Sukkari dates seed improves type-2 diabetes mellitus-induced memory impairment by reducing blood glucose levels and enhancing brain cholinergic transmission: In vivo and molecular modeling studies

Cognitive decline is one of the serious complications associated with diabetes mellitus (T2DM) of type-2. In this reported work, the effect of aqueous sukkari dates seed extract (ASSE) was evaluated in T2DM-induced rats. T2DM was induced using intraperitoneal injection of nicotinamide and streptozocin (STZ) administration. The diabetic rats were then treated orally with 200 mg/kg and 400 mg/kg of dates seed extract for 30 days and results were compared with metformin-treated groups. The memory functions were assessed using three maze models. Glucose and insulin levels in the blood and acetylcholine, acetylcholinesterase brain homogenates were estimated. The results showed a significant reduction in transfer latency (TL) (p < 0.001) during the elevated plus maze (EPM) test. The novel object recognition (NOR) test revealed a longer exploration time (p > 0.05) with novel objects and a higher discrimination index (p > 0.05). The Y-maze test also showed a significant increase in the number of entries to the novel arm (p > 0.05) and the total number of entries in the trial (p > 0.01) as well as in test (p > 0.05) sessions. Reduction in blood glucose (p > 0.05) and improvement in blood insulin (p > 0.05) levels were also noted. Improvement in ACh levels (p > 0.001) with 400 mg/kg of ASSE and reduction in AChE (p > 0.001) with both doses of ASSE were also observed in the brain homogenates. The results of ASSE were found comparable with the metformin-treated rats. The estimation of phytochemical constituents displayed a significant presence of phenolic content. Further, molecular modeling studies showed ellagic acid, catechin, and epicatechin as the potential molecule interacting with GSK-3β, α-amylase, and AChE and may be responsible for observed bioactivity. In conclusion, ASSE has the ability to alleviate T2DM-related cognitive impairments.     

Post-Traumatic Epilepsy: Cellular Mechanisms and Implications for Treatment

Summary: Epilepsy complicates severe head trauma. Development of persistent seizures appears to correlate with the extent of trauma. Although early reports suggested that prophylactic administration of antiepileptic drugs would prevent epileptogenesis, controlled studies have failed to corroborate this assumption. Head trauma initiates a sequence of responses that includes altered blood flow and vasoregulation, disruption of the blood-brain barrier, increases in intracranial pressure, focal or diffuse ischemia, hemorrhage, inflammation, necrosis, and disruption of fiber tracts. The presence of an intracranial hematoma has a robust association with the development of post-traumatic epilepsy. Extravasation of blood is followed by hemolysis and deposition of heme-containing compounds into the neuropil, initiating a sequence of univalent redox reactions and generating various free radical species, including superoxides, hydroxyl radicals, peroxides, and perferryl ions. Free radicals initiate peroxidation reactions by hydrogen abstraction from methylene groups adjacent to double bonds of fatty acids and lipids within cellular membranes. Intrinsic enzymatic mechanisms for control of free radical reactions include activation of catalase, peroxidase, and superoxide dismutase. Steroids, proteins, and tocopherol also terminate per-oxidative reactions. Tocopherol and selenium are effective in preventing tissue injury initiated by ferrous chloride and heme compounds. Treatment strategies for prevention or prophylaxis of post-traumatic epilepsy must await absolute knowledge of mechanisms. Antioxidants and chelators may be useful, given the speculation that peroxidative reactions may be an important component of brain injury responses. However, potential treatment strategies involving -y-aminobutyric acid (GABA) agonists, NMDA receptor antagonists, and barbiturates need further scientific assessment.     

注射用奥拉西坦治疗颅脑损伤的随机、双盲、对照、多中心临床研究

目的 通过对注射用奥拉西坦与注射用吡拉西坦比较的临床研究,评价注射用奥拉西坦治疗颅脑损伤引起的神经功能缺失的临床疗效及安全性. 方法 本研究为随机、双盲、阳性药平行对照、多中心临床试验,收集自2006年9月至2009年1月珠江医院等5家医院收治的239例颅脑损伤和颅脑手术后患者,按照随机数字表法分为试验组(采用注射用奥拉西坦治疗,120例)和对照组(采用注射用吡拉西坦治疗,119例).比较2组治疗前后美国国立卫生研究院卒中量表(NIHSS)评分、GCS评分、肢体肌力分级、简易智能状态检查量表(MMSE)评分,观察2组的不良反应并进行心电图和实验室检查以了解其安全性. 结果 试验组和对照组NIHSS、GCS评分和肢体肌力分级治疗后较治疗前均有明显改善,差异有统计学意义(P＜0.05),但改善的程度二者差异无统计学意义(P＞0.05),且2组均无药物严重不良事件发生. 结论 注射用奥拉西坦与注射用吡拉西坦一样,在治疗颅脑损伤引起的神经功能缺失中疗效显著,安全性好.

