抑郁症患者血清脑源性神经营养因子、神经元特异性烯醇化酶和S-100B的表达及相关性

目的观察抑郁症患者血清中脑源性神经营养因子(BDNF)、神经元特异性烯醇化酶(NSE)和S-100B蛋白(S-100B)的表达水平及相关性。方法确诊为抑郁症患者的血清标本82例为观察组,16例体检证实为健康成人血清标本为对照组,检测两组血清中BDNF、NSE和S-100B的表达。结果两组血清中BDNF、NSE和S-100B的表达差别显著(P<0.05)。观察组BDNF、NSE和S-100B的表达与病程有关,BDNF的表达与首发抑郁症有关。三者均与性别和年龄无相关性。线性相关分析显示观察组BDNF和S-100B正相关。结论抑郁症患者血清中BDNF低表达、NSE和S-100B高表达与病变的形成和进程有关,BDNF和S-100B可能具有协同作用。     

脑梗死后患者认知障碍与血清脑源性神经营养因子和神经元特异性烯醇化酶表达的关系

目的观察脑梗死后认知障碍与血清中脑源性神经营养因子(BDNF)和神经元特异性烯醇化酶(NSE)表达的关系。方法 30例无明显器质性病变的成人血清作为对照组,106例脑梗死的患者作为观察组,依据蒙特利尔认知评估(Mo CA)评分情况将观察组分为认知障碍组76例和非认知障碍组30例,同时应用酶联免疫吸附(ELISA)法检测两组血清中BDNF和NSE的表达。结果认知障碍组血清BDNF的表达明显低于非认知障碍组,血清NSE的表达明显高于非认知障碍组(均P<0.05)。线性相关分析显示观察组认知障碍评分与BDNF和NSE的表达有一定相关性。结论脑梗死患者血清中BDNF和NSE的表达异常,部分患者存在认知障碍,其与BDNF和NSE的表达具有一定的相关性。     

康复训练对脑梗死患者神经功能转归及血清神经元特异性烯醇化酶、脑源性神经营养因子含量的影响

目的观察不同时期介入康复训练对脑梗死患者神经功能转归及血清神经元特异性烯醇化酶(NSE)、脑源性神经营养因子(BDNF)含量的影响。方法将150例急性脑梗死(ACI)患者随机分为早期康复组、非早期康复组及对照组,早期康复组患者在生命体征稳定且神经功能障碍停止进展48 h进行早期规范化的康复训练,非早期康复组在生命体征稳定、神经功能障碍停止进展7 d且头颅影像提示脑梗死周围水肿区处于吸收消退期进行规范化康复训练,对照组患者仅给予常规内科治疗,不进行规范化的康复训练。3组患者药物治疗基本相同。分别采用临床神经功能缺损程度评分、Barthel指数(BI)评分对患者入院时、发病14 d及发病2个月的疗效进行评定,并同时检测入院时、发病7、14 d、2个月的血清NSE、BDNF含量变化。结果 3组在入院时临床神经功能缺损程度和BI评分比较无明显差异(P>0.05),发病14 d、2个月3组比较有明显差异(P<0.05);3组血清NSE含量入院时、发病7 d及2个月比较无明显差异(P>0.05),发病14 d早期康复组血清NSE下降明显(P<0.05);3组血清BDNF含量入院时及发病2个月比较无明显差异(P>0.05),发病7 d、14 d比较血清BDNF升高明显,与其他两组有明显差异(P<0.05)。结论早期规范化的康复训练可促进ACI患者神经功能的恢复,并不会加重神经损伤,恢复的机制可能与促进ACI患者BDNF的表达有关。     

高血压脑出血病人血清S100B蛋白和神经元特异性烯醇化酶的变化及意义

目的 探讨高血压脑出血病人血清S100B蛋白和神经元特异性烯醇化酶（NSE）浓度变化及其与出血量、脑组织损伤情况及预后之间的关系.方法 高血压脑出血病人52例,对照组30例.测定脑出血病人起病第1、3、7天血清S100B蛋白和NSE浓度,分析浓度的变化与出血量、格拉斯哥预后评分（GOS）之间的关系.结果 脑出血组血清S100B蛋白和NSE浓度明显高于对照组（P＜0.001）,与出血量呈正相关（P＜0.05）,其浓度的变化与预后有关.结论 高血压脑出血病人血清S100B蛋白和NSE浓度变化能在一定程度上反映出血量的大小、脑组织损伤的情况,有助于评估病人预后.     

