胸水、血清中CEA、NSE、CYFRA21-1对恶性胸腔积液的诊断价值

目的探讨胸水、血清中CEA、NSE、CYFRA21-1对恶性胸腔积液的诊断价值。方法测定40例恶性胸水和40例非恶性胸水及其血清中CEA、NSE、CYFRA21—1的水平。结果恶性胸水组胸水及其血清中CEA、NSE、CYFRA21-1的水平明显高于非恶性胸水组,有显著性差异（P〈0．05）。恶性胸水组3项联合检测的阳性率明显高于单项检测（P〈0．05）。结论联合检测胸水及其血清中CEA、NSE、CYFRA21-1对鉴别良、恶性胸水有一定的临床价值。     

脑出血继发癫痫患者血清NSE和炎症细胞因子浓度测定对病情的预测价值

目的:探讨脑出血急性期继发癫痫患者血清NSE,炎症细胞因子的变化及对病情的预测价值。方法:检测脑出血继发癫痫组,单纯脑出血组和健康对照组各31例对象的血清肿瘤坏死因子(TNF-α),白介素-β(IL-1β),白介素-6(IL-6),C-反应蛋白(CRP)与神经元特异性烯醇化酶(NSE)的含量,并同步采用美国卫生研究院卒中量表(NIHSS)进行评分。结果:组间脑出血继发癫痫组和单纯脑出血组患者各指标水平均高于健康对照组,(P<0.001),有非常显著差异。多元回归分析显示炎症细胞因子的变化与NSE及NIHSS有线性关系,NSE是NIHSS的独立预测因子。结论:脑出血急性期继发癫痫的病理机制是炎症细胞因子进一步表达导致神经元再次受损,NSE升高,检测血清中NSE浓度对患者的病情预测有重要意义。     

病毒性脑炎患儿治疗前后血清NSE、血浆NPY检测的临床意义

目的:探讨了病毒性脑炎患儿治疗前后血清NSE和血浆NPY水平的变化及意义.方法:应用放射免疫分析对32例病毒性脑炎患儿进行了血清NSE和血浆NPY水平测定,并以30例正常健康儿进行比较.结果:在治疗前病毒性脑炎患儿血清NSE和血浆NPY水平非常显著地高于正常儿水平(P＜0.01),经治疗一个月血清NSE和血浆NPY水平与正常儿比较仍有显著性差异(P＜0.05).结论:病毒性脑炎患儿血清NSE和血浆NPY水平的变化与病毒性脑炎的发病机理有密切的关系.     

血清神经元特异性烯醇化酶水平与2型糖尿病患者认知功能障碍的相关性研究

目的 探讨血清神经元特异性烯醇化酶(NSE)水平与T2DM患者认知功能障碍的相关性.方法 选取T2DM患者300例,根据简易智力状态检查量表(MMSE)评分分为认知功能正常组、轻度认知功能障碍组、中度认知功能障碍组和重度认知功能障碍组,检测各组血清NSE水平. 结果 与认知功能正常组相比,轻、中、重度认知功能障碍组血清NSE水平升高[(10.91±3.58)vs(13.78±4.76)、(18.35±5.29)、(24.19±5.64) ng/ml,P＜0.01].认知功能障碍程度越严重,血清NSE水平越高(P＜0.01). 结论 血清NSE水平与T2DM患者认知功能障碍密切相关,可用于判断认知功能障碍的严重程度.     

