前列腺素E1治疗椎基底动脉供血不足的临床疗效观察

目的探讨前列腺素E1对椎-基底动脉供血不足(VBI)的临床疗效。方法对60例VBI患者随机分为30例前列腺素E1组(治疗组)和30例丁咯地尔组(对照组),疗程10d,并进行治疗前、后临床症状、体征评分。结果前列腺素E1和丁咯地尔分别对治疗组和对照组有效(P<0.001),前列腺素E1能明显改善VBI患者的症状和体征,尤其是眩晕和共济失调,且不良反应少而轻;2种药物的疗效无明显差异(P>0.05)。结论前列腺素E1是治疗VBI安全、有效的药物。     

尼莫地平与前列腺素E1治疗偏头痛对比研究

目的观察尼莫地平与前列腺素E1合用对偏头痛的疗效.方法将前列腺素E1100μg加入5%糖水250ml中静滴,每日一次,尼莫地平20mg,一日3次口服,2周为一疗程.结果研究表明,治疗组有效率95.5%,对照组有效率72%,两组比较有显著差异,p＜0.01.结论尼莫地平与前列腺素E1合用治疗偏头痛,特别是顽固性偏头痛疗效显著.     

前列腺素E1治疗脑梗死临床血液流变学观察

目的观察前列腺素E1治疗脑梗死的疗效.方法将100例脑梗死患者随机分为治疗组和对照组.治疗组用PGE1,对照组用低分子右旋糖酐和血塞通,对比疗效.结果治疗组治愈率及显效率明显优于对照组.治疗组用药后血流变学各项指标均有降低,尤以全血比粘度、血小板粘附率下降明显.结论PGE1能有效治疗脑梗死.     

前列腺素E1治疗急性脑梗塞的疗效观察

本文报道前列腺素E1治疗50例急性脑梗塞的结果和复方丹参对照组相对照,病例数相同,年龄相似,性别差异不大,有可比性.治疗组中50例用PGE1注射液200μgQd×15天.开始用药时间均在起病24小时内.结果为PGE1治疗组的显效率及血液流变学指标降低明显优于对照组.结论为PGE1治疗急性脑梗塞有肯定疗效.     

尼莫地平与前列腺素E1治疗偏头痛对比研究

目的：观察尼莫地平与前列腺素E1合用对偏头痛的疗效。方法：将前列腺素E1 100ug加入5％糖水250ml中静滴。每日一次，尼莫地平20mg，一日3次口服，2周为一疗程。结果：研究表明，治疗组有效率95．5％，对照组有效率72％，两组比较有显著差异，P＜0．01。结论：尼莫地平与前列腺素E1合用治疗偏头痛，特别是顽固性偏头痛疗效显著。     

前列腺素E1注射液治疗急性脑梗死50例

目的：观察前列腺素Ｅ１（ＰＧＥ１）治疗急性脑梗死疗效。方法：经临床及ＣＴ或ＭＲＩ确诊的脑梗死病人１００例,随机分为两组并按病情分成两组。治疗组用ＰＧＥ１注射液,观察各组的疗效。结果：经过统计分析,治疗组神经功能缺损症状改善显著（Ｐ〈０．０５）。特别对重症患者显示了独特的疗效。结论：ＰＧＥ１可有效的改善急性脑梗死患者的神经功能缺损症状,提高有效率。     

前列腺素E1治疗脑梗死临床血液流变学观察

目的：观察前列腺素E1治疗脑梗死的疗效。方法：将100例脑梗死患者随机分为治疗组和对照组。治疗组用PGE1，对照组用低分子右旋糖酐和血塞通，对比疗效。结果：治疗组治愈率及显效率明显优于对照组。治疗组用药后血流变学各项指标均有降低，尤以全血比粘度、血小板粘附率下降明显。结论：PEG1能有效治疗脑梗死。     