神经元特异性烯醇化酶和S—100蛋白在脑血管疾病？…

脑脊液或血清中的神经元特异性烯醇化醇和Ｓ－１００蛋白是脑组织损伤后的两种生化标记物,具有较高的敏感性和特异性。前者主要存在于神经细胞和神经内分泌细胞内,后者主要存在于神经胶质细胞内。脑组织损伤后通过对它们的测定,不仅可以对神经经细胞和神经胶质细胞的损伤程度提供定量信息,而且也是评价疗效、估计预后的一个重要参数。     

奥拉西坦对脑梗死患者血清S100B、神经元特异性烯醇化酶和vWF的影响

目的观察奥拉西坦对脑梗死患者的治疗效果及血清中S100B、神经元特异性烯醇化酶(NSE)和v WF的变化。方法 114例脑梗死患者随机分为两组,对照组(57例)应用常规治疗,并加用丁苯酞胶囊。观察组57例在上述基础上加用奥拉西坦注射液,治疗10 d后观察疗效,并关注血清中S100B、NSE和v WF的变化。结果两组治疗前美国国立卫生研究院脑卒中量表(NIHSS)评分无统计学差异,治疗10 d后,两组NIHSS评分均下降,但是观察组下降值明显高于对照组。两组治疗10 d后血清中S100B、NSE和v WF的表达均下降,但是观察组S100B、NSE和v WF的下降值明显高于对照组。结论奥拉西坦对脑梗死的临床疗效明显,且能有效下调血清中S100B、NSE和v WF表达,保护神经细胞,优化体液环境。     

外周血S-100B蛋白及神经元特异性烯醇化酶水平与进展性脑梗死的相关性研究

目的探讨外周血S-100B蛋白及神经元特异性烯醇化酶(NSE)水平与进展性脑梗死的关系。方法选择2011年1月—2013年1月贵港市人民医院收治的急性脑梗死患者83例,根据美国国立卫生院卒中量表(NIHSS)评分将患者分为进展组(NIHSS评分≥4分)35例和非进展组(NIHSS评分<4分)48例。两组患者均于治疗第1天、第3天、第7天及第14天采集肘静脉血检测S-100B蛋白和NSE水平,并分析进展组患者NIHSS评分与外周血S-100B蛋白及NSE水平的关系。结果治疗第1天两组患者血清S-100B蛋白及NSE水平比较,差异无统计学意义(P>0.05);治疗第3天、第7天及第14天进展组患者血清S-100B蛋白及NSE水平高于非进展组(P<0.05)。进展组患者NIHSS评分与血清S-100B蛋白和NSE水平呈正相关(r值分别为0.373、0.384,P值分别为0.000、0.000)。结论外周血S-100B蛋白及NSE水平可反映急性脑梗死患者脑损伤程度,动态监测外周血S-100B蛋白及NSE水平有助于早期判断进展性脑梗死的发生。     

老年颅脑损伤患者CT图像评分与血清中髓鞘碱性蛋白、神经元特异性烯醇化酶和S100B蛋白表达的关系

目的观察颅脑损伤老年患者头颅CT图像评分与血清中髓鞘碱性蛋白(MBP)、神经元特异性烯醇化酶(NSE)和S100B蛋白(S100B)的关联性。方法 98例颅脑损伤的老年患者,均于伤后24 h内行头颅CT检查,计量CT图像评分,同时检测伤后24 h内空腹静脉血中MBP、NSE和S100B的含量。结果不同CT图像评分分组MBP、NSE和S100B表达差异显著,CT图像评分与格拉斯哥昏迷评分(GCS)具有负相关性,CT图像计分与MBP、NSE和S100B的表达均具有正相关性。结论老年人颅脑损伤后CT图像评分与MBP、NSE和S100B具有一定的相关性,因此早期积极检测MBP、NSE和S100B表达对诊断及治疗可能有重要价值。     

