S100B蛋白、胶质纤维酸性蛋白和神经元特异性烯醇化酶在早产儿脑损伤中的意义

早产儿脑损伤是造成早产儿伤残的重要原因,影像学检查有时间滞后性.寻找一种简单、及时、准确地预测早产儿脑损伤的生物学标志物尤为重要.本文对早产儿脑损伤的生物标志物S100B蛋白、胶质纤维酸性蛋白和神经元特异性烯醇化酶在早产儿脑损伤中的作用作一综述,探讨其对早产儿脑损伤早期诊断的意义.     

雄激素对HIBD新生鼠phosphacan和NG2蛋白聚糖表达与轴突再生的影响研究

目的：了解雄激素对缺氧缺血脑损伤（HIBD）新生鼠脑组织磷酸蛋白聚糖（phosphacan,PC）及NG2蛋白聚糖（NG2）表达变化及其与缺血缺氧脑损伤后轴突再生的关系，探讨其神经保护作用机制。方法：制作新生鼠HIBD模型，随机分为假手术组、HIBD组、雄激素干预组（于模型制成后即刻注射丙酸睾丸酮25 mg/kg）。于缺氧缺血（HI）后24 h、72 h、7 d、10 d取脑组织制作石蜡切片和电镜切片，用免疫组化法观察PC和NG2蛋白聚糖在各组大鼠皮质和海马表达的动态变化，应用透射电镜对比观察各组海马和皮层神经元超微结构变化、细胞凋亡、神经元轴突再生及胶质细胞增生情况。结果：①HI后脑组织超微结构变化：假手术组于术后24 h细胞表面见较小的突起，72 h、7 d及10 d细胞表面可见大小不等的突起，未见凋亡细胞；HIBD组HI 24 h、72 h、7 d和10 d时细胞表面无突起或仅有较小突起；雄激素干预组的神经元轴突较HIBD组后增长明显，但较假手术组弱。②HI后脑组织PC和NG2的表达：假手术组海马和皮层均存在少量PC和NG2的表达，海马的表达高于皮层。HIBD组在HI后24 h 表达开始呈阳性反应，HI后72 h明显增多，7 d达高峰，10 d后开始下降，但仍高于正常对照组；雄激素干预组，PC和NG2的表达时程和分布与HIBD组相似，HI后24 h、72 h、7 d和10 d在皮层和海马的表达水平明显低于HIBD组，均有统计学意义（P<0.01）。结论：PC和NG2可能是HIBD后抑制神经元轴突再生的重要因子之一，雄激素可能通过调节胶质细胞形态结构和功能抑制PC和NG2表达促进神经元轴突再生，从而发挥神经保护作用。     

组织型纤溶酶原激活物与缺氧缺血性脑损伤

组织型纤溶酶原激活物(tPA)参与正常脑组织中神经元、神经胶质的迁移和轴突或树突的重塑,它在神经组织中的异常表达与神经元退变和某些神经系统疾病有关.研究表明,tPA表达升高参与了缺氧缺血性脑损伤的发生.该文综述了生理和病理状态下tPA在中枢神经系统的表达、作用以及tPA参与缺氧缺血性脑损伤的可能机制.     

沉默信息调节因子3调控小胶质细胞对早产儿脑损伤的神经保护作用研究进展

随着围生医学发展,早产儿存活率已逐年上升,但脑损伤发生率依旧不低.尽管神经康复使脑损伤得到一定改善,但不可避免地遗留不同程度神经功能障碍.最近研究表明,沉默信息调节因子3可调控脑内小胶质细胞而减轻神经元受损,在早产儿脑损伤保护中具有极大潜力.文章综述了沉默信息调节因子3通过小胶质细胞对早产儿脑损伤的神经保护作用机制,以...     

