黄疸、肝昏迷为主要临床表现的出血热血液净化治疗

目的：探讨出血热肝损害为主的黄疸、肝昏迷联合血液净化治疗的作用。方法：在内科综合治疗基础上同时应用联合血液净化进行治疗。结果：在总胆红素、ALT、AST、BUN、肌酐比较,差异有统计学意义（P〈0.01）;在肝性脑病的清醒方面也有明显的效果。结论：出血热肝损害为主的黄疸、肝昏迷联合血液净化治疗有很好的疗效,能清除体内许多有害物质,同时补充机体需要的物质,出血热以肝脏损伤为主的黄疸及肝性脑病,应把联合血液净化作为治疗的首选方法。     

依达拉奉和醒脑静治疗急性一氧化碳中毒98例疗效观察

目的：研究依达拉奉和醒脑静合用治疗急性一氧化碳中毒（ACOP）的疗效及其预防迟发性脑病的作用。方法：将196例ACOP患者,分为对照组（常规治疗组）和治疗组（加用依达拉奉和醒脑静注射液）,治疗前、后观察两组疗效及迟发性脑病发生率。结果：治疗组临床疗效明显高于对照组,迟发性脑病发生率明显低于对照组,两组间差异有统计学意义（P〈0.05）。结论：依达拉奉和醒脑静合用可以明显缩短ACOP患者的意识障碍时间,显著提高疗效,有效减少迟发性脑病的发生率。     

米氮平治疗伴发抑郁的皮质下动脉硬化性脑病疗效分析

目的观察抗抑郁治疗对皮质下动脉硬化性脑病伴发抑郁患者的抑郁症状、神经功能缺损及日常生活能力的改善情况。方法 110例患者随机分为米氮平组(n=38),阿米替林组(n=36),对照组(n=36),各组均行常规神经营养药物和促智药物治疗。米氮平组同时口服米氮平30mg/次,1次/晚;阿米替林组同时口服阿米替林25mg/次,分早晚2次口服,最大剂量为100mg/d,总疗程均为12～24周,治疗期间不合并其他抗抑郁或精神障碍药,治疗前、治疗后1、2、4、8、12周及6个月,分别采用汉密顿抑郁量表评定患者的抑郁症状。于治疗前及治疗后12周、6个月进行神经功能缺损和日常生活能力评定。并于6个月对各组患者并发症及预后进行评定。结果①米氮平组在治疗第1、2、4、8、12周和6个月时,汉密顿抑郁量表得分均明显低于治疗前及对照组(P<0.05),阿米替林组在治疗后第2、4、8、12周及6个月时,汉密顿抑郁量表得分低于治疗前及对照组(P<0.05)。②米氮平组及阿米替林组在治疗后12周、6个月时,神经功能缺损评分均明显低于治疗前及对照组(P<0.05),日常生活能力得分明显高于治疗前及对照组(P<0.05)。③治疗期间米氮平导致口干、便秘、视力模糊、恶心、呕吐、心电图异常、脑卒中、心血管事件的发生率明显少于阿米替林治疗组(P<0.05)。④各组治疗后并发症及预后比较:对照组肺部感染、尿路感染、脑卒中、心血管事件的发生率高于米氮平治疗组、阿米替林治疗组(P<0.05),其死亡率也明显增高(P<0.05)。结论米氮平能有效改善皮质下动脉硬化性脑病伴抑郁的症状,副作用少,安全可靠。     

CT对新生儿缺血缺氧性脑病的诊断价值

目的通过对54例经临床确诊的缺血缺氧性脑病新生儿CT表现进行分析,正确认识CT诊断HIE的作用,以指导临床治疗及愈后评估。方法对有围产期窒息史,且有临床症状的54例缺血缺氧性脑病患儿进行CT扫描,将其CT表现特征进行归纳。结果所有病例均出现了低密度灶。结合国内外文献按受累脑范围分轻、中、重度,其中轻度16例、中度23例、重度15例,HIE易并发颅内出血,其中以蛛网膜下腔出血多见。结论 CT检查对HIE的诊断有较大作用,对其临床治疗及预后判断有重要价值。     

单唾液酸四己糖神经节苷脂治疗新生儿缺氧缺血性脑病临床疗效

目的探讨单唾液酸四己糖神经节苷脂（GM1）治疗新生儿缺氧缺血性脑病的临床疗效。方法：48例新生儿缺氧缺血性脑病患儿,随机分为治疗组25例,对照组23例,两组均采用常规治疗,治疗组在常规治疗基础上加用GM1静脉滴注,1次／天,20mg／次,10～14天为一疗程。比较两组患儿治疗前后新生儿神经行为评分（NBNA）及CT测量值。结果：两组患儿治疗5～7天和治疗10～14天NBNA评分有显著差异．且治疗组评分明显高于对照组。两组患儿治疗前和治疗一疗程CT值均无显著差异（P〉0．05）,出生后28天治疗组CT值明显高于对照组（P〈0．05）。结论：GM1治疗新生儿缺氧缺血性脑病疗效显著,未见不良反应发生。     

