水疗治疗痉挛型脑瘫患儿疗效的Meta分析

目的 评价水疗治疗痉挛型脑瘫患儿的临床疗效。 方法 检索中国知网、万方数据、维普、PubMed、Cochrane library等数据库,以痉挛型脑瘫患儿为研究对象,收集水疗治疗痉挛型脑瘫患儿的随机对照试验(RCT),检索时限设定为建库至2018年11月。全部文献由2名评价员独立筛选、提取资料,并进行纳入研究的偏倚风险评价,采用RevMan 5.3软件进行Meta分析。 结果 检索到249篇相关文献,最终6篇文献纳入Meta分析,共计464例患者。Meta分析结果显示,水疗联合常规康复的总有效率高于常规康复［OR=4.04,95%CI（2.11,7.73）,P<0.05］,差异有统计学意义。 结论 水疗联合常规康复治疗可以改善痉挛型脑瘫患儿的症状,缓解肌张力,提高运动功能。     

Primary Cerebral Neuroectodermal Tumors: Neuroblastoma,Differentiated Neuroblastoma,and Composite Neuroectodermal Tumor

Seven cases of primary cerebral neuroectodermal tumors with predominant neuroblastic features were studied ultrastructurally and five were evaluated immunohistochemically. The fine structural features were indicative of neuroblastic differentiation by the presence of elongated cytoplasmic processes, electron-dense neurosecretory granules, and neurotubules. Five of the seven cases had the morphologic findings of classic cerebral neuroblastoma, and the sixth case, originally diagnosed as an oligodendroglioma, had the features of a differentiated neuroblastoma. Desmoplastic and/or stromal foci were intermingled with neuronal-ganglionic cells and neuroblasts in the seventh case. In addition to strong immunoreactivity for S-100 protein and glial fibrillary acidic protein in the desmoplastic areas, the spindle cells had fibroblastic and Schwannian features by electron microscopy in the latter case. The neuroblastic cells and fibrillary network were immunoreactive for neuron-specific eno-lase and neurofilament in the five study cases. It is concluded that cerebral neuroectodermal tumors may express an range of phenotypic features from the exclusive neuroblastic stage to a neuronal and stromogenic phase analogous to the classic neuroblastoma of the sympathetic nervous system.     

Ischemia preconditioning is neuroprotective in a rat cerebral ischemic injury model through autophagy activation and apoptosis inhibition

Sublethal ischemic preconditioning (IPC) is a powerful inducer of ischemic brain tolerance. However, its underlying mechanisms are still not well understood. In this study, we chose four different IPC paradigms, namely 5 min (5 min duration), 5×5 min (5 min duration, 2 episodes, 15-min interval), 5×5×5 min (5 min duration, 3 episodes, 15-min intervals), and 15 min (15 min duration), and demonstrated that three episodes of 5 min IPC activated autophagy to the greatest extent 24 h after IPC, as evidenced by Beclin expression and LC3-I/II conversion. Autophagic activation was mediated by the tuberous sclerosis type 1 (TSC1)-mTor signal pathway as IPC increased TSC1 but decreased mTor phosphorylation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and hematoxylin and eosin staining confirmed that IPC protected against cerebral ischemic/reperfusion (I/R) injury. Critically, 3-methyladenine, an inhibitor of autophagy, abolished the neuroprotection of IPC and, by contrast, rapamycin, an autophagy inducer, potentiated it. Cleaved caspase-3 expression, neurological scores, and infarct volume in different groups further confirmed the protection of IPC against I/R injury. Taken together, our data indicate that autophagy activation might underlie the protection of IPC against ischemic injury by inhibiting apoptosis.     

Influence of butyphthalide combined with urinary kallikrein in ACI treatment on neuro-cytokines and vascular endothelial function and its clinical effect

Abstract

Objective: To study the influence of butyphthalide combined with urinary kallikrein in acute cerebral infarction (ACI) treatment on neuro-cytokines and indicators of vascular endothelial function, observe the curative effect and adverse effects, and discuss its safety and feasibility.

Method: 110 ACI patients were chosen as the objects, and classified into observation group (55 cases) and control group (55 cases) according to the method of random number table. Butyphthalide injection combined with urinary kallikrein was adopted for the observation group based on conventional treatment, while cinepazide maleate injection combined with alprostadil injection was applied for the control group based on conventional treatment. The following indicators of both groups were compared before and after treatment: neurotrophic factor (NTF), nerve growth factor (NGF), neuron specific enolase (NSE); content of CXC chemotactic factor ligand 16 (CXCL16), soluble CD ligand (CD40L), Fibulin-5 and high mobility group box B1 (HMGB1); the content of indicators of vascular endothelial function including plasma endothelin ?1 (ET-1) and no therapeutic effects and adverse effects were recorded.

Results: NSE of both groups after treatment decreased obviously, and the content of NTF and NGF increased obviously. NSE content of observation group was lower than that of control group. NTF content and NGF content of observation group were higher than those of control group. The differences had statistical significance (p?<?0.05). The levels of CXCL16, CD40L, Fibulin-5 and HMGB1 declined obviously, compared with pre-treatment, and the levels of observation groups were significantly lower than those of control grip. The differences had statistical significance (p?<?0.05). ET-1 level rose significantly after treatment, and NO level declined obviously after treatment. ET-1 level of observation group was significantly higher than that of control group, and NO level of observation group was significantly lower than that of control group. The difference had statistical significance (p?<?0.05). Clinical effect of observation group was significantly higher than that of control group. The difference had statistical significance (p?<?0.05). The comparison difference of both groups in the occurrence rate of adverse effects had no statistical significance (p?>?0.05).

Conclusion: The application of butyphthalide combined with urinary kallikrein in ACI treatment can effectively inhibit secretion and release of neuro-cytokines, and improve patients’ vascular endothelial function, with significant treatment effect and high safety. Therefore, it deserves to be promoted clinically.     

急性脑梗死后抑郁患者血清iNOS,MIP-1 α水平变化及其临床意义

目的 探讨急性脑梗死后抑郁(Post-stroke depression,PSD)患者血清诱导型一氧化氮合酶(Inducible nitric oxide synthase,iNOS)、巨噬细胞炎性蛋白-1α(Macrophage inflammatory protein-1α,MIP-1α)水平变化及其临床意义。方法 收集2017年6月-2020年4月本院收治的143例急性脑梗死患者为研究对象,根据患者发病后1个月内是否发生PSD分为PSD组(n=42)和非PSD组(n=101),并于同期随机选取60例体检健康者为对照组; 采用酶联免疫吸附法检测各组血清iNOS,MIP-1α水平,绘制受试者工作特征(Receptor operating characteristic,ROC)曲线评估其对PSD的预测价值。结果 PSD组和非PSD组血清iNOS,MIP-1α水平高于对照组,且PSD组高于非PSD组(P<0.05); 随着抑郁程度的加重,PSD组患者血清iNOS,MIP-1α水平逐渐升高(P<0.05); 经Pearson积矩相关分析显示,PSD组患者血清iNOS,MIP-1α水平与HAMD评分呈正相关(r=0.692、0.658,P<0.05)。ROC曲线显示,iNOS水平预测PSD的AUC为0.862,灵敏度、特异性分别为83.33%、86.14%; MIP-1α水平预测PSD的AUC为0.832,灵敏度、特异性分别为78.57%、81.19%; iNOS联合MIP-1α水平预测PSD的AUC为0.902,灵敏度、特异性分别为88.10%、91.09%。结论 PSD患者血清iNOS,MIP-1α水平异常升高,并与病情严重程度密切相关,早期联合检测可作为预测急性脑梗死患者PSD发生风险的生化指标。     

慢性脑低灌注大鼠海马Arc低表达与其认知功能障碍的相关性研究

目的 探讨慢性脑低灌注大鼠海马活性调节的细胞骨架相关蛋白(activity-regulated cytoskeletal-associated protein,Arc)的低表达与其认知功能障碍的相关性。方法 大鼠慢性脑低灌注模型使用持久性双颈总动脉结扎术(2-vessel occlusion,2-VO); 大鼠随机分成假手术组和2-VO组,每组各6只。术后第8周行Morris水迷宫评价其认知功能; 实时定量聚合酶链式反应(Real time quantitative polymerase chain reaction,RT-qPCR)及蛋白免疫印迹法检测大鼠海马Arc mRNA及蛋白表达水平。结果(1)2-VO组大鼠第2～5 d的逃逸潜伏期比假手术组明显延长(P<0.01)及其在原平台区域游泳时间明显比假手术组短(P<0.01);(2)2-VO组大鼠海马Arc mRNA水平及免疫反应条带相对灰度值分别比假手术组明显降低(P均<0.01);(3)空间探索实验中2-VO大鼠在原平台区域游泳时间与海马Arc免疫反应条带相对灰度值呈正相关(r=0.7085,P<0.05)。结论 慢性脑低灌注大鼠的认知功能障碍可能与海马Arc的低表达相关。     

Effects of mild chronic cerebral hypoperfusion and early amyloid pathology on spatial learning and the cellular innate immune response in mice

Understanding the contribution of cerebrovascular factors in the progression of cognitive decline in Alzheimer's disease (AD) is a key step for the development of preventive therapies. Among these factors, chronic cerebral hypoperfusion is an early component of AD pathogenesis that can predict the progression from mild cognitive impairment to AD. Here, we investigated the effects of a protocol of mild chronic cerebral hypoperfusion in the APPswe/PS1 transgenic mouse model of AD. We observed that the permanent occlusion of the right common carotid artery induced spatial learning impairments in young APPswe/PS1 mice, but not in their wild type littermates. Furthermore, the extent of learning deficits strongly correlated with the number of cortical β-amyloid plaques, with the mobilization of monocytes into the blood and with the number of bone marrow-derived microglia in the brain. These results indicate that a mild reduction of cerebral blood flow can selectively induce cognitive deficits at an early stage of amyloid pathology, eliciting a cellular innate immune response, even without causing neuronal death.