缺血性脑卒中患者血清中S100B、半乳糖凝集素-3和神经元特异性烯醇化酶的表达及意义

目的检测缺血性脑卒中患者血清中S100B蛋白(S100B)、半乳糖凝集素(Galectin)-3和神经元特异性烯醇化酶(NSE)的表达,关注其临床价值。方法 59例缺血性脑卒中患者作为观察组,30例经体检成年人血清标本作为对照组,应用酶联免疫吸附法检测两组中S100B、Galectin-3和NSE的表达。结果观察组血清中S100B、Galectin-3和NSE的表达量明显高于对照组,观察组血清中S100B、Galectin-3和NSE的表达量与梗死灶的体积及病变严重程度相关。相关分析显示S100B和NSE具有正相关性,而S100B和Galectin-3、Galectin-3和NSE的表达未见明显相关性。结论缺血性脑卒中患者血清中S100B、Galectin-3和NSE的表达升高,三者不仅可以促进疾病的形成,还对疾病的进展起一定作用。S100B和NSE可能具有一定的协同作用。     

脑卒中患者血清神经元特异性烯醇化酶变化及意义

用免疫学方法测定脑梗死和脑出血患者的血清神经元特异性烯醇化酶(N SE)水平,并与正常健康者进行对照。结果显示,脑梗死患者血清N SE(30.54±12.66)ng/m l,脑出血患者(31.30±13.78)ng/m l,均显著高于对照组的(13.89±6.76)ng/m l(P<0.05);脑梗死和脑出血患者发病后不同时期血清N SE有明显变化,N SE水平与脑损伤程度呈正相关,与病情转归及患者预后有明显关系。提示血清N SE水平是急性脑血管病所致脑损害较敏感的生化指标,可较早反映脑损伤程度,并与病情的严重程度及预后关系密切,有助于其早期诊断、指导临床和评价疗效。     

血清脑源性神经营养因子水平与缺血性卒中后抑郁的相关性

目的 探讨血清脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)与卒中后抑郁(post-stroke depression,PSD)的相关性.方法 前瞻性纳入90例缺血性卒中患者,入院后检测血清BDNF含量,采用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评定神经功能缺损,采用Barthel指数(Barthel index,BI)评定日常生活活动能力.6个月随访时采用17项汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)进行抑郁评定,≥17分为抑郁,＞24分为重度抑郁.结果 共40例患者(44.4％)发生PSD,轻度抑郁30例(33.3％),中度抑郁8例(8.9％),重度抑郁2例(2.2％).单变量分析显示,PSD组多发性梗死的患者比例(65.0％对32.0％;x2=9.723,P=0.002)、基线NIHSS评分[(7.05±4.25)分对(4.35±3.14)分;t=3.465,P =0.001]和出院时NIHSS评分[(5.43±3.02)分对(3.11±2.56)分;=3.944,P＜0.001]显著高于非PSD组,而受教育年限[(9.03±4.51)年对(13.45 ±5.02)年;=4.340,P＜0.001]、血清PDNF浓度[(16.754 ±4.451) pg/ml对(29.551 ±3.213)pg/ml;t =15.827,P＜0.001]以及出院时BI[(55.00±28.10)分对(83.11±27.11)分;=4.809,P＜0.001]显著低于非PSD组.多变量logistic回归分析显示,高血清BDNF水平是PSD的独立保护因素(优势比0.571,95％可信区间0.416 ～0.967;P=0.003).结论 高血清BDNF水平是PSD的独立保护因素.     

