对大鼠PC12细胞用于定量测定神经生长因子活性两种方案的评价

建株的大鼠肾上腺嗜铬细胞瘤ＰＣ１２细胞，在神经生长因子ＮＧＦ的作用下，会长出神经突起。这一现象被用于神经生长因子的活性测定。但就定量测定而言、目前已 方法，方案，包括判定阳性细胞的标准，均有一定差异，而我国也尚未建立起对这一重要的 活性的标准测定法。     

神经的生长与再生

神经的生长与再生与胚胎学极其相似.在胚胎期神经的诱导是与可弥散的物质有关,这些物质可称为神经生长因子.神经的存活和生长是离不开神经生长因子的.在神经轴突膜上有一个能识别并能结合神经生长因子分子的特异受体,从而导致神经生长因子分子促使轴突生长和维持神经元存活起生化活动的作用.成年个体的神经损伤以后,在受伤的部位总要产生一些胶状渗出物,这些物质对损伤的神经起诱导作用,从而诱导神经再生.这就是神经的诱导性.     

老年痴呆症的药物治疗进展

老年痴呆症（ＡＤ）是一种神经退行性疾病，至今病因未明，且尚无特效药，近年来，临床运用促智药、胆碱酯酶抑制剂、乙酰胆碱释放增强剂、ＮＳＡＩＤ、神经生长因子等药物，对改善症状、延缓疾病表一定的作用。此病的病因及药的治疗有待作更深入的研究 。     

老年痴呆症的药物治疗进展

老年痴呆症（AD）是一种神经退行性疾病，至今病因未明，且尚无特效药。近年来，临床运用促智药、胆碱酯酶抑制剂、乙酸胆碱释放增强剂、NSAID、神经生长因子等药物，对改善症状、延缓疾病的发生有一定的作用。此病的病因及药物治疗尚有特作更深入的研究。     

基因工程菌E.Coli2426／pMN表达产物的纯化

用基因工程菌Ｅ．Ｃｏｌｉ２４２６／ｐＭＮ高效表达了麦芽糖结合蛋白—人神经生长因子（β）融合蛋白，菌体经超声波破碎后，上清液经Ａｍｙｌｏｓｅ亲和柱一步即可获得ＳＤＳ－ＰＡＧＥ纯蛋白质，回收率为１０％左右，按标准分子量计，该融合蛋白（５５ＫＤａ）确是麦芽糖结合蛋白（４２ＫＤａ）与人神经生长因子（β）（１３ＫＤ）的络合物     

蛇毒的研究进展及其在医药领域的应用

就国内外主要毒蛇的蛇毒组分、对凝血系统的影响及蛇毒在医药领域的应用进行了综述．蛇毒的化学成分十分复杂,主要包括酶、神经毒性多肽、神经生长因子、膜活性多肽及其他生物活性肽,其中酶类包含多种与凝血系统、纤溶系统相关的成分．蛇毒在医药领域具有非常重要的作用,主要有促凝作用、溶栓作用、镇痛作用、降压作用和抗肿瘤作用．     

人18周胎儿脑cDNA文库的构建及鉴定

许多脑基因的特异性表达对人脑的发育，分化有着重要的作用，为了研究这些基因的结构和功能，构建了一个人１８周胎儿脑ＣＤＮＡ文库，抽提总ｍＲＮＡ后，经过一系列的酶促反应合成ｃＤＮＡ，分有分离柱除去小片段后克隆到λｇｔ１０载体中，转染宿主菌Ｃ６００ｊｆｌ后文库包装效率为４．６×１０＾６ｐｆｕ／μｇ，ｃＤＮＡ平均郫在于１．２ｋｂｐ已知序列设计引物，从ｃＤＮＡ文库中扩增出神经生长因子（ＮＧＦ）的生长编码基因     

神经生长因子有助修复受损心肌

[科技日报]英国布里斯托尔人学的一项研究发现，提升心脏病患者心脏部位的神经生长因子（NGF）水水平，可帮助受损心肌快速修复，从而有效提高患者的生存几率。这一研究结果发表在最近出版的《循环研究》杂志上。     

神经生长因子及其受体在雌性哺乳动物生殖系统中的作用

神经生长因子（nerve growth factor,NGF）属于靶蛋白的一种,通过与其受体trkA与p75结合来发挥其旁分泌或自分泌作用。最初的研究表明NGF的作用仅限于神经系统,但越来越多的证据里示NGF也可作用于非神经细胞。在哺乳动物生殖系统中,NGF及其受体在卵巢,输卵管,子宫及胎盘中都有不同程度的表达,并对生殖系统的生长、发育、细胞的分化与增殖产生一定的作用。     

