依达拉奉对急性脑出血患者脑水肿及自由基的影响

目的观察依达拉奉对急性脑出血患者脑水肿及自由基的影响。方法 72例急性脑出血患者随机分为对照组和观察组,对照组采用常规对症治疗,观察组加用依达拉奉治疗。观察治疗前后脑水肿面积、神经功能及自由基改善情况。结果 2组治疗后脑水肿面积显著小于治疗前,观察组治疗后脑水肿面积显著小于对照组(P0.05)。观察组治疗后神经功能缺损评分、GCS评分及APACHE?Ⅱ评分显著优于对照组(P0.05)。观察组治疗后7dNO、LPO水平显著低于对照组,SOD、GSHPX水平显著高于对照组(P0.05)。结论依达拉奉治疗急性脑出血可显著缩小脑水肿面积,促进神经功能恢复。     

依达拉奉对局灶性脑缺血大鼠神经功能恢复及海马病理形态学改变的影响

目的 探讨大鼠局灶性脑缺血后神经功能恢复及海马病理形态学改变,评价依达拉奉的干预作用.方法 126只雄性SD大鼠随机分为3组:假手术组(A组,6只),生理盐水组(B组,MCAO后6h、12h、24h、48h、72h、5d、7d7时点,各6只),依达拉奉处理组(C组,同B组),术后即刻予以依达拉奉干预.行神经功能缺损评分测定;TTC染色观察脑梗死体积改变;用HE染色方法观察病理形态学改变.结果 术后进行神经缺损评分发现,由于麻醉和手术创伤的影响,假手术组术后出现6～24h神经功能减退.与假手术组相比,在6～24h时间段盐水组神经功能下降明显(P＜0.05).依达拉奉组神经功能明显好于盐水组(P＜0.05).术后7d盐水组和依达拉奉组神经功能基本恢复.同时,在依达拉奉组和盐水组中,缺血24h脑梗死体积最大;与盐水组相比,术后6～24h依达拉奉组脑梗死体积明显减小(P＜0.05).HE染色显示术后6h在脑缺血区神经元细胞无明显改变,6h后缺血区脑组织逐渐出现肿胀与坏死;在依达拉奉组,脑水肿和神经元坏死病理损害明显较轻,在假手术组,脑组织无明显改变.结论 依达拉奉具有改善神经功能缺损、缩小脑梗死体积和减轻缺血性病理损害程度的作用;研究还提示依达拉奉对缺血性脑卒中早期神经功能恢复具有十分重要的临床意义.     

丁苯酞软胶囊联合依达拉奉注射液治疗急性脑梗死的效果观察

目的：观察丁苯酞软胶囊联合依达拉奉注射液治疗急性脑梗死的疗效。方法急性脑梗死患者60例随机分为依达拉奉组和联合治疗组,每组30例。2组均采用相同的基础治疗和对症处理。依达拉奉组静滴依达拉奉注射液30mg＋生理盐水150mL,2次／d,连用14d;联合治疗组给予丁苯酞软胶囊空腹口服,2粒（0.2g）／次,3次／d,静滴依达拉奉注射液30mg＋生理盐水150mL,2次／d,均连续用14d。分别在治疗前及治疗第15天进行MRI检查评估患者脑梗死体积,并进行神经功能缺损评分（NIHSS）。结果治疗第15天时,联合治疗组脑梗死体积显著小于依达拉奉组（P＜0.01）,2组NIHSS评分与治疗前比较均明显降低,差异有统计学意义（P＜0.05）;2组NIHSS评分比较,联合治疗组明显低于依达拉奉组（P＜0.05）;显效率明显高于对照组,差异有统计学意义（P＜0.05）;2组不良反应发生率比较差异无统计学意义（P＞0.05）。结论丁苯酞软胶囊联合依达拉奉注射液治疗急性脑梗死,可明显缩小脑梗死体积,显著改善神经功能,减少致残率,疗效确切,无严重不良反应,值得临床推广应用。     