东莨菪碱对兔肝性脑病模型的保护作用研究

目的:研究东莨菪碱对兔肝性脑病模型的保护作用。方法:采用肝叶大部分切除术联合十二指肠注入复方氯化铵溶液的方法复制肝性脑病模型兔28只,于第2次注入复方氨化铵后分为4组,即空白对照组(5%葡萄糖注射液),东莨菪碱组(0.015mg·kg-1)、复方谷氨酸钠组(0.5g·kg-1)及合用组(2药同剂量),进行一次性耳缘静脉给药后,观察各组兔给药后抽搐情况、存活时间和给药前与给药10min后的血氨水平变化。结果:与空白对照组比较,东莨菪碱组、复方谷氨酸钠组和合用组兔抽搐潜伏期和存活时间延长、抽搐持续时间缩短、血氨降低(P<0.05或P<0.01),其中合用组保护作用最显著。结论:东莨菪碱与复方谷氨酸钠合用对肝性脑病具有协同保护作用。     

门冬氨酸鸟氨酸联合乳果糖治疗肝硬化并发肝性脑病临床观察

目的观察应用门冬氨酸鸟氨酸联合乳果糖治疗肝硬化所并发肝性脑病的疗效。方法 68例肝性脑病患者被随机分为乙酰谷酰胺治疗组17例、门冬氨酸鸟氨酸治疗组28例、门冬氨酸鸟氨酸联合乳果糖治疗组23例。结果 25%（7/28）门冬氨酸鸟氨酸治疗组患者,21.7%（5/23）联合治疗组患者死亡,而47.1%（8/17）乙酰谷酰胺治疗组患者死亡。死亡率有差异性P〈0.05。结论在基础治疗的前提下,应用门冬氨酸鸟氨酸治疗肝性脑病在降低血浆氨、减少死亡率、改善肝肾功能等方面有一定效果,联合乳果糖后可明显减少死亡率,减少并发症的发生。     

Oligodendrocyte/myelin injury and repair as a function of the central nervous system environment

Multiple sclerosis is a chronic neurologic disorder considered to result from relatively selective immune mediated injury of central nervous system (CNS) myelin and/or its cell of origin, the oligodendrocyte (OGC). Constituents of both the innate and adaptive immune systems are potential contributors to this process. Endogenous (microglia) and infiltrating (macrophages, dendritic cells) constituents of the innate immune system serve as sensors of events occurring within the CNS; their response to such events underlies the extent of their interaction (chemoattraction, antigen presentation) with the components of the adaptive immune system (alphabeta T cells, B cells) and ultimately the extent of the resultant inflammatory response. Constituents of both the innate and adaptive immune system can serve as effectors of tissue injury. The susceptibility of specific types of neural cells to injury further reflects the extent to which immune mediators modulate expression of crucial molecules (adhesion molecules, receptors) involved in effector-target interactions. Ongoing interactions between the constituents of the immune system themselves and between these constituents and neural cells are important determinants of disease recurrence and/or progression. Conversely, these interactions also impact on the mechanisms involved in target protection and repair.     

The expression of nNOS, iNOS and nitrotyrosine is increased in the rat cerebral cortex in experimental hepatic encephalopathy

The changes in the distribution and amount of nitric oxide (NO) synthases (nNOS and iNOS) and the appearance of nitrotyrosine (NT) in the rat cerebral cortex were investigated following portacaval anastomosis (PCA), an experimental hepatic encephalopathy (HE) model. One month after PCA, rats showed more neurones immunoreactive to nNOS than did control animals. At 6 months post PCA, the number of neurones expressing nNOS had again increased and the intensity of the immunoreactions was stronger. Immunohistochemical analysis also showed that iNOS was increasingly expressed in pyramidal-like cortical neurones and in perivascular astrocytes from 1 to 6 months post PCA. In addition, a significant increase in cerebral iNOS concentration, at both post-PCA periods, was determined by Western blotting. The iNOS induction appears to be correlated with the length of the post-PCA period. PCA also induced the expression of NT, a nitration product of peroxynitrite. NT immunoreactivity was found in pyramidal-like cortical neurones. At 6 months, NT immunoreactivity was also evident in perivascular astrocytes, which was concomitant with a significant increase in NT protein level. PCA therefore not only increases the expression of nNOS but also induces the expression of iNOS and NT in both neurones and astrocytes. Taken together, these findings indicate that the induction of iNOS in pyramidal neurones and cortical astrocytes 6 months after PCA contributes to the generation of NT, and demonstrate the clear participation of NO in the pathogenic process of HE in this model.     

Oligodendrocyte progenitor cell (OPC) transplantation is unlikely to offer a means of preventing X-irradiation induced damage in the CNS

Oligodendrocyte lineage cells [oligodendrocytes and their parent cells, the oligodendrocyte progenitor cells (OPCs)] are depleted by X-irradiation and progenitor cell transplantation has been proposed as a therapeutic strategy to counteract radiation induced myelopathy. Previous studies have demonstrated that oligodendrocyte progenitor cell (OPC) depletion is a prerequisite for establishing transplanted OPCs in normal tissue. One can therefore predict that the extent and timing of OPC depletion and regeneration following X-irradiation will be crucial factors in determining the feasibility of this therapeutic approach. To address this issue, we have examined the time course of OPC depletion and regeneration following a range of X-irradiation doses (5 to 40 Gy), and its relationship to establishing transplanted OPCs in X-irradiated tissue. Doses above 10 Gy resulted in rapid death of OPCs. With doses up to 20 Gy, surviving X-irradiated OPCs were capable of robust regeneration, restoring normal densities within 6 weeks. Transplanted OPCs could only be established in tissue that had been exposed to > or =20 Gy. Since 20 Gy is close to the ED50 for radiation necrosis, our findings demonstrate the limitation of OPC replacement strategies.