Bcl-2、Bax蛋白产物在脑缺血耐受中的表达及前列腺素E1的干预作用

目的探讨大鼠脑缺血时凋亡相关基因Bcl-2、Bax蛋白的表达与脑缺血耐受的关系及前列腺素E1 (PGE1)对脑缺血耐受的影响。方法采用大鼠全脑-局灶脑缺血耐受模型。观察预缺血组、PGE1组在大脑中动脉梗死2h再灌注(MCAO)24h后神经行为评分、脑梗死体积、Bcl-2、Bax蛋白表达和TUNEL、流式细胞仪检测神经细胞凋亡。结果MCAO后24h,PGE1组的神经行为评分、脑梗死体积、Bax蛋白表达更少,Bcl-2蛋白表达较高,神经细胞凋亡降低。结论预缺血及PGE1预处理后,使Bax蛋白表达减少,Bcl-2蛋白表达增高能够诱导脑缺血耐受,且PGE1的作用优于预缺血。     

前列腺素E_1针联合甲钴胺针治疗糖尿病周围神经病变

目的观察前列腺素E1（PGE1）联合甲钴胺治疗糖尿病周围神经病变的临床疗效及神经电生理改善情况。方法收集2010-01-2011-03我院住院治疗的糖尿病周围神经病变患者97例,随机分为治疗组（49例）和对照组（48例）,对照组给予维生素B12治疗,治疗组给予前列腺素E1注射液（商品名凯时）联合甲钴胺注射液（商品名弥可保）治疗,2周后比较2组疗效。结果 2组糖尿病周围神经病变患者麻木疼痛减轻的程度、神经传导速度均明显改善,且治疗组优于时照组（P〈0.05）。结论前列腺素E1针与甲钴胺针联合治疗糖尿病周围神经病变疗效较好。     

促红细胞生成素对大鼠激光脑损伤神经保护作用的实验研究

目的探讨外源性促红细胞生成素（EPO）对大鼠激光脑损伤的神经保护作用,为激光脑损伤的治疗提供新思路。方法80只健康雄性SD大鼠制作激光脑损伤模型,随机分为假手术（A）组、模型（B）组、EPO治疗（C）组、生理盐水对照（D）组,每组20只。对术后大鼠进行运动神经功能评分,采用免疫组织化学方法检测大鼠脑中热休克蛋白70（HSP70）的表达。结果激光损伤后24h,C组神经功能评分显著改善。A组HSP70表达较弱,B组HSP70表达增加,C组HSP70表达显著升高（P〈0.01）,D组HSP70表达增加。结论促红细胞生成素对大鼠激光脑损伤神经保护作用可能与HSP70表达有关。     

下调lncRNA-MALAT1表达对新生大鼠缺氧缺血性脑损伤的保护作用

目的 探讨小图lncRNA-MALAT1表达对新生大鼠缺氧缺血性脑损伤（HIBD）的影响。方法 取SPF级7 d龄SD大鼠40只,随机分为假手术组、模型组、lncRNA对照组、silncMALAT1组,每组10只。Rice-Vannucci法建立新生大鼠HIBD模型,造模后2 h,侧脑室分别注射生理盐水、生理盐水、空载体重组腺病毒液、silncMALAT1各5μl。造模后7 d,Morris水迷宫试验评估空间学习和记忆能力,TUNEL染色检测海马组织神经元凋亡,PCR和免疫印迹法检测海马组织BDNF/TrkB信号通路mRNA和蛋白表达变化。结果 模型组造模失败2只,lncRNA组失败2只,silncMALAT1组失败1只,造模成功率为83.33%。下调lncRNAMALAT1表达,明显增加新生大鼠学习和记忆能力（P<0.05）,明显减少海马组织神经元凋亡率（P<0.05）,明显下调BDNF/TrkB mRNA和蛋白表达水平（P<0.05）。结论 下调lncRNA-MALAT1表达可减轻新生大鼠HIBD,其机制可能与抑制BDNF/TrkB信号通路、减轻海马组织神经元凋亡...     