亚低温联合依达拉奉治疗脑出血疗效观察

目的 观察亚低温联合依达拉奉治疗脑出血疗效。方法 对40例患者行亚低温联合静点依达拉奉治疗，观察治疗前后神经功能、脑血肿脑水肿体积的变化，并与对照组比较。结果 治疗组神经功能恢复、血肿及水肿体积较对照组明显减少。结论 亚低温联合依达拉奉能促进脑出血患者神经功能的恢复，促进血肿吸收抑制水肿形成。     

依达拉奉治疗重型颅脑外伤的疗效观察

目的观察依达拉奉对重型颅脑外伤的治疗效果。方法60名急性重型颅脑损伤病人随机分成依达拉奉治疗组（n=30）和对照组（n=30），观察病人颅内压、头颅CT变化和远期疗效。结果依达拉奉治疗组伤后10d内颅内压显著升高和重度脑水肿者均较对照组明显减少；依迭拉奉组10d后格拉斯哥计分及伤后3个月恢复良好率显著高于对照组。结论依达拉奉可以降低急性重型颅脑外伤病人颅内压的升高幅度，缩短昏迷时间，降低伤残率，促进病人神经功能恢复，改善预后。     

依达拉奉对脑出血患者脑水肿及预后的影响

目的探讨依达拉奉对脑出血患者脑水肿及预后的影响。方法选取我院急性脑出血患者82例,随机分为治疗组与对照组各41例,对照组给予常规性治疗,治疗组在常规治疗的基础上加用依达拉奉注射液,疗程3周。2组患者治疗前、治疗后第5天、第14天、第28天做头部CT检查,比较2组患者脑水肿体积以及神经功能缺损评分(NIHSS)的变化情况。结果治疗组与对照组患者在治疗后第14天和第28天脑水肿的体积均发生明显缩小,在体积缩小程度方面,治疗组明显高于对照组,2组间差异具有统计学意义(P0.05)。与治疗前比较,治疗组与对照组患者在治疗后的第28天NIHSS评分均明显降低,治疗组患者降低幅度明显高于对照组,2组间差异具有统计学意义(P0.05)。结论早期使用依达拉奉能够使脑出血患者的脑水肿程度减轻,促进脑神经功能的恢复,并能够改善预后,无明显不良反应发生。     

依达拉奉联合七叶皂苷钠治疗脑出血的疗效观察

目的研究依达拉奉联合七叶皂苷钠治疗脑出血的疗效。方法 58例脑出血患者随机分为实验组与对照组各29例。实验组采取依达拉奉联合七叶皂苷钠治疗,对照组仅采用七叶皂苷钠治疗,比较2组治疗效果,通过神经功能缺损程度评分评估神经功能。结果 2组治疗后脑水肿、脑血肿均显著降低,实验组脑水肿面积、脑血肿体积与对照组相比差异均有统计学意义(P0.05);2组治疗前后NIHSS评分相比差异具有统计学意义(P0.05),组间比较差异具有统计学意义(P0.05);实验组治疗总有效率为93.3%,对照组为62.1%,2组比较差异有统计学意义(P0.05)。结论依达拉奉与七叶皂苷钠联合治疗脑出血疗效显著,且可降低对患者的神经功能损伤,值得临床推广应用。     

尤瑞克林联合依达拉奉治疗进展性脑梗死疗效观察

目的观察尤瑞克林联合依达拉奉治疗进展性脑梗死的临床疗效。方法进展性脑梗死85例随机分为尤瑞克林联合依达拉奉治疗组(n=45例)和对照组(n=40例),2组均给予抗凝、抗血小板、活血化瘀、神经康复等治疗。治疗组同时给予0.9%生理盐水100mL+0.15PNAU尤瑞克林静滴,1次/d,连用7～14d,给予依达拉奉针30mg+糖水或盐水100mL静滴,2次/d,连用2周,于治疗前后评定神经功能缺损程度(NIHSS)、日常生活活动能力(ADL)和临床疗效。结果治疗后2组患者的神经功能缺损、日常生活活动能力均有改善,与对照组相比差异有统计学意义(P<0.01)。治疗组临床有效率91.11%,近期治愈率55.55%,显著高于对照组(P<0.01),且无明显不良反应。结论尤瑞克林联合依达拉奉治疗进展性脑梗死疗效较好,且无明显不良反应,值得进一步观察探讨。     

