蓝光照射辅助治疗新生儿黄疸53例疗效观察

新生儿黄疸是新生儿常见症状,它既可以是生理现象,又可以是多种疾病的重要表现.原因是新生儿自身胆红素代谢特点致胆红素在体内积聚而发病.分为生理性、病理性黄疸两大类.部分病理性黄疸可致中枢神经系统受损而产生胆红素脑病,危及生命或留有严重的后遗症.故应加强对新生儿黄疸的临床观察,找明病因及时治疗.     

FGF与中枢神经系统

成纤维细胞生长因子 (fibroblastgrowthfactor ,FGF)是一类结构上相类似的多肽家族。家族许多成员在中枢神经系统表达 ,它们与其特异性受体 (FGFRs)结合发挥广泛的生理作用。尤其对中枢神经系统的发育、损伤、修复以及神经干细胞的增殖和分化方面有重要意义。本文综述了GFFs及其受体的研究进展及其在中枢神经系统发育及损伤修复中作用。     

纳米技术在中枢神经系统中的作用

纳米技术是指在0.1-100nm量度范围内对物质结构和制造技术进行研究。纳米粒子能够进入细胞并与细胞及其组织发生作用,从而在分子水平上产生生物效应。由于纳米粒子可以和有机高分子多肽、无机盐等结合通过血脑屏障,已经在中枢神经系统药物转运、中枢神经系统疾病的诊断和治疗中发挥重要作用。本文从纳米粒子与血脑屏障的关系、纳米粒子在神经系统的保护、神经系统的再生中的作用等几方面阐述纳米技术在中枢神经系统应用中的现状与前景。     

PI3K和Akt在心血管疾病中的作用

PI3K-Akt信号通路在细胞增殖和代谢中发挥了重要作用,并且PI3K-Akt信号通路在心脏保护机制——缺血预适应和缺血后适应中发挥重要作用。本文通过分析PI3K分子和Akt分子以及PI3K-Akt信号通路对心脏和血管生理性和病理性的影响,旨在了解其在心血管疾病中的作用。     

中枢神经系统中星形胶质细胞作用的研究进展

星形胶质细胞是中枢神经系统中维持生理动态平衡的关键细胞，具有广泛功能，在正常生理和疾病状态中发挥多样的调节作用，包括提供信息传递和代谢支持、调控血脑屏障功能、调控突触形成、建立和维持适当的突触连接、调节神经保护及神经毒性作用等功能，在中枢神经系统的生长，各种生理、病理环境下均发挥重要作用。该文旨在阐明星形胶质细胞在中枢神经系统中的作用，总结其具体的调节过程和相关机制，为神经系统相关疾病的诊断和治疗提供新思路和方向。     

免疫系统中细胞的程序性死亡：文献综述

细胞的程序性死亡是一种生理性死亡。近年来这种过程在免疫系统的发生与发展中也起着很重要的作用。影响免疫细胞程序性死亡的因素多种多样。本文简要综述了近年来在这方面的研究进展。     

用免疫组化法检测肾母细胞瘤过度表达基因蛋白在大鼠中枢神经系统的分布

为探讨肾母细胞瘤过度表达基因（ＮＯＶ）在中枢神经系统发育和分化过程中的作用，用免疫组织化学ＡＢＣ方法辅以微波抗原修复技术研究ＮＯＶ原癌基因蛋白的分布和定位。结果发现，ＮＯＶ蛋白在成年大鼠的中枢神经系统中有较为广泛的存在，其分布区域包括大脑皮质、海马、丘脑和下丘脑的部分核团、脑桥及脊髓前角。结果提示：ＮＯＶ基因在中枢神经系统的功能活动中可能起重要作用。有关研究正在深入进行中     

腺苷A_(2A)受体在中枢神经系统损伤中的相关研究进展

中枢神经系统损伤以其高发生率和高死残率,已经成为紧迫的世界性公众健康问题,但目前还缺乏公认安全有效的疗法。腺苷A_(2A)受体(A_(2A)R)作为神经精神活动及中枢神经系统损伤的重要调控因子,引起了普遍的关注。目前,研究发现在中枢神经系统损伤中,激活A_(2A)R有加重神经损伤与神经保护的复杂作用。本文即对A_(2A)R在中枢神经损伤中的作用与机制进行探讨。     