神经系统相关蛋白质标志物与脑损伤的关系

血清或脑脊液中神经系统相关蛋白质标志物在不同类型的脑损伤中有不同的临床意义,本文总结S-100B、胶质纤维酸性蛋白、神经元特异性烯醇化酶和髓鞘碱性蛋白的特点及应用价值,对协助判断脑损伤及预后有重要指导作用。     

惊厥性脑损伤与细胞自噬的相关性

自噬是溶酶体降解利用细胞内物质成分的过程,对应激状态下神经细胞存活及清除衰老细胞器和错误折叠蛋白等起重要作用;其可作为神经细胞的保护机制,也可作为神经细胞死亡方式之一.反复惊厥可以导致脑损伤,但具体机制尚不清楚,最近研究表明,惊厥时可启动细胞凋亡途径,并且也可启动细胞自噬,从而介导神经元适应、损伤或凋亡,惊厥性脑损伤与细胞自噬密切相关.细胞自噬作为一条新的重要的信号途径,为惊厥脑损伤的防治提供新的治疗方向.     

热休克蛋白对缺氧缺血性脑损伤神经元凋亡的保护作用及机制

热休克蛋白(HSP)是机体在受到应激刺激后诱导产生的一组蛋白质,对细胞损伤具有保护作用.近年来较多文献报道HSP对缺氧缺血性脑损伤神经元的凋亡具有保护作用.本文就HSP的特点、脑缺氧缺血后神经元中HSP的表达及其对神经元凋亡的保护作用和机制进行综述.     

癫(癎)的脑损伤研究进展

癫痫是一种慢性、反复出现的发作性疾病,是多种原因引起脑功能障碍的表现,严重危害人类健康。癫痫发作引起脑损伤一直是人们长期关注的问题。在脑损伤的发病过程中,炎性介质和免疫因素相互作用,导致神经元丧失和胶质增生。神经元的丧失方式除坏死外还存在凋亡。胶质增生是脑损伤的结果,又可促进癫痫的发作。可通过检测脑损伤的标志蛋白对其做出诊断。     

我国早产儿脑室内出血的早期诊断和防治现状

在新生儿医学所有问题中，早产儿的脑损伤及其预防尤为重要。早产儿脑损伤包括脑室内出血(IVH)、脑室周围白质软化(PVL)、出血后脑积水以及其他一些脑损伤如选择性神经元坏死和基底神经节丘脑损伤等，其中以IVH和PVL最为常见。尽管IVH发生率近年来国际上似呈下降趋势，但在发生     

丙戊酸钠对癫癎脑损伤的神经保护作用

癫癎发作引起的脑损伤主要表现为神经元丢失及胶质细胞增生.广谱的抗癫癎药丙戊酸钠具有复杂的药理作用,近年来研究发现丙戊酸钠不仅具有抗癫癎效应,其在一定剂量范围内还对癫脑损伤具有神经保护作用,可诱导神经营养,减少癫癎发作后神经元的缺失及阻止细胞的凋亡等.但丙戊酸钠发挥神经保护作用的同时也存在一些不良反应.该文重点就丙戊酸钠神经保护作用及其机制的研究现状作一综述.     

诱导型一氧化氮合酶和缺氧缺血脑损伤

缺氧缺血可导致严重的神经系统疾病,如脑卒中、新生儿缺氧缺血性脑病。诱导型一氧化氮合酶在缺氧、缺血过程中被诱导表达,产生过量一氧化氮,导致神经系统的炎症反应及神经元死亡,加重神经损伤。抑制诱导型一氧化氮合酶表达在体内体外实验及临床应用中显示了一定的神经保护作用。该文综述了诱导型一氧化氮合酶在中枢神经系统中的表达及与缺氧缺血脑损伤的相关性,展望了诱导型一氧化氮合酶抑制剂作为缺氧缺血脑损伤治疗策略的前景。     

缺氧缺血性脑病大鼠脑多巴胺含量的动态变化及病理观察

目的：探讨多巴胺（DA）在缺氧缺血性脑损伤（HIBD）中的变化规律，揭示HIBD中细胞形态变化及其死亡形式，为缺氧缺血性脑病（HIE）的发病机制提供实验和理论依据。方法：利用7日龄SD大鼠99只，随机分为对照组，假手术组和实验组，用高效液相－电化学检测法测定脑损伤后0min,30min,1h,3h,6h,9h,12h,24h,48h皮层、纹状体、脑干DNA含量的动态变化。光镜下观察组织的病理改变。结果：1．动物缺氧缺血（HI）后DA在30min即有明显上升，纹状体和皮层、脑干内DA含量分别在HI后6h,9h达高峰，之后缓慢下降。2．细胞病理改变；HI后3h时水肿，6h时有局灶性坏死，12h,24h及48h出现大量坏死的神经细胞。3．凋（APO）出现在细胞坏死之前，HI后3h APO细胞出现，6h后APO细胞明显增加。结论：1．新生鼠HI后早期脑细胞内DA含量即增高，6h,9h可达到最高水平，脑细胞损伤与DA含量有关。2．HI后脑细胞死亡有APO和坏死两种形式。     

Neonatal brain infections

Infections of the brain in the neonatal period differ considerably from infections in the older child, due to a variety of age-specific factors that are related not only to the child, but also to the mother, and to specific pathogenic organisms. It has been recognized that clinical and neurological signs are often non-specific, sometimes scarce, and seldom correlate with the extent of neuroimaging findings, thus warranting early imaging to ensure timely therapy and improved outcome.     

Hypoglycemic brain injury

Hypoglycemia frequently occurs in newborn infants who previously have suffered asphyxia, who are offspring of diabetic mothers, or who are low birthweight for gestational age (IUGR). Many infants who are hypoglycemic do not exhibit clinical manifestations, while others are symptomatic and at risk for the occurrence of permanent brain damage. This review emphasizes the clinical, neuropathologic, and neuro-imaging features of hypoglycemia in newborn infants, especially those who are symptomatic. Neurologic morbidity occurs particularly in those infants who have suffered severe, protracted, or recurrent symptomatic hypoglycemia. Experimental observations emphasize the resistance of the immature brain to the damaging effect of hypoglycemia; such resistance occurs as a consequence of compensatory increases in cerebral blood flow, lower energy requirements, higher endogenous carbohydrate stores, and an ability to incorporate and consume alternative organic substrates to spare glucose for energy production. Hypoglycemia combined with hypoxia-ischemia (asphyxia) is more deleterious to the immature brain than either condition alone.     

Childhood brain tumors

Primary malignant tumors of the central nervous system (CNS) account for about 16% of all childhood malignancies. These tumors are the second most common type of childhood cancer and the most frequent of the solid tumors. The small increase in incidence noted over the past two decades most likely represents advancements in diagnostic technologies rather than true changes in disease frequency, though this is controversial. CNS tumors are diverse, representing many histological types and arising in a variety of anatomic sites. The most common malignant tumors include astrocytomas (52%), medulloblastomas/primitive neuroectodermal tumors (PNETs) (21%), gliomas (19%), and ependymomas (9%). The current 5-year survival rate for all pediatric CNS tumors is 67%, but rates differ considerably among tumor types. Treatment modalities also differ according to histological type. Currently, about 25% of patients are treated with surgery alone, 40% undergo surgery plus radiation, and 30% are treated with surgery, radiation, and chemotherapy. Survivors of childhood brain tumors are at substantial risk for increased morbidity and late mortality. Five-year survivors of brain tumors are 13 times more likely to die than healthy age- and sex-matched peers. Disease recurrence remains the single most common cause of late deaths (70%). Neurological, neurocognitive, and endocrine disturbances are the most prevalent disabilities observed among long-term survivors of pediatric brain tumors.     

Neonatal brain injury

Complacency about long-term outcomes in newborns is being eroded rapidly with new information. We have examined developments in the area from an explicitly clinical approach, focusing on etiology, diagnostic modalities, and therapies. We attempt to discuss relevance from the preterm and the term perspective. Emerging evidence implicating chorioamnionitis as a significant contributor to neonatal brain injury is discussed. Therapeutic modalities such as magnetic resonance imaging and electrophysiological monitoring offer some potentially new tools for the clinician. An exploding series of basic advances suggest several potentially new strands of therapy. We discuss two that deserve further clinical exploration, namely anti-inflammatory strategies and thread hormone supplementation. In the arena of therapy, however, the paucity of large trials from which to guide therapies is a predominant theme, leaving a large reservoir of uncertainty for the clinician.