依达拉奉治疗急性重型颅脑创伤的临床研究

目的探讨依达拉奉对急性重型颅脑创伤的治疗作用及安全性。方法108例患者随机分为2组,依达拉奉组54例：常规治疗基础上加用依达拉奉治疗；依达拉奉30mg稀释后30min内静滴完,1次/12h,连续10d。对照组54例：采用常规治疗,不给予脑保护治疗。研究开始10d后,观测颅内压、头部CT变化、GCS,APACHE-Ⅱ评分及不良反应。结果给药组伤后10d内颅内压显著升高和重度脑水肿者比例均较对照组明显减少；且给药组GCS评分升高,APACHE-Ⅱ评分下降,组间差异具有显著性。结论早期应用依达拉奉治疗急性重型颅脑创伤,可以降低急性重型颅脑创伤患者颅内压的升高幅度,缩短昏迷时间,促进患者神经功能恢复,降低伤残率,促进患者神经功能恢复,改善预后,且副作用少,安全可靠。     

尤瑞克林联合依达拉奉治疗急性脑梗死的疗效及对炎症介质水平的影响

目的探讨尤瑞克林联合依达拉奉治疗急性脑梗死的临床效果以及治疗前后的炎症介质水平。方法选取2011—2013年我院收治的急性脑梗死患者80例,随机分为2组,分别给予依达拉奉治疗与依达拉奉联合尤瑞克林治疗。结果治疗2周后观察组有效率显著高于对照组,2组治疗后NIHSS评分与血清CRP相比治疗前均明显改善,观察组改善更为显著。结论尤瑞克林联合依达拉奉治疗急性脑梗死效果良好,明显改善患者神经功能,降低血清CRP水平,改善预后。     

视频脑电图在小儿癫痫诊断中的应用

目的评价视频脑电图(video-EEG)在小儿癫诊断中的应用价值。方法对126例具有发作性症状的患儿进行连续8h的包括清醒、睡眠、诱发试验及必要的认知测验的视频脑电图监测。结果经发作期视频脑电图证实,39例初诊为癫性发作的患儿中14例(35%)为非癫性发作;15例其他症状发作中13例(86%)为非癫性发作。64例样放电患儿中51例(80%)确定发作类型,22例(34%)确定癫类型。视频脑电图可发现短暂轻微的癫发作及样放电引起的一过性认知损伤。结论视频脑电图在排除非癫性发作、确定癫性发作的类型、评价脑电-临床关系方面可提供准确可靠的证据,进一步提高癫的临床诊断水平。     

Neuroprotective properties of memantine in different in vitro and in vivo models of excitotoxicity

The pathogenesis of stroke, trauma and chronic degenerative diseases, such as Alzheimer's disease (AD), has been linked to excitotoxic processes due to inappropriate stimulation of the N-methyl-D-aspartate receptor (NMDA-R). Attempts to use potent competitive NMDA-R antagonists as neuroprotectants have shown serious side-effects in patients. As an alternative approach, we were interested in the anti-excitotoxic properties of memantine, a well-tolerated low affinity uncompetitive NMDA-R antagonist presently used as an anti-dementia agent. We explored in a series of models of increasing complexity, whether this voltage-dependent channel blocker had neuroprotective properties at clinically relevant concentrations. As expected, memantine protected neurons in organotypic hippocampal slices or dissociated cultures from direct NMDA-induced excitotoxicity. However, low concentrations of memantine were also effective in neuronal (cortical neurons and cerebellar granule cells) stress models dependent on endogenous glutamate stimulation and mitochondrial stress, i.e. exposure to hypoxia, the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+) or a nitric oxide (NO) donor. Furthermore, memantine reduced lethality and brain damage in vivo in a model of neonatal hypoxia-ischemia (HI). Finally, we investigated functional rescue (neuronal capacity to migrate along radial glia) by memantine in cerebellar microexplant cultures exposed to the indirect excitotoxin 3-nitropropionic acid (3-NP). Potent NMDA-R antagonists, such as (+)MK-801, are known to block neuronal migration in microexplant cultures. Interestingly, memantine significantly restored the number of neurons able to migrate out of the stressed microexplants. These findings suggest that inhibition of the NMDA-R by memantine is sufficient to block excitotoxicity, while still allowing some degree of signalling.     