神经元特异性烯醇化酶对急性ST段抬高型心肌梗死患者发生心力衰竭的预测价值

目的:评价神经元特异性烯醇化酶(NSE)对急性ST段抬高型心肌梗死(STEMI)患者住院期间发生心力衰竭(心衰)的预测价值。方法:连续收集2011年1月至2012年12月住院的STEMI患者508例。收集患者临床资料,检测血清NSE及氨基末端B型脑钠肽前体(NT-pro-BNP)浓度、血肌酐(Cr)、肝功能和心肌酶。观察患者住院期间发生心衰的情况。依据心衰Killip分级分为心衰组和非心衰组,比较2组临床特征及NSE、NT-pro-BNP浓度的差异。采用Spearman秩相关分析NSE与各临床因素间的关系;应用多因素Logistic回归分析影响住院期间STEMI患者发生心衰的相关因素;采用受试者工作特征(ROC)曲线评价NSE和NT-pro-BNP对住院期间STEMI患者发生心衰的预测价值。结果:与非心衰组相比,心衰组患者NSE、NT-pro-BNP浓度高。随着患者心功能的恶化,NSE、NT-pro-BNP浓度逐渐升高(P0.001)。Spearman秩相关分析显示NSE与天冬氨酸转氨酶(AST)、肌酸激酶(CK)呈明显正相关(AST:r=0.342,P0.001;CK:r=0.377,P0.001),与左心室射血分数(LVEF)呈显著负相关(r=-0.342,P0.001)。多因素Logistic回归分析显示NSE是住院期间STEMI患者发生心衰的独立危险因素[风险比(HR)=1.021,95%可信区间(CI):1.003~1.040,P=0.023],其预测住院期间心衰发生的ROC曲线下面积(AUC)为0.674(P0.001)。结论:NSE是STEMI患者住院期间心衰发生的独立危险因素,对预测STEMI患者住院期间心衰的发生有一定价值。     

New striatal neurons form projections to substantia nigra in adult rat brain after stroke

Previous studies have demonstrated that newborn striatal neurons can functionally integrate with local neural networks in adult rat brain after injury. In the present study, we determined whether these newly generated striatal neurons can develop projections to the substantia nigra, a target of striatal projection neurons. We used 5′-bromodeoxyuridine (BrdU) and a retroviral vector expressing green fluorescent protein (GFP) combined with multiple immunostaining labels of newborn striatal neurons, and nigral microinjection of fluorogold (FG) to trace the striatonigral projection in adult rat brain at different weeks following a transient middle cerebral artery occlusion (MCAO). We found that FG positive (FG⁺) cells could be detected in newly generated neurons (BrdU⁺-NeuN⁺ and GFP⁺-NeuN⁺) in ipsilateral striatum clearly at 12, but not 2 weeks after MCAO. The data suggest that ischemia-induced newborn striatal projection neurons could form long axons that targeted the substantia nigra (striatonigral projection pathway) and that have intact axonal transport from the nerve terminal to cell body. These new striatal neurons express glutamate NR2 and dopamine D2L receptors, which form the molecular basis for responding to the inputs from cortical glutamatergic and nigral dopaminergic projection neurons. Our data provide the first morphological evidence that newborn neurons in the striatum, a non-neurogenic region, can establish new striatonigral neural circuits, important pathways for the maintenance of motor function. These results help us to understand endogenous cellular mechanisms of brain repair, and suggest that increasing adult neurogenesis could be a practical strategy for enhancing the efficacy of rehabilitative therapy in stroke patients.     

An increase in S-glutathionylated proteins in the Alzheimer's disease inferior parietal lobule, a proteomics approach

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by neurofibrillary tangles, senile plaques, and loss of synapses. Many studies support the notion that oxidative stress plays an important role in AD pathogenesis. Previous studies from our laboratory employed redox proteomics to identify oxidatively modified proteins in the AD inferior parietal lobule (IPL) and hippocampus. The proteins were consistent with biochemical or pathological alterations in AD and have been central to further investigations of the disease. The present study focused on the identification of specific targets of protein S-glutathionylation in AD and control IPL by using a redox proteomics approach. For AD IPL, we identified deoxyhemoglobin, alpha-crystallin B, glyceraldehyde phosphate dehydrogenase (GAPDH), and alpha-enolase as significantly S-glutathionylated relative to these brain proteins in control IPL. GAPDH and alpha-enolase were also shown to have reduced activity in the AD IPL. This study demonstrates that specific proteins are sensitive to S-glutathionylation, which most likely is due to their sensitivity to cysteine oxidation initiated by the increase in oxidative stress in the AD brain.     