Abstract：

Objective To evaluate the efficacy and safety of oxiracetam in the treatment of neurological deficits resulting from brain injury through the comparison of oxiracetam for injection and piracetam for injection in clinical trials. Methods A multiple-center, randomized, double-blind,parallel study was performed on 239 patients; these patients were divided into experimental group (oxiracetam for injection, n=120) and control group (piracetam, n=119). National institutes of health stroke scale (NIHSS), Glasgow coma scale (GCS), myodynamia grading, mini-metal state examination (MMSE) were employed to evaluate the therapeutic effects; electrocardiogram and laboratory examination were performed, and the side effects were also observed. Results The scores of NIHSS,GCS and myodynamia grading after treatment in the 2 groups were all significantly higher than those before treatment (P＜0.05); however, no significant differences on these scores were noted between the experimental group and control group (P＞0.05). No serious adverse events were noted in both groups.Conclusion Oxiracetam, the same as piracetam, is safe and effective in the treatment of neurological deficits secondary to brain injury.     

脑梗死患者血同型半胱氨酸与炎症因子及神经功能缺损相关性研究

目的探讨脑梗死(CI)患者血同型半胱氨酸(Hcy)与炎症因子及神经功能缺损的相关性。方法收集2015年2月至2016年3月就诊的首次发病的CI患者90例,为CI组;选取同期于健康体检中心体检的健康人群90例,为对照组(C组)。检测血清中Hcy、高敏C反应蛋自(hs-CRP)、肿瘤坏死因子(TNF-α)、白细胞介素(IL)-1β、IL-6及IL-10;记录患者临床神经功能缺损评分(CNDS)评分;分析Hcy与炎症因子、CNDS的相关性。结果与C组比较,CI组患者血清中Hcy[(23.57±8.64)μmol/L比(9.89±4.58)μmol/L]、hs-CRP[(4.32±1.41)mg/L比(0.69±0.31)mg/L]、TNF-α[(31.24±6.34)pg/ml比(6.15±2.59)pg/ml]、IL-1β[(1.31±0.25)pg/ml比(0.34±0.11)pg/ml]、IL-6[(15.62±3.59)pg/ml比(2.19±1.42)pg/ml]均显著升高,IL-10[(5.19±2.13)pg/ml比(15.12±3.42)pg/ml]显著降低,差异均有统计学意义(P<0.01)。根据CNDS评分标准,将CI组患者分为3个亚组,其中,CI轻度组23例,CI中度组36例,CI重度组31例;与C组比较,CI组3个亚组患者CNDS评分均显著升高(P<0.05)。相关性分析显示,Hcy与hs-CRP、TNF-α、IL-1β、IL-6呈正相关(Rs>0,P<0.05),与IL-10呈负相关(Rs<0,P<0.05)。血清中Hcy与CI轻度、中度患者的CNDS评分呈正相关(r=0.691、r=0.632,P<0.05),而重度患者CNDS评分与血清中Hcy无相关性(r=0.049,P>0.05)。结论 CI患者血清中Hcy与炎症因子及神经功能缺损具有相关性,可反应CI患者的炎症状态和病情的严重程度。     

案例教学法在神经病教学中的应用

案例教学法是根据教学目的和培养目标的要求，教师在教学过程中以案例为基本素材，把学生带入具体的问题情境中进行分析问题和解决问题，培养学生运用理论知识并形成技能、技巧的一种方法．阐述了神经病学教学中导入病例教学法尝试所获得的成功与经验，认为开展病例导入教学是启迪学生的临床思维、培养学以致用的能力的有效途径．     

急性脑卒中患者早期综合康复治疗的临床研究

目的探讨早期综合康复治疗对脑卒中患者神经功能缺损、运动功能及日常生活活动能力（ADL）的影响。方法72例急性脑卒中患者随机分为康复组及对照组，康复组在采用常规药物治疗同时，进行早期综合康复治疗；对照组仅采用常规药物治疗。治疗前后的运动功能和日常生活能力（ADL）分另q用Fugl-meyer assessment（FMA）和改良的Barthel指数评定。结果治疗后康复组患者神经功能缺损积分、运动功能和ADL的改善程度明显优于药物治疗组，两组的变化均数相比。差异具有显著性（P〈0．05）。结论急性脑卒中患者早期综合康复治疗与单纯药物治疗相比，在降低其神经功能缺损积分，提高运动功能、ADL的积分上效果更好。     