Storage of lipofuscin in neurons in mucopolysaccharidosis

Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.Supported by a grant from the Expressen Prenatal Research Foundation     

Role of vincristine in the inhibition of angiogenesis in glioblastoma

Objective: Vincristine, a microtubule-destabilizing drug, was found to exhibit anti-angiogenic effects and anti-tumoral activity. However, the precise mechanism by which vincristine inhibits angiogenesis in glioblastomas is not well understood. Our aim was to investigate whether vincristine affects vascular endothelial growth factor (VEGF) expression in glioblastoma cells and determine whether it is mediated by the downregulation of hypoxia-inducible factor-1α (HIF-1α).

Methods: We investigated the expression of HIF-1α in glioblastoma tissues resected from patients and in human glioblastoma cell lines using immunohistochemistry, Western blot analysis, and immunocytochemistry. In addition to an MTT assay assessing the effect of vincristine on cell proliferation and viability, the effects of vincristine on VEGF mRNA expression and HIF-1α protein were examined using real-time RT-PCR and Western blot analysis under 1% O₂ (hypoxia).

Results: HIF-1α was expressed in the majority of glioblastoma tissues and was detected mainly in the nucleus. Strong immunoreactivity for HIF- 1 α was found often in the hypercellular zones. Under hypoxic conditions, HIF-1α protein levels in the glioblastoma cell lines increased, primarily localizing into the nucleus similar to glioblastoma tissues. Exposure of glioblastoma cells to vincristine resulted in enrichment of the G₂-M fraction of the cell cycle, which suggests that vincristine-mediated growth inhibition of glioblastoma is correlated with mitotic inhibition. Using doses lower than those found to reduce the viability and proliferation of cells by 50% (IC₅₀), vincristine decreased both the expression of VEGF mRNA and the level of HIF-1α protein in hypoxic glioblastoma cells. In addition, following exposure to vincristine, the expression of VEGF mRNA was correlated with HIF-1α protein levels.

Conclusions: Our results suggest that the mechanism by which vincristine elicits an anti-angiogenic effect in glioblastomas under hypoxic conditions might be mediated, in part, by HIF-1α inhibition.     

脑电图预测痫性发作研究进展

癫痫(epilepsy)是由脑部神经元高度同步化异常放电所致的临床综合征,系神经系统的常见病,困扰着全世界约1%的人群.每次神经元的阵发性放电或短暂的脑功能异常称为痫性发作(seizures).     

The Burden of Agoraphobia in Worsening Quality of Life in a Community Survey in Italy