Alterations of brain-derived neurotrophic factor serum levels in patients with alcohol dependence

Background: Alcohol dependence is a chronic relapsing disorder characterized by repetitive alcohol drinking patterns and a loss of control over alcohol consumption. Recent studies have hypothesized that dysregulations in brain neurotrophic support regulated by neurotrophins may be involved in the vulnerability to dependence and in the brain damage caused by chronic alcohol consumption. The neurotrophin brain‐derived neurotrophic factor (BDNF) plays a pivotal role in neurodevelopment and in the maintenance of adult brain homeostasis through the regulation of neurogenesis and neuronal plasticity. The role of BDNF and its signaling in the mechanisms of alcohol dependence has been well documented in studies of animal models, but a few studies have been conducted in human peripheral tissues. On the basis of this rationale, we compared BDNF levels in both serum and plasma in alcohol‐dependent patients and healthy volunteers. Methods: Thirty‐seven patients with a principal diagnosis of alcohol dependence were recruited. In parallel, a control group of 37 unrelated volunteers matched for gender and age was enrolled. Serum and plasma BDNF levels were measured by ELISA. Results: A significant reduction in BDNF serum levels was observed in the patient group compared to healthy subjects (p = 0.028). On the contrary, no difference in BDNF plasma levels was evident between patients and controls. Conclusions: In conclusion, our data show an alteration of BDNF peripheral content in patients with alcohol dependence, suggesting the involvement of this neurotrophin in this psychopathology.     

血清脑源性神经营养因子预测急性缺血性卒中患者卒中后认知损害

目的:探讨血清脑源性神经营养因子（brain-derived neurotrophic factor, BDNF）与急性缺血性卒中患者卒中后认知损害（post-stroke cognitive impairment, PSCI）的相关性,并评估其对PSCI的预测价值。方法:前瞻性纳入2018年4月至2020年9月济宁医...     

急性脑梗死患者血清S100蛋白B及胶质纤维酸性蛋白的变化及其临床意义

目的 研究S100蛋白B(S100B)、胶质纤维酸性蛋白(GFAP)在急性脑梗死患者不同病程时期的水平变化规律,分析其在疾病发生发展中的临床意义.方法 检测急性发病不超过24小时的脑梗死患者不同时期血清中S100B、GFAP的水平变化,结合神经功能缺失程度,并通过前后自身对照,分析S100B、GFAP在疾病发生发展中的意义.结果 急性缺血性脑梗死患者血清中S100B、GFAP明显高于对照组.最初24小时内S100B的水平与第3～5天、7～10天神经功能缺失程度显著相关.结论 S100B水平与神经功能缺失程度相关,其在发病后24小时内的血清浓度可提示之后的神经功能缺损.S100B可作为监测急性脑梗死预后的标记物.     

血清BDNF,皮质醇以及血脂水平在阻塞性睡眠呼吸暂停低通气综合征患者中的变化研究

目的检测阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清脑源性神经生长因子(BDNF)、皮质醇和血脂水平的变化。方法设置OSAHS组(n=45)和健康对照组(n=30),测定并比较血清BDNF、皮质醇和血脂水平在两组间的差异;分析OSAHS患者中部分血清指标与呼吸暂停低通气指数(AHI)的相关性。结果 OSAHS组和健康对照组在血压、AHI、最低血氧饱和度(LSa O2)上有统计学差异(P0.05);OSAHS组血清BDNP水平较对照组低(P=0.0008),而皮质醇、TC、LDL-C水平要高(P0.05);血清BDNP、LDL-C在OSAHS轻度组、中度组和重度组间也具有统计学差异(P0.05);OSAHS患者中血清BDNP与AHI呈负相关(r=-0.04,P=0.015),与LDL-C呈正相关(r=0.12,P=0.041)。结论 OSAHS患者血清BDNP、皮质醇和部分血脂指标的水平发生改变,BDNP和LDL-C或可作为OSAHS严重程度的参考指标。     

Clinical significance of serum neuron-specific enolase in patients with adult T-cell leukemia

The present study examines the clinical significance of serum neuron-specific enolase (NSE) in patients with adult T cell-leukemia (ATL). Serum NSE values were measured using a radioimmunoassay in 35 patients (acute type, n = 15; lymphoma type, n = 10; chronic type, n = 10) and in 7 controls carrying T lymphotropic virus type-1 (HTLV-1). Serum NSE values >10 ng/mL were detected in 9 of 15 patients with acute type (60%), 5 of 10 with lymphoma type (50%), and in one of 10 patients with chronic type (10%) ATL, but in none of the HTLV-1 carriers. Contrary to previous findings demonstrating that 20% of patients with non-Hodgkin's lymphoma (NHL) had positive serum NSE, the frequency of a high NSE value in patients with acute and lymphoma type ATL was much higher (60% and 50%, respectively). The serum NSE value positively correlated with serum thymidine kinase activity (TK) and serum soluble interleukin-2 receptor (sIL-2R) levels (P < 0.04 and P < 0.01, respectively). Serum NSE values at the initial diagnosis were adversely related to overall survival time according to the log-rank test (P < 0.02). Pathological examinations demonstrated that both patients with anaplastic large cell lymphoma type ATL had cytoplasmic NSE and CD30 markers on cell membranes. These findings suggest that serum NSE is partially produced by ATL cells and that ATL tumor cells seem preferentially produce NSE compared with other NHL cells. Serum NSE may be a novel marker of disease aggressiveness as well as a prognostic factor for ATL.     

2型糖尿病患者血清脑源性神经营养因子的变化及其临床意义

目的 探讨T2DM患者血清脑源性神经营养因子（BDNF）与APN、瘦素（LP）、胰岛素抵抗指数（HOMA-IR）和ISI的相关性. 方法 选取T2DM组102例和健康对照（NC）组97名,将T2DM组进一步分为体重正常（N-OB）亚组53例和超重（OB）亚组49例.采用RT-PCR检测BDNF表达水平.对T2DM组BDNF表达水平的相关因素行Pearson相关性及多因素线性回归分析. 结果 OB亚组BMI、TG、APN、LP和BDNF较N-OB亚组、NC组低（P＜0.05或P＜0.01）.多因素线性回归分析显示,仅LP进入回归方程. 结论 T2DM患者BDNF表达水平降低,与LP呈正相关.     

Decreased plasma brain-derived neurotrophic factor levels in patients with alcohol dependence

BACKGROUND: Many reports have suggested possible relationships between brain-derived neurotrophic factor (BDNF) and alcohol dependence. A protective effect of BDNF against ethanol-induced cell damage has been suggested, and this effect may contribute to the development or maintenance of alcohol dependence. This study was carried out in order to verify the significance of BDNF in alcohol dependence. METHODS: Peripheral BDNF levels were measured in alcohol-dependent patients and control subjects using an enzyme-linked immunosorbent assay. A physician's interview and standardized questionnaire were used to obtain information regarding each patient's history of alcohol consumption. RESULTS: The mean BDNF level was lower in the alcohol dependence group (389.5 +/- 501.7 pg/ml) than in the normal controls (822.5 +/- 420.7 pg/ml) by analysis of covariance (ANCOVA) (F = 25.79, p < 0.01). The mean BDNF level was lower in the alcohol-dependent patients with a positive family history of alcohol dependence (247.6 +/- 289.2 pg/ml) than in those with a negative family history of alcohol dependence (583.9 +/- 652.8 pg/ml) by ANCOVA (F = 6.51, p = 0.01). The BDNF levels did not correlate significantly with any of the variables analyzed in this study, including Beck depression inventory, state and trait anxiety inventory (STAI-S and T), and various drinking behaviors. CONCLUSIONS: Changes in the levels of BDNF might play a role in the pathophysiology and inheritance of alcohol dependence.