胆汁酸在中枢神经系统疾病中的作用

胆汁酸是胆固醇代谢的产物，主要在肝脏及肠道微生物的共同作用下产生，少部分可由中枢神经系统内神经元和星形胶质细胞产生。中枢神经系统中不但有合成胆汁酸的多种酶类，还有多种胆汁酸的结合受体，比如法尼醇X受体(FXR)、武田G蛋白偶联受体5(TGR5)、鞘氨醇1-磷酸受体2(S1PR2)等，在脑内的物质和能量代谢、神经元电活动过程中发挥重要作用，并与阿尔茨海默病(AD)、帕金森病(PD)、亨廷顿病(HD)、脑卒中等多种神经系统疾病有关。以上表明胆汁酸是肠道微生物调节神经系统功能的重要介质。深入研究胆汁酸对中枢神经系统的影响，将有助于丰富脑-肠轴的理论，为中枢神经系统疾病的治疗提供新的思路。     

免疫系统中细胞的程序性死亡

细胞的程序性死亡是细胞的一种生理性死亡。近年来发现这种过程在免疫系统的发生与发展中也起着很重要的作用。影响免疫细胞程序性死亡的因素多种多样。本文简要综述了近年来在这方面的研究进展。     

一氧化氮在中枢神经系统发育中的作用

一氧化氮作为中枢神经系统内的非经典性细胞递质和信使分子,有着多方面的生物效应。在神经发育的过程中,一氧化氮可通过NO/cGMP系统调节突触的形成及修饰,介导成熟期突触可塑性等过程。本文结合其生物学特性和作用机制就一氧化氮对中枢神经系统发育的影响作一综述。     

Impairment of TNF-Receptor-1 Signaling but not Fas Signaling Diminishes T-Cell Apoptosis in Myelin Oligodendrocyte Glycoprotein Peptide-Induced Chronic Demyelinating Autoimmune Encephalomyelitis in Mice

T-cell apoptosis in inflammatory demyelinating lesions of chronic myelin oligodendrocyte glycoprotein peptide35-55 induced autoimmune encephalomyelitis was studied in several different gene knockout mice as well as their wild-type counterparts. The gene deletions included tumor necrosis factor (TNF) alpha, lymphotoxin, TNF receptor 1 or 2, Fas-L, inducible nitric oxide synthase, perforin, and interleukin1beta-converting enzyme. Impairment of the TNF receptor 1 pathway led to a 50% reduction of T-cell apoptosis in the central nervous system lesions, whereas the other genetic deletions showed no significant effect. Our study thus identified the TNF receptor 1 signaling pathway as one mechanism responsible for the removal of T lymphocytes from inflammatory demyelinating lesions of the central nervous system.     

Roles of fibrinolytic system components in the nervous system

Recent studies have remarkably clarified the physiological roles of fibrinolytic system components on memory formation, neuronal plasticity, neuronal migration, neuronal cell death and axonal regeneration, together with their pathophysiological roles in ischemic stroke, intracerebral hemorrhage and Alzheimer disease in the central nervous system. Fibrinolytic system components also have various roles in the peripheral and autonomic nervous system, not only under physiological conditions but also under pathophysiological conditions. In these roles, fibrinolytic system components work not only through the extracellular proteolytic cascade but also through activation of their own receptors. This paper reviews the roles of fibrinolytic system components in the nervous system.     

小胶质细胞及其相关炎性信号通路

小胶质细胞作为中枢系统重要的免疫效应细胞，在中枢神经系统损伤及疾病处理中发挥着不可忽视的作用。本文从小胶质细胞的生物学特性及其相关的炎性信号通路（Notch信号通路、Toll样信号通路、AMPK信号通路、NF-κB信号通路）两大方面探讨，以期为临床抗炎药物的开发提供新思路。     

RAM7,一种新的核蛋白分子在小鼠中枢神经系统的表达

Notch信号途径参与动物多种组织和器官尤其是神经系统的发育调节。 RBP-Jκ是 Notch信号途径中的关键分子 ,RAM7是近年通过酵母双杂交技术发现的与 RBP-Jκ相互作用的蛋白。本实验表达 RAM7C-末端 60 k D的多肽片段 ,并制备特异性的多克隆抗体 ,检测 RAM7在小鼠中枢神经系统的分布。结果显示 :RAM7主要呈细胞核染色 ,在中枢神经系统中广泛分布 ;尾壳核、丘脑室旁核、下丘脑室旁核、室周核等核团内没有 RAM7阳性神经元 ,但存在着一定数量的 RAM7阳性神经纤维 ;另有相当多 RAM7胞浆染色的细胞和神经元以及一些胶质细胞 ,局限在脑室和脑室周围的神经组织中。RAM7分子的分布对其可能的生理功能有一定的提示作用     

Pathological systems in CNS performance

The occurrence of new pathological integrations from the altered nervous structures in the central nervous system (CNS) is a highly important mechanism of nervous disorders. At the level of systemic relations, such an integration represents a new pathodynamic arrangement from the primarily and secondary altered formations of the CNS. The results of its performance are of a biologically negative, pathogenic value for the body. So such a pathodynamic arrangement is determined by the author as a pathological system (PS). PS substantially and basically differs from the physiological system in the mechanisms of occurrence, clinical manifestations, and performance results. PS is formed and fixed due to the plastic processes intrinsic to the nervous system, under the influence of the pathological determinant the hyperactive CNS formation that can also determine the nature of PS activity. The pathological systems are a pathobiological basis and a pathophysiological mechanism of neuropathological syndromes that are a clinical manifestation of PS performance. Each neuropathological syndrome has its PS. The pathological systems may consist of different formations, levels, and spheres of CNS performance, which determines the content of neuropathological syndromes, including those applied to higher nervous performance, behavior, and the mental sphere.     

细胞型朊蛋白分子结构及其相关疾病的研究进展

细胞型朊蛋白(cellular prion protein,PrPC)是一种高度保守且广泛表达的糖磷脂酰基醇(glycosyl phosphatidyl inositol,GPI)锚定糖蛋白,定位于脂筏.在哺乳动物体内,PrPC在中枢神经系统和网状内皮系统中大量存在,其它组织中有少量分布.目前研究表明,PrPC分子结构具有重要的生理功能之外,还与神经系统疾病和肿瘤发生等相关.本文重点阐述了PrPC的分子结构、组织分布及其相关疾病研究进展.     

Identification of differentially expressed genes in the denervated rat hippocampus by cDNA arrays

To elucidate the molecular mechanism underlying the physiological responses to injury in the central nervous system, gene expression profiles in rodent hippocampus following perforant path transection were investigated using cDNA array hybridization. Of the 8000 arrayed clones, 47 exhibited differential expression by >3-fold difference in the denervated hippocampus from control, with 15 up-regulated and 22 down-regulated. They can be functionally assigned into several classes, among which the most prominent are those coding proteins involved in macromolecules synthesis and processing. Northern blot analysis verified the validation of the aforementioned array data. These results throw some new light on the physiological responses of the hippocampus to entorhinal deafferentation at molecular level.     

Pavlovian conditioning of corticotropin-releasing factor-induced increase of blood pressure and corticosterone secretion in the rat

Corticotropin-releasing factor (CRF) is clearly involved in the central regulation of the pituitary-adrenal axis and, moreover, of autonomic nervous system functions. Enhanced sympathetic activity with subsequent increases in blood pressure and heart rate and attenuation of the baroreceptor reflex results from the intracerebroventricular (i.c.v.) administration of CRF. Additionally, the peptide has a variety of potent effects on behavioural responses in animals similar to those observed after an experimentally evoked stress. It was therefore of obvious interest to examine whether CRF is a possible mediator of the learning processes associated with physiological stress reaction patterns. This report clearly demonstrates a classical conditioning of the endocrine (i.e. corticosterone secretion) and haemodynamic (i.e. blood pressure) sequelae following central CRF application and thus indicates that this mechanism is of physiological significance for learned stress responses.     

Auditory neuropathy in streptozotocin-induced diabetic mouse

An investigation of the mechanism of damage to the peripheral nervous system and central nervous system in diabetes mellitus (DM) is highly important in current neurological research. Auditory neuropathy is a hearing disorder in which the auditory brainstem evoked potential is absent or severely abnormal. This study investigated auditory neuropathy caused by streptozotocin in mouse model. In order to assess diabetic auditory neuropathy, we evaluated auditory brainstem response (ABR) for the evaluation of sensorineural function in peripheral auditory nerve. Auditory middle latency response (AMLR) was employed to assess the middle response in the midbrain. STZ groups significantly increased the absolute latencies IV and the interpeak latencies I-III and I-IV of ABR compared with STZ 0 group. Pa latency of AMLR also significantly increased in proportion to STZ dosage. Taken together, our results demonstrate that STZ-induced DM may impair the auditory pathway from peripheral auditory nerve to midbrain in the mouse model. We suggest that the STZ-induced diabetic mouse model may be useful for the evaluation of auditory pathway impairment by using ABR and AMLR tests.