Tropic1808基因重组蛋白对损伤坐骨神经脊髓细胞凋亡的影响

探讨Tropic1808基因重组蛋白对损伤坐骨神经的新生大鼠脊髓细胞凋亡影响,将新生SD大鼠一侧坐骨神经切断后,用无菌止血海绵包裹断离的神经近侧端,海绵内加入Tropic1808基因重组蛋白,阳性用神经生长因子、阴性用生理盐水作为对照;术后3、6、12h经TUNEL法染色,在光镜、电镜和图像分析系统下,了解L4－L5段脊髓细胞凋亡情况。得到生理盐水组的脊髓出现大量绸亡细胞;Tropic1808基因重组蛋白组凋亡细胞数量较生理盐水组显减少;Tropic1808基因重组蛋白组与神经生长因子组之间凋亡细胞数量的差别无显性意义。说明Tropic1808基因重组蛋白有保护受损神经组织,减少细胞凋亡的作用。     

Alterations in the surface properties of cells responsive to nerve growth factor.

An initial effect of nerve growth factor on a responsive nerve cell line is to increase intracellular cyclic AMP, which in turn leads to a mobilisation of calcium ions. These events are correlated with structural changes in the plasma membrane, increased cell-substratum adhesion, and neurite outgrowth.     

根据神经类型测定综合心理运动能力的实验分析

大脑神经细胞的结构和功能是影响综合心理运动能力的重要因素.掌握按照神经类型测定综合心理运动能力的方法,对运动选材、教学训练、运动竞赛等方面有着重要意义.     

Proliferation and differentiation of neuronal stem cells regulated by nerve growth factor

Nerve growth factor plays an important part in neuron-target interactions in the late embryonic and adult brain. We now report that this growth factor controls the proliferation of neuronal precursors in a defined culture system of cells derived from the early embryonic brain. Neuronal precursor cells were identified by expression of the intermediate filament protein nestin. These cells proliferate in response to nerve growth factor but only after they have been exposed to basic fibroblast growth factor. On withdrawal of nerve growth factor, the proliferative cells differentiate into neurons. Thus, in combination with other growth factors, nerve growth factor regulates the proliferation and terminal differentiation of neuroepithelial stem cells.     

前列腺素E1,锌离子对大鼠感觉神经元的保护作用

目的探讨环化酶激活剂(AdenyIate cyclase activator)对周围神经损伤后感觉神经元存活和变性的影响.方法大鼠坐骨神经夹毁模型、分组,术后每d分别局部注射一定剂量的PGE1,hβNGF,共14 d.另一组从术前10 d开始喂以高锌饲料各组术后21 d取背根节(DRG)制片染色,用图像分析法观测PGE1和锌对DRG细胞数、核偏心率和核等圆径的影响,以人胎盘神经生长因子(hβNGF)作阳性对照.结果锌显著降低感觉神经元的死亡率,显著减轻核偏移、抑制核等圆径增大,与NGF组相比,P＞0 05.PGE1也明显减少神经元死亡,与夹毁组相比,P＜0 05结论神经损伤后锌促进感觉神经元存活和减轻细胞变性的保护作用与NGF无差别.PGE1对感觉神经元的保护作用不及NGF和锌.     

Structure, expression and function of a schwannoma-derived growth factor

During the development of the nervous system, cells require growth factors that regulate their division and survival. To identify new growth factors, serum-free growth-conditioned media from many clonal cell lines were screened for the presence of mitogens for central nervous system glial cells. A cell line secreting a potent glial mitogen was established from a tumour (or 'schwannoma') derived from the sheath of the sciatic nerve. The cells of the tumour, named JS1 cells, were adapted to clonal culture and identified as Schwann cells. Schwann cells secrete an autocrine mitogen and human schwannoma extracts have mitogenic activity on glial cells. Until now, neither mitogen has been purified. Here we report the purification and characterization of a mitogenic molecule, designated schwannoma-derived growth factor (SDGF), from the growth-conditioned medium of the JS1 Schwann cell line. SDGF belongs to the epidermal growth factor family, and is an autocrine growth factor as well as a mitogen for astrocytes, Schwann cells and fibroblasts.     

Restricted growth of Schwann cells lacking Cajal bands slows conduction in myelinated nerves

Nerve impulses are propagated at nodes of Ranvier in the myelinated nerves of vertebrates. Internodal distances have been proposed to affect the velocity of nerve impulse conduction; however, direct evidence is lacking, and the cellular mechanisms that might regulate the length of the myelinated segments are unknown. Ramón y Cajal described longitudinal and transverse bands of cytoplasm or trabeculae in internodal Schwann cells and suggested that they had a nutritive function. Here we show that internodal growth in wild-type nerves is precisely matched to nerve extension, but disruption of the cytoplasmic bands in Periaxin-null mice impairs Schwann cell elongation during nerve growth. By contrast, myelination proceeds normally. The capacity of wild-type and mutant Schwann cells to elongate is cell-autonomous, indicating that passive stretching can account for the lengthening of the internode during limb growth. As predicted on theoretical grounds, decreased internodal distances strikingly decrease conduction velocