亚低温对大鼠急性缺血脑保护作用的研究

脑缺血性疾病由于高致死率，高致残率成为神经科医生研究的热点，缺血性脑卒中治疗的中心环节是如何在实现脑保护基础上恢复血流，挽救半暗带。而亚低温对脑外伤的脑保护作用已为临床所证实并广泛应用于临床，为此，我们采用亚低温方法通过改良的不开颅栓塞法来观测脑缺血不同时间段缺血局部兴奋氨基酸，脑水肿，梗死体积及其光镜下形态的变化。结果表明亚低温具有脑保护作用。现将研究报告介绍如下。     

CT、PET、SPECT及MRI在脑卒中溶栓治疗中的作用

溶栓疗法在缺血性脑卒中治疗中已经被证明是有效的，缺血半暗带在决定采取溶栓治疗中起关键作用．本文从能否超早期诊断、影像诊断征象与溶栓治疗预后的相关性等方面对CT、PET、SPECT及MRI在脑卒中溶栓治疗中的作用进行综述，认为随着影像技术对缺血半暗带识别能力的增强，溶栓治疗缺血性脑卒中将会更加准确与灵活．     

CT、PET、SPECT及MRI在脑卒中溶栓治疗中的作用

溶栓疗法在缺血性脑卒中治疗中已经被证明是有效的,缺血半暗带在决定采取溶栓治疗中起关键作用.本文从能否超早期诊断、影像诊断征象与溶栓治疗预后的相关性等方面对CT、PET、SPECT及MRI在脑卒中溶栓治疗中的作用进行综述,认为随着影像技术对缺血半暗带识别能力的增强,溶栓治疗缺血性脑卒中将会更加准确与灵活.     

缺血性脑卒中影响因素的条件Logistic回归分析

目的应用条件Logistic回归模型探讨深圳市缺血性脑卒中的危险因素，为制定相关政策和措施提供科学依据。方法采用1：1配比的病例对照研究设计，选择深圳市两家综合性医院的309例缺血性脑卒中患者为病例组，同时选择年龄、性别匹配309例健康者作为对照组，对研究因素进行单因素及多因素条件Logistic回归分析。结果高血压、吸烟、家庭压力和高血糖是缺血性脑卒中的危险因素。OR值分别为3．507、5．420、3．990和1．183；而饮茶、体育锻炼是缺血性脑卒中的保护因素，OR值分别为0．250、0．100。结论在脑卒中的社区防治中，应尽早、及时地控制高血压、吸烟和体重，同时培养健康的生活方式是预防缺血性脑卒中发生的重要措施。     

PINK1/Parkin介导的线粒体自噬在缺血性脑卒中的作用研究进展

PTEN诱导推定激酶1(PINK1)/人帕金森蛋白2(Parkin)介导的线粒体自噬过程作为线粒体质量控制的关键机制之一，与缺血性脑卒中的凋亡、氧化应激及炎症反应等病理机制密切相关，极大地影响着该病的发生发展过程。本文将对PINK1、Parkin蛋白的结构与功能、该通路介导的线粒体自噬在缺血性脑卒中的作用展开综述，并分析其作为治疗缺血性脑卒中新靶点的优势。     

Toll样受体对缺血性脑卒中的作用及中医药干预

Toll样受体(TLRs)通过与相应配体结合,通过介导多种信号通路在缺血性脑卒中的病理生理机制中发挥着重要作用。本文综述近年国内外有关TLRs对缺血性脑卒中的作用及中医药干预对脑缺血保护的研究进展。     