缺血修饰白蛋白在缺血性脑卒中早期诊断中的临床应用研 究简

目的 观察缺血性脑卒中患者血清中缺血修饰白蛋白（IMA）的动态变化,并探讨其相关的临床意义.方法 选择2012年3月～2013年6月深圳市南山区人民医院（以下简称“我院”）收治的缺血性脑卒中患者42例为缺血性脑卒中组,根据NIHSS评分将其分为轻度（n=12）、中度（n=16）、重度（n=14）神经功能受损组,选取同期我院体检中心健康体检者40例为对照组.使用比色法测定IMA的表达情况.结果 缺血性脑卒中组IMA表达情况与对照组比较,差异有统计学意义（P＜0.05）;入院3、6、12、24、48 h时缺血性脑卒中组患者血清中IMA的表达水平相比较,差异均有统计学意义（均P＜ 0.05）;轻度、中度、重度神经功能受损组IMA水平分别为（59.8±5.6）、（49.9±4.8）和（42.8±3.7） U/mL,各组之间差异有统计学意义（P＜0.05）.结论 血清IMA水平的变化可以作为缺血性脑卒中的早期诊断指标,同时血清IMA水平的高低可以反映出患者神经功能损伤的严重程度.     

血清同型半胱氨酸与急性脑梗死的相关研究

目的：探讨急性脑梗死患者血清同型半胱氨酸（Hcy）水平变化,并分析其与神经功能缺损程度的关系.方法：检测急性脑梗死患者280例和对照组200例的血浆Hcy水平,采用美国国立卫生院制订的标准（NIHSS评分）对脑梗死神经功能缺损程度进行评定,对血浆Hcy与急性脑梗死的神经功能缺损相关性进行分析,线性回归分析危险因素GLU,TG,TC,HDL,LDL,Hcy与急性脑梗死的关系.结果：急性脑梗死患者血浆Hcy水平高于对照组,血清Hcy水平与NIHSS评分呈正相关（r=0.430,P＜0.01）,Hcy是急性脑梗死的危险因素.结论：脑卒中患者血清Hcy水平升高,血清Hcy水平可反映脑卒中病情的严重程度,高Hcy血症是脑卒中的独立危险因素.     

黄体酮对脑梗死大鼠脑损伤程度及神经功能的影响

目的 研究黄体酮对脑梗死体积及行为学的影响,评价其对脑梗死大鼠的治疗价值.方法 按随机数字表法将健康成年雄性Sprague-Dawley大鼠分为4组,即假手术组、模型组、溶剂治疗组和黄体酮治疗组.后3组采用线栓法制作大脑中动脉栓塞大鼠模型,假手术组只分离暴露血管、不结扎动脉、不插入尼龙鱼线;黄体酮治疗组造模成功后腹腔注射黄体酮,溶剂治疗组给予等体积的环糊精溶液治疗.分别于脑梗死后1d、2d、3d用Zea-Longer评分评价大鼠神经功能的缺损程度,并于脑梗死后3d通过TTC染色检测脑梗死体积.结果 Zea-Longer评分显示,造模前所有大鼠均没有神经功能缺损症状,评分为0.成模后,除假手术组外,其余大鼠均有不同程度的神经功能缺损;黄体酮治疗组大鼠[(3.00±0.63)分,(2.83±0.75)分,(2.00±0.89)分]在脑梗死后1d、2d、3d神经功能评分低于模型组[(4.00±0.89)分,(3.83±0.75)分,(3.16 ±0.75)分]及溶剂治疗组[(3.67±1.21)分,(3.50±1.05)分,(2.83±0.76)分],差异有显著性(P＜0.05).TTC染色表明,脑梗死体积在模型组[(23.74±4.48)％]与溶剂治疗组[(24.42±7.07)％]均比较大,且二者比较差异无统计学意义(P＞0.05);经黄体酮治疗后[(15.03±3.75)％]脑梗死体积明显缩小,较模型组与溶剂治疗组差异均有显著性(P＜0.05).结论 黄体酮治疗可以显著减小脑梗死体积并明显促进脑梗死大鼠神经功能的恢复,其对脑梗死大鼠动物模型具有很好的治疗价值.     

大脑中动脉狭窄患者侧枝循环开放相关因素分析及其对预后的影响

目的 评估大脑中动脉患者的侧枝循环状况,进一步探讨大脑中动脉狭窄患者的相关影响因素及其对预后的影响.方法 选择住院患者经头颅磁共振成像（MRI）及磁共振血管成像（MRA）确诊的单侧大脑中动脉中-重度狭窄（其为责任血管）的急性脑梗死患者60例,采用经颅多普勒（TCD）评估侧枝循环,分为侧枝循环开放组及未开放组各30例,对患者的相关影响因素及NIHSS评分进行相关性分析.结果 大脑中动脉狭窄的急性脑梗死患者侧枝循环开放组与未开放组卒中量表（NIHSS）评分差异有统计学意义（P＜0.05）;其侧枝循环开放情况与冠心病、年龄、糖尿病、吸烟、饮酒无相关性（P＞0.05）,而与高血压病、高脂血症、高同型半胱氨酸血症及性别有相关性（OR =0.145、0.226、6.507、4.164,P＜0.05）.结论 大脑中动脉狭窄患者侧枝循环的建立与开放及多种缺血性脑血管病的危险因素有一定相关性.