ObjectiveCurrent nosology redefined agoraphobia as an autonomous diagnosis distinct from panic disorder. We investigated the lifetime prevalence of agoraphobia, its association with other mental disorders, and its impact on the health-related quality of life (HR-QoL). MethodsCommunity survey in 2,338 randomly selected adult subjects. Participants were interviewed with the Advanced Neuropsychiatric Tools and Assessment Schedule (ANTAS), administered by clinicians. The diagnoses were based on the ICD-10 criteria. The Short-Form Health Survey (SF-12) was used to quantify HR-QoL. ResultsIn the sample, 35 subjects met the criteria for agoraphobia (1.5%), with greater prevalence among women (2.0%) than men (0.9%): odds ratio (OR) 2.23; 95% CI: 1.0-5–2. Agoraphobia was more often seen among those with (n=26; 1.1%) than without (n=9; 0.4%) panic disorder: OR=8.3; 2.9–24.4. Co-morbidity with other mental disorders was substantial. The mean score of SF-12 in people with agoraphobia was 35.2±7.8, with similar levels of HR-QoL in people with (35.3±7.9) or without (34.8±7.3) panic disorder: ANOVA: F(1;33)=0.0; p=1.00. ConclusionOne out of seventy people may suffer from agoraphobia in their lifetime. The attributable burden in terms of HR-QoL is substantial and comparable to the one observed for chronic mental disorders such as major depression, post-traumatic stress disorder, or obsessive-compulsive disorder.     

自噬参与帕金森病发病的研究进展

近年来,蛋白质的降解障碍被认为是帕金森病（Parkinson’Sdisease,PD）发病过程中的重要因素,人们已经公认泛素一蛋白酶体系统（ubiquitin--pro—teasomesystem,UPS）功能异常或衰竭能够导致细胞内异常蛋白蓄积、细胞功能障碍,甚至细胞凋亡。与此同时,蛋白降解的另一条途径——自噬-溶酶体途径（autophagy—lysosomepathway,ALP）也已成为了生命科学领域的研究热点,自噬与神经变性疾病,尤其是PD的关系日益受到人们的重视。     

Developmental effects of in vivo and in vitro inhibition of nitric oxide synthase in neurons

The diffusible chemical messenger nitric oxide (NO) is involved in neuronal plasticity and it is, therefore, supposed to play a role in brain development. A shortage of NO during the critical period of brain maturation may theoretically have long-lasting consequences on the organization of the adult brain. We have performed in neonatal rats a chronic inhibition of the enzyme responsible for NO production, nitric oxide synthase (NOS), from postnatal day 3 to postnatal day 23, through administration of the competitive antagonist N-nitro-L-arginine methylester (L-NAME). The calcium-dependent catalytic activity resulted almost completely inhibited throughout the period of treatment and it took more than 4 days after its suspension to get a full recovery. The expression of the neuronal isoform of the enzyme (nNOS), revealed by immunoblotting, was unchanged during the treatment and after it. The histochemical reaction for NADPH diaphorase was reduced at the end of the treatment and recovered in concomitance with the recovery of the catalytic NOS activity. No gross structural alterations were detected in brain morphology. The levels of three neurotransmitter-related and one astrocytic marker were unchanged in the cerebellum, hippocampus and cortex of 60-day-old rats which had been neonatally treated. A similar lack of significant effects on neurochemical brain maturation was also noticed in a parallel series of experiments, in which a short pulse of NOS inhibition was performed at a critical prenatal time of brain development, from gestational day 14 to gestational day 19. In vitro, chronic exposure of cerebellar granule cells to L-NAME (500 microM) resulted in slight decrease of surviving neurons after 8 days in culture and in better resistance to the challenge of stressful culture conditions. The present results suggest that the basic plan of brain organization can be achieved despite an almost complete NOS inhibition during the maturation period. In vitro, NOS inhibition may bring to more pronounced consequences on neuronal viability and function.     

Midazolam in treatment of various types of seizures in children

Midazolam is a recently developed water-soluble benzodiazepine that shares anxiolytic, muscle relaxant, hypnotic and anticonvulsant actions with other members of this class. There are limited studies that midazolam can be used successfully to treat seizures in adults and children. In this study, 0.2 mg/kg intramuscular (IM) midazolam was administered to 11 children (eight boys and three girls), aged 3 days to 4 years (mean age 1.8±1.4 years), with seizures of various types. In all but one child, seizures stopped in 15 s–5 min after injection. No side effects were observed. These results suggest that IM administration of midazolam may be useful in a variety of seizures during childhood, especially in case of intravenous (IV) line problem.