星形胶质细胞调节缺血性脑卒中的胶质瘢痕形成

背景：缺血性脑卒中是临床上主要的致死及致残性疾病之一，经血管再通获益的患者数量极其有限，故探索有效治疗手段迫在眉睫。以星形胶质细胞为主所形成的胶质瘢痕作为缺血性脑卒中的重要病理变化之一，是阻碍脑卒中后期轴突再生和神经修复的主要原因。目的：通过对缺血性脑卒中后星形胶质细胞瘢痕形成的病理过程、关键的信号调节机制和潜在治疗靶点进行分析，旨在为干预星形胶质细胞瘢痕形成以有效治疗缺血性脑卒中提供理论依据，并为促进脑卒中后康复提供新策略。方法：全面检索2010-2022年在中国知网、Pub Med和Web of Science数据库收录的相关文献，中文检索词：“缺血性脑卒中、脑缺血、星形胶质细胞、胶质瘢痕、胶质增生、星形胶质细胞增多症”，英文检索词：“Ischemic stroke,Brain ischemi*,Cerebral ischemi*,Astrocyt*,Astroglia*,Glial scar,Gliosis,Astrogliosis”，经筛选后纳入78篇文献进行综述。结果与结论：(1)星形胶质细胞在中枢神经系统稳态的维持中具有重要作用，缺血性脑卒中发生后，星形胶质细胞从静息态转变...     

内源性神经干细胞在缺血性脑卒中治疗中的研究进展

<正>缺血性脑卒中又称脑梗死,是一类因脑局部血液循环中断引起神经功能障碍的疾病,其发病率约占脑卒中总发病率的60～80%[1],严重威胁着人类的生命与健康。目前,缺血性脑卒中的临床治疗除一般治疗方法外还主要包括溶栓治疗和神经保护治疗等。溶栓治疗是通过使用溶栓药物如重     

长链非编码RNA GAS5在缺血性脑卒中及相关疾病中的研究进展

缺血性脑卒中是全世界范围内致残和死亡的主要原因之一,发病后持续的神经功能缺损给患者和社会带来很大的经济负担。迄今为止,人们不断寻找更加有效的诊断方法和治疗缺血性脑卒中的药物,越来越多的研究证实了长链非编码RNA GAS5在缺血性脑卒中发病机制中的重要作用,并认为其是脑梗死的潜在治疗药物。     

Kalirin-7在缺血性脑卒中中的作用

缺血性脑卒中是由多种因素共同引起的致残致死疾病,其发病机制涉及信号转导通路、兴奋性谷氨酸受体活化、NO作用等。Kalirin是Rho蛋白家族中小GTP酶的一种神经特异的鸟嘌呤核苷酸转化因子,kalirin-7是成熟大脑中最丰富的kalirin同种型,对树突棘的维持等方面具有重要作用。多研究显示,kalirin-7在缺血性脑卒中也起一定作用,此分子对神经元具有保护作用,在缺血性脑卒中中其含量的减少加重了神经元的损伤。其机制可能包括:与PSD-95结合而改变了JNK信号传导通路,与NMDA受体亚单位结合减少以至兴奋性谷氨酸作用增强,以及对iNOS的抑制减少。     

Case report: Detection of a hepatitis B surface antigen variant emerging in an elderly patient after an ischemic cerebral vascular accident

HBV reactivations are observed frequently in patients with past hepatitis B infection receiving cytotoxic and/or immunosuppressive chemotherapy for hemato‐oncological malignancies or autoimmune diseases. Recent ischemic stroke was shown to induce immunodepression by misunderstood mechanisms. To our knowledge, the association between HBV reactivation and ischemic stroke has not been reported before. This study reports the case of an anti‐HBs‐ and anti‐HBc‐positive patient who presented HBV reactivation in a context of recent ischemic stroke, with no other intercurrent iatrogenic phenomenon or usual immunosuppressive pathology. J. Med. Virol. 84:1897–1900, 2012. © 2012 Wiley Periodicals, Inc.     

Pathogenic mechanisms in ischemic damage: a computational study

The pathogenesis of penumbral tissue infarction during acute ischemic stroke is controversial. This peri-infarct tissue may subsequently die, or survive and recuperate, and its preservation has been a prime goal of recent therapeutic trials in acute stroke. Two major hypotheses currently under consideration are that penumbral tissue is recruited into an infarct by cortical spreading depression (CSD) waves, or by a non-wave self-propagating process such as glutamate excitotoxicity (GE). Careful experimental attempts to discriminate between these two hypotheses have so far been quite ambiguous. Using a computational metabolic model of acute focal stroke we show here that the spatial patterns of tissue damage arising from artificially induced foci of infarction having specific geometric shapes are inherently different. This is due to the distinct propagation characteristics underlying self-regenerating waves and non-wave diffusional processes. The experimental testing of these predicted spatial patterns of damage may help determine the relative contributions of the two pathological mechanisms hypothesized for ischemic tissue damage.     

Phosphodiesterase 4D Gene and Risk of Noncardiogenic Ischemic Stroke in a Korean Population

Recently published studies from different populations provide apparently conflicting evidence on the association between the phosphodiesterase 4D (PDE4D) gene and ischemic stroke. The relationship between a representative PDE4D genotype and ischemic stroke was explored in a case-control study of 205 consecutive Korean patients with noncardiogenic ischemic stroke and 103 healthy controls who were neurologically and radiologically proven to be stroke-free. We selected and genotyped a PDE4D single nucleotide polymorphism (SNP 41, rs152312) as a candidate marker for susceptibility to ischemic stroke because SNP 41 has shown the most significant association with stroke in both a meta-analysis and the original Icelandic study of the PDE4D gene. No significant difference was observed between the cases and controls in the distribution of the PDE4D SNP 41 genotypes. The results from the adjusted conditional logistic regression analysis (adjusted for age, hypertension, diabetes and smoking status) showed no significant association between PDE4D SNP 41 genotypes and an increased risk of noncardiogenic ischemic stroke. The PDE4D gene is not a major risk factor for noncardiogenic ischemic stroke in a Korean population, which supports the recent evidence suggesting that the causative genetic variants of ischemic stroke may differ across populations.     

外泌体在缺血性脑卒中的研究进展

正1外泌体概述外泌体是直径在30~100 nm的胞外囊泡,通过细胞被释放到细胞外液中~([1])。它们存在于生物体液中,诸如血液和脑脊液。外泌体携带有DNA、RNA、蛋白质和脂质等。由于外泌体的微泡结构为其内在的小分子提供了一个安全稳定的环境,同时这些信号小分子利用循环系统在胞间信号交换发挥重要作用,这让外泌体表现出一个成熟、稳定的信号传输系统~([2])。研究发现,外泌体中的m RNA和micro RNA     

Complications of hydroxyethyl starch in acute ischemic stroke and other brain injuries

Serious complications of hydroxyethyl starch (HES) administration have been repeatedly demonstrated in clinical trials of acute ischemic stroke and other brain injuries. Such complications have prompted the premature termination of several randomized trials. Coagulopathy and bleeding have been the most frequently documented complications in the brain injury setting and have occurred after exposure to HES solutions of widely varying molecular weight and substitutions. Severe, protracted, refractory pruritus is another HES complication. Claims of safety for HES solutions have often been made on the basis of small trials with inadequate statistical power. Additionally, the safety has been typically assessed in highly selected low-risk patient populations receiving relatively small HES doses, so that the results cannot be generalized to routine clinical practice. The preponderance of available evidence suggests that HES solutions should be avoided in acute ischemic stroke and other brain injuries.     

颈动脉内膜剥脱术在防治缺血性脑卒中的临床分析

目的对颈动脉内膜剥脱术预防和治疗缺血性脑卒中的临床疗效进行评价。方法对30例经检查确诊为脑卒中患者,行颈动脉内膜剥脱术,剥离颈动脉斑块。结果30例患者术后恢复良好,脑缺血症状有明显改善,围手术期内未出现死亡及脑卒中事件。随访6-24个月未出现脑卒中,未出现严重并发症,且病人的生活质量有明显改善。结论颈动脉内膜剥脱术对预防和治疗缺血性脑卒中是安全有效的。     

Schlafbezogene Atmungsstörungen und zerebrovaskuläre Erkrankungen

Sleep-related breathing disorders comprise obstructive sleep apnea (OSA), central sleep apnea (CSA), Cheyne–Stokes respiration (CSR), and central alveolar hypoventilation. OSA is significantly associated with known cardiovascular risk factors, e.g., arterial hypertension, atrial fibrillation, and carotid atheromatosis. In addition, OSA has been shown to independently increase stroke risk. Thus, OSA is a direct and indirect risk factor of ischemic stroke, and early diagnosis and treatment of OSA may be crucial for stroke prevention. Acute ischemic stroke may cause any type of sleep-related breathing disorder in an affected patient. Nocturnal breathing abnormalities may be present transiently or persist for a longer period of time, affecting both neurological outcome and the risk of recurrent stroke. Sleep-disordered breathing is highly prevalent in patients with large supratentorial or bihemispheric infarctions, brainstem and cerebellar infarctions. It is associated with worse prognosis, increased disability, and higher mortality. Recently, several interventional studies showed that early implementation of continuous positive airway pressure (CPAP) treatment overnight is feasible and significantly improves neurological outcome in patients with ischemic stroke even if overall mortality may not be significantly reduced.     

The Relationship Between Serum Lipoprotein (a) Levels and Ischemic Stroke Risk: A Cohort Study in the Chinese Population

The role of atherosclerosis in ischemic stroke has been intensively investigated in recent years, and lipoprotein (a) [Lp(a)] is found to have roles during the process. The aim of this study was to investigate the relationship between acute ischemic stroke (AIS) and serum Lp(a) levels in the Chinese population. All consecutive patients with first-ever acute ischemic stroke during 2011–2012 were recruited to participate in the study. Serum Lp(a) levels and routine tests were examined in both groups. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to Lp(a) levels. In this study, 181 patients with acute ischemic stroke were included. There was a significant difference in median serum Lp(a) levels between acute ischemic stroke patients and control cases (328 [IQR, 173–554] vs. 145 [IQR, 66–254] mg/L, respectively; P?=?0.000). Lp(a) levels increased with increasing severity of stroke as defined by the NIHSS score (P?=?0.000). For the entire group, when adjusting for other possible risk factors, an elevated Lp(a) level was an independent risk factor for stroke, and a serum Lp(a) level ≥300 mg/L was associated with a 2.23-fold increase in AIS (P?=?0.015). In addition, this association was stronger in male than in female patients. High Lp(a) levels are significantly related to stroke, independent from other traditional and emerging risk factors, suggesting that they may play a role in its pathogenesis. It should be considered as a routine risk factor for stroke in the Chinese population.     

A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke

Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood–brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. This article reviews recent developments in understanding the mechanisms underlying BBB dysfunction, neuroinflammation, and oxidative stress after ischemic stroke, and focuses on how cav-1 modulates a series of activities after ischemic stroke. In general, cav-1 reduces BBB permeability mainly by downregulating MMP9, reduces neuroinflammation through influencing cytokines and inflammatory cells, promotes nerve regeneration and angiogenesis via cav-1/VEGF pathway, reduces apoptosis, and reduces the damage mediated by oxidative stress. In addition, we also summarize some experimental results that are contrary to the above and explore possible reasons for these differences.     

Elevated blood pressure management in acute ischemic stroke remains controversial: Could this issue be resolved?

A transient elevated arterial blood pressure is common in acute ischemic stroke and is often associated with a poor prognosis. The underlying mechanisms of blood pressure elevation are not well understood and its management is still unresolved. This article focuses on pathophysiology and management of elevated blood pressure in acute ischemic stroke. There is evidence that the main causes of a transient blood pressure elevation in acute ischemic stroke are the focal cerebral hypoperfusion and the stress responses with neuroendocrine systems activation. Clinical trials have reported that blood pressure lowering in acute ischemic stroke may have detrimental effect, probably because of impaired cerebral autoregulation. However, quantitative assessment of cerebral perfusion has not been performed during emergency blood pressure reduction in acute ischemic stroke. We suggest that ultrasound carotid artery disease evaluation and cerebral hemodynamics monitoring using bilateral transcranial ultrasonography, during blood pressure management in acute ischemic stroke might contribute to maintaining of an adequate penumbral perfusion and prevent infarct enlargement. Such an approach could individualize the antihypertensive treatment in acute ischemic stroke and improve functional outcome. Prospective studies are needed to confirm such a treatment strategy.