脑死亡器官捐献移植过程中的问题

背景：采用国际标准的供肾来源,即脑死亡无偿肾脏捐献可缓解目前肾移植中供肾的严重短缺问题。近年脑死亡无偿器官捐献及移植已在中国成功开始实施,但在脑死亡无偿器官捐献肾移植方面的报道较少。 目的：探讨脑死亡器官捐献肾移植在中国的可行性及保证移植成功的必要条件。 方法：总结2007-01/2010-07脑死亡器官捐献肾移植12例患者的经验和体会,包括供者/供肾的评估、供肾的摘取与保存、肾移植情况、移植后受者肾功能及并发症、住院时间、生活质量等。 结果与结论：12例脑死亡器官捐献肾移植受者中10例在移植后2~5 d肾功能恢复正常,移植后14~21 d出院;2例出现肾功能延迟恢复,分别于移植后10,15 d肾功能正常,移植后第28天出院。在2~42个月随访过程中,8例患者肾功能均正常,尿蛋白阴性,已从事正常工作,生活质量良好;2例出现蛋白尿,但肾功能正常;1例肾功能正常,肝功能异常,经治疗好转;1例在术后3个月死于严重肺部感染。提示,脑死亡器官捐献肾移植在中国可以得到开展;脑死亡供者必须有满意的血流动力学和尿量及良好的肾功能才能作为理想的肾移植供体;选择最佳移植时机,重视移植后系统性随访,才能确保脑死亡无偿器官捐献肾脏移植成功。     

Retinoic acid enhances prostaglandin E2 production through increased expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in rat brain microglia

Retinoic acid (RA) is a well-known antiinflammatory agent. In this study, we show that RA has a dual effect on cyclooxygenase-2 (COX-2) expression in inflammatory activated microglia, the resident brain macrophages. After treatment of microglia with LPS or thrombin, COX-2 expression was induced in two phases, specifically, an initial increase at about 12 hr after stimulation followed by a decrease, and another increase at about 48-72 hr. However, PGE(2) and 15d-PGJ(2) were detected at about 12 hr, and the levels continuously increased thereafter. Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. ATRA enhanced PGE(2) production but had little effect on 15d-PGJ(2). Moreover, ATRA selectively up-regulated the expression of a PGE(2) synthase, mPGES-1, but had little effect on the PGD(2) synthase, H-PGDS. The results collectively suggest that ATRA modulates microglial responses to inflammatory stimulators, particularly at the late phase, via enhancement of COX-2 expression and PGE(2) production.     

Facial myokymia in brain death

BACKGROUND: Brain death (BD) is the irreversible loss of all functions of the brain and brainstem. Spontaneous and reflex movements of the limbs have been described in this condition. However, facial myokymia (FM) in BD has not been previously reported. The origin of that motor phenomenon in alive patients is still uncertain, since supranuclear, nuclear and peripheral mechanisms have been proposed. OBJECTIVE: We describe the presence of FM in a patient who fulfilled the criteria for BD. A 40-year-old-man had right-sided weakness and impaired consciousness. After 14 h admission, he fulfilled the criteria for BD. A CT scan of the head showed a large putaminal hemorrhage. The EEG was isoelectric. At that time, fine spontaneous twitches of the left cheek were noticed. They consisted of repetitive and rhythmic movements in groups of 3-5 lasting for < 5 s. These movements appeared every 2-10 min during 6 h. DISCUSSION: Spinal reflexes have been described in BD. The presence of any movements other than the recognized reflexes may question this diagnosis and limit organ procurement for transplantation. The recognition of FM as an accepted movement in BD patients has practical and legal implications.     

