检出率和具有不稳定斑块的比例均显著高于对照组(χ2=75.996、69.283,P0.05),未检出斑块组和对照组血清FG水平、血浆D-D水平均显著低于检出斑块组(q=2.633~4.662,P0.05),不稳定斑块组均显著高于稳定斑块组,稳定斑块组均显著高于对照组(q=3.025~4.817,P0.05);Logistic多元回归分析显示,ACI的发病与颈动脉硬化斑块稳定性(OR=1.836)、血清FG水平(OR=2.332)、血浆D-D水平(OR=1.928)具有相关性(Waldχ2=4.336、5.013、4.257,P0.05),颈动脉硬化斑块的形成与血清FG水平(OR=2.053)、血浆D-D水平(OR=1.799)具有相关性(Waldχ2=5.027、4.288,P0.05),颈动脉硬化斑块的不稳定性与血清FG水平(OR=2.655)、血浆D-D水平(OR=3.231)具有相关性(Waldχ2=4.933、4.639,P0.05)。结论 ACI患者表现为血清FG水平、血浆D-D水平显著升高,是影响颈动脉硬化斑块形成风险和稳定性及ACI发病风险的独立危险因素,可作为ACI发病风险监测、病情评价的辅助指标。     

炎症因素与脑梗死患者颈动脉粥样硬化的关系

目的 探讨炎症因素与脑梗死患者颈动脉粥样硬化的关系.方法 对244例急性缺血性脑卒中患者的颈动脉内膜中层厚度(IMT)及斑块情况和血液炎症性生化指标进行相关性分析.结果 炎症因素(单核细胞比例,纤维蛋白原,C-反应蛋白水平,血沉)和颈动脉粥样硬化相关,其中单核细胞比例(ORIMT=1.231,P<0.01;OR斑块=1.175,P<0.05)及血沉增高(ORIMT=1.024,OR斑块=1.029,均P<0.01)具有独立预测性,单核细胞比例的独立预测性最高.炎症因素和斑块稳定性之间无相关性.结论 单核细胞比例及血沉可独立预测颈动脉粥样硬化的发生.     

急性脑梗死患者血清纤维蛋白原、D-二聚体与颈动脉粥样硬化斑块的相关性研究

目的 探讨急性脑梗死患者血清纤维蛋白原、D-二聚体与颈动脉粥样硬化斑块的关系. 方法 选择解放军第三医院神经内科自2009年4月至2011年4月收治的120例急性脑梗死患者(脑梗死组)、同期单纯颈动脉粥样硬化而无脑梗死患者60例(颈动脉粥样硬化组)和健康体检者80例(正常对照组)作为研究对象,采用双抗体夹心法测定血清D-二聚体含量,全自动血凝仪测定纤维蛋白原含量,颈动脉彩色多普勒超声检测患者颈动脉粥样硬化斑块和颈动脉内一中膜厚度(IMT)值. 结果 脑梗死组、颈动脉粥样硬化组及正常对照组血清纤维蛋白原、D-二聚体水平及颈动脉IMT值依次降低,差异有统计学意义(P＜0.05);进展性卒中患者血清纤维蛋白原、D-二聚体水平高于非进展性卒中患者,差异有统计学意义(P＜0.05);随着动脉粥样硬化严重程度的升高,脑梗死患者血清纤维蛋白原及D-二聚体水平逐渐升高,差异有统计学意义(P＜0.05);脑梗死患者血清纤维蛋白原、D-二聚体水平均与颈动脉粥样硬化严重程度呈正相关关系(r=0.426,P=0.006; r=0.535,P=0.001). 结论 纤维蛋白原及D-二聚体参与了急性脑梗死的发生发展,与病情进展密切相关.二者做为急时相反应物参与动脉粥样硬化的发生机制提示,相对于高凝状态,动脉粥样硬化的形成与慢性炎症反应关系更为密切.     

脑梗死患者颈动脉粥样硬化斑块的相关危险因素分析

目的探讨脑梗死患者的颈动脉粥样硬化发生情况及其主要危险因素。方法对170例脑梗死患者应用彩超进行颈动脉检查,观察动脉粥样硬化的发生情况和记录相关危险因素的资料,同时实验室检测血脂、血糖、纤维蛋白原水平。结果脑梗死患者有颈动脉粥样硬化斑块者131例(77.1%),颈动脉狭窄11例(6.5%)。经Logistic回归分析发现,年龄(OR 1.352,95%CI:1.087~1.569)、吸烟(OR 1.854,95%CI:1.362~2.258)及糖尿病(OR 2.774,95%CI:1.612~5.956)可能是导致斑块发生的独立危险因素。颈动脉有斑块组其总胆固醇、低密度脂蛋白、血糖及纤维蛋白原水平较无斑块组显著增高(P<0.01)。结论年龄、吸烟和糖尿病是发生脑梗死颈动脉粥样硬化斑块的独立危险因素,应对存在多种危险因素的患者进行积极干预。     