急性脑卒中患者血清神经元特异性烯醇化酶、S-100B蛋白、髓鞘碱性蛋白水平的变化

目的探讨急性脑卒中患者血清神经元特异性烯醇化酶(NSE)、S-100B蛋白、髓鞘碱性蛋白(MBP)水平变化及其临床意义。方法回顾性对照分析发病在48 h内的45例急性脑卒中患者(其中脑梗死组19例,脑出血组15例,短暂性脑缺血发作组11例)血清NSE、S-100B蛋白、MBP水平变化及其与脑梗死、脑出血患者神经功能缺损程度的相关性。结果脑梗死组和脑出血组患者血清NSE、S-100B蛋白、MBP水平均较对照组有不同程度增高(P<0.05),而短暂性脑缺血发作组与正常对照组比较均无明显变化。脑梗死组和脑出血组患者中神经功能缺损较重的中重型亚组患者血清NSE、S-100B蛋白、MBP水平较轻型亚组水平高(P<0.05)。结论血清NSE、S-100B蛋白、MBP水平可作为急性脑卒中患者病情判断、预后评估的指标之一,对早期脑梗死与短暂性脑缺血发作也有鉴别诊断价值,尤其适用于无法进行影像学检查的脑卒中患者。     

依达拉奉对急性颅脑损伤血清神经元特异性烯醇化酶的影响

目的通过观察依达拉奉注射液对急性颅脑损伤患者血清中神经元特异性烯醇化酶(NSE)的影响,探讨依达拉奉对脑的保护作用。方法将60例急性颅脑损伤患者随机分为依达拉奉治疗组(30例)和常规治疗组(30例),并另取30例为正常对照组,利用ELISA法分别测定患者入院时、第3d、第7d及第14d血清NSE浓度。结果依达拉奉治疗组第3、7d血清NSE浓度低于常规治疗组;治疗后第14d及3个月,依达拉奉治疗组GOS评分高于常规治疗组。结论依达拉奉注射液对急性颅脑损伤有保护作用。     

Autoimmunity to specific citrullinated proteins gives the first clues to the etiology of rheumatoid arthritis

Summary: Rheumatoid arthritis (RA) is now clearly a true autoimmune disease with accumulating evidence of pathogenic disease-specific autoimmunity to citrullinated proteins. Citrullination, also termed deimination, is a modification of arginine side chains catalyzed by peptidylarginine deiminase (PAD) enzymes. This post-translational modification has the potential to alter the structure, antigenicity, and function of proteins. In RA, antibodies to cyclic citrullinated peptides are now well established for clinical diagnosis, though we argue that the identification of specific citrullinated antigens, as whole proteins, is necessary for exploring pathogenic mechanisms. Four citrullinated antigens, fibrinogen, vimentin, collagen type II, and α-enolase, are now well established, with others awaiting further characterization. All four proteins are expressed in the joint, and there is evidence that antibodies to citrullinated fibrinogen and collagen type II mediate inflammation by the formation of immune complexes, both in humans and animal models. Antibodies to citrullinated proteins are associated with HLA ‘shared epitope’ alleles, and autoimmunity to at least one antigenic sequence, the CEP-1 peptide from citrullinated α-enolase (KIHAcitEIFDScitGNPTVE), shows a specific association with HLA-DRB1*0401, *0404, 620W PTPN22, and smoking. Periodontitis, in which Porphyromonas gingivalis is a major pathogenic bacterium, has been linked to RA in epidemiological studies and also shares similar gene/environment associations. This is also the only bacterium identified that expresses endogenous citrullinated proteins and its own bacterial PAD enzyme, though the precise molecular mechanisms of bacterial citrullination have yet to be explored. Thus, both smoking and Porphyromonas gingivalis are attractive etiological agents for further investigation into the gene/environment/autoimmunity triad of RA.