Comparable effect of prostaglandin E1 in decreasing in vivo platelet deposition on human lesion sites after intravenous and intraarterial application

It had been claimed that prostaglandin E1 is degraded during first lung passage to a major extent. Clinical results, however, as well as various platelet function tests and coagulation parameters revealed no apparent difference after i.v. and i.a. infusion. Thus, we examined the question what the quantitative difference between i.v. and i.a. PGE1-application would be upon in-vivo platelet function assessed by platelet uptake over active lesion sites as well as platelet half-life monitoring after autologous 111-In-oxine platelet labelling. In patients suffering from peripheral vascular disease stage II according to Fontaine PGE1 was able to decrease platelet uptake after i.v. and i.a. therapy to a comparable extent; similarily, a significant prolongation in platelet half-life was noted, again revealing no difference. As the decrease in platelet uptake is assumed to be predominantly a vascular effect, it is hypothetized that more stable derivatives of PGE1 are active, counterbalancing a lower biological activity with a longer half-life.     

SP600125对大鼠肝缺血再灌注损伤的保护作用

背景：SP600125作为JNK激酶抑制剂,可特异性阻断JNK细胞转导通路,对肝脏缺血再灌注又起到怎样的作用,目前尚无相关研究。 目的：应用SP600125对肝脏缺血再灌注进行干预,分析JNK信号转导通路在该病理生理过程中的作用。 方法：将30只雄性SD大鼠按随机数字表法分为3组,假手术组、缺血再灌注组及SP600125组各10只。假手术组仅行进腹手术;缺血再灌注组行进腹手术,阻断肝左中叶的血供;SP600125组于术前半小时腹腔注射SP600125 15 mg/kg,其他操作同缺血再灌注组。于复灌后2 h取材,分别测定各组血清肝功能酶活性,通过苏木精-伊红切片染色观察肝组织结构的病理变化,运用免疫组织化学法检测肝组织中p-JNK表达并进行半定量分析,以比色法检测肝脏丙二醛含量及髓过氧化物酶活性。 结果与结论：相对于缺血再灌注组,SP600125组血清肝功能酶活性明显下降,肝脏p-JNK表达较低,肝脏髓过氧化物酶活性以及丙二醛含量下降,病理损伤有所缓解。提示JNK细胞信号转导通路在肝缺血再灌注损伤过程中被广泛激活,应用JNK抑制剂SP600125对缺血再灌注损伤有保护作用。     

Scalp EMG in brain death electroencephalogram

Electromyograms (EMGs) are usually considered artifacts during electroencephalographic (EEG) recording for determination of electrocerebral silence (ECS). Appearance of scalp motor unit activity, however, may reflect residual brainstem function and can introduce difficulty in establishing a secure diagnosis of brain death. In this study, ECS patients with and without scalp EMG were compared in terms of relationship to brainstem survivability. There was no correlation between length of survivability and presence of scalp EMG activity. No patient recovered brainstem function clinically. This study provides firm support for the usual practice of ignoring the EMG in brain death EEG. Scalp has no prognostic value.     

Heart rate variability in brain death

The sensitivity and specificity of heart rate variability (HRV) in the corroboration of brain death diagnosis in patients with acute traumatic intracranial lesions was evaluated in 20 patients with clinical criteria of brain death, nine patients in deep coma (Glasgow scale <7) and 18 normal controls, all age matched. The electrocardiogram was sampled at 650 Hz and several parameters of HRV were calculated, in both time and frequency domains. The HRV parameters were significantly lower in the brain death group compared with the deep coma group. Linear discriminant analysis between brain death and deep coma patients was performed on a data set made of nine randomly selected patients with clinical criteria of brain death and nine patients in deep coma. Cross-validation was performed on the remaining 11 patients with clinical criteria of brain death. All patients in the data set were correctly classified (sensitivity and specificity of 100%). All patients in the cross-validation set were correctly classified (sensitivity of 100%). Further studies are necessary to evaluate the specificity of the method in the independent set of deep coma patients and in the follow-up of comatose and vegetative patients to identify irreversibility of HRV. Nevertheless, these results suggest that HRV analysis constitutes a fully sensitive and specific method for assessing brain death in potential organ donors with acute traumatic lesions of the brain. This fast, quantitative and bedside method seems very promising for the early confirmation of brain death, which is an important factor for the success of transplantation procedures and could have a high predictive value of brain death in comatose patients with brain injuries without fully diagnostic criteria.