急性脑梗死患者颈动脉粥样硬化与血清高敏C反应蛋白水平的关系

目的 探讨颈动脉粥样硬化与高敏C反应蛋白(hs-CRP)、急性脑梗死之间的关系.方法 应用彩色多普勒超声检测仪对58例急性脑梗死患者及35例健康对照者进行颈动脉超声检查,观测颈动脉内膜-中膜厚度(IMT)、粥样斑块类型,同时检测血清hs-CRP水平.结果 脑梗死组患者血清hs-CRP、颈动脉IMT及粥样斑块发生率较对照组明显增加(P＜0.05);脑梗死患者中不稳定斑块、稳定斑块、无斑块组血清hs-CRP水平差异有统计学意义(P＜0.05);血清hs-CRP水平与颈动脉IMT呈正相关.结论 颈动脉IMT、粥样硬化斑块、血清hs-CRP与脑梗死有密切的关系,hs-CRP能反映颈动脉粥样硬化的程度及斑块的稳定性.     

Desire, disease, and the origins of the dopaminergic system

The dopaminergic neurons in the midbrain region of the central nervous system project an extensive network of connections throughout the forebrain, including the neocortex. The midbrain-forebrain dopaminergic circuits are thought to regulate a diverse set of behaviors, from the control of movement to modulation of cognition and desire--because they relate to mood, attention, reward, and addiction. Defects in these pathways, including neurodegeneration, are implicated in a variety of psychiatric and neurological diseases, such as schizophrenia, attention-deficit/hyperactivity disorder, drug addiction, and Parkinson disease. Based on the importance of the midbrain dopaminergic neurons to normal and pathological brain function, there is considerable interest in the molecular mechanisms that regulate their development. The goal of this short review is to outline new methods and recent advances in identifying the molecular networks that regulate midbrain dopaminergic neuron differentiation and fate. Midbrain dopaminergic neurons are descended from progenitor cells located near the ventral midline of the neural tube floor plate around the cephalic flexure. It is now clear that their initial formation is dependent on interactions between the signaling molecules Sonic hedgehog, WINGLESS 1, and FIBROBLAST growth factor 8, but there is still an extensive wider network of molecular interactions that must be resolved before the complete picture of dopaminergic neuron development can be described.     

Blindness,Psychosis, and the Visual Construction of the World

The relationship between visual loss and psychosis is complex: congenital visual loss appears to be protective against the development of a psychotic disorder, particularly schizophrenia. In later life, however, visual deprivation or visual loss can give rise to hallucinosis, disorders of visual insight such as blindsight or Anton syndrome, or, in the context of neurodegenerative disorders, more complex psychotic presentations. We draw on a computational psychiatric approach to consider the foundational role of vision in the construction of representations of the world and the effects of visual loss at different developmental stages. Using a Bayesian prediction error minimization model, we describe how congenital visual loss may be protective against the development of the kind of computational deficits postulated to underlie schizophrenia, by increasing the precision (and consequent stability) of higher-level (including supramodal) priors, focusing on visual loss-induced changes in NMDA receptor structure and function as a possible mechanistic substrate. In simple terms, we argue that when people cannot see from birth, they rely more heavily on the context they extract from the other senses, and the resulting model of the world is more impervious to the false inferences, made in the face of inevitably noisy perceptual input, that characterize schizophrenia. We show how a Bayesian prediction error minimization framework can also explain the relationship between later visual loss and other psychotic symptoms, as well as the effects of visual deprivation and hallucinogenic drugs, and outline experimentally testable hypotheses generated by this approach.     

Distribution of the protein IMPACT, an inhibitor of GCN2, in the mouse, rat, and marmoset brain

IMPACT is an inhibitor of GCN2, a kinase that phosphorylates the alpha subunit of the translation initiation factor 2 (eIF2 alpha). GCN2 has been implicated in regulating feeding behavior and learning and memory in mice. IMPACT is highly abundant in the brain, suggesting its relevance in the control of GCN2 activation in the central nervous system. We describe here the distribution of IMPACT in the brain of rodents (mice and rats) and of a primate (marmoset) using highly specific antibodies raised against the mouse IMPACT protein. Neurons expressing high levels of IMPACT were found in most areas of the brain. In the hippocampal formation the lack of IMPACT in the dentate gyrus granule cells was striking. The hypothalamus is exceptionally rich in neurons expressing high levels of IMPACT, particularly in the suprachiasmatic nucleus. The only exception to this pattern was the ventromedial nucleus. The thalamic neurons are mostly devoid of IMPACT, with the exception of the paraventricular, reuniens and reticular nuclei, and intergeniculate leaf. The brainstem displayed high levels of IMPACT. For the marmoset, IMPACT expression in the brain is not as prominent when compared to other organs. In the marmoset brain the pattern of IMPACT expression was similar to rodents in most areas, except for the very strong labeling of the Purkinje cells, the lack of IMPACT-positive neurons in the nucleus reuniens, and weak labeling of interneurons in the hippocampus. GCN1, the activator of GCN2 to which IMPACT binds, is widely distributed in all neuronal populations, and all IMPACT-positive cells were also GCN1-positive. The data presented herein suggest that IMPACT may be involved in biochemical homeostatic mechanisms that would prevent GCN2 activation and therefore ATF4 (CREB-2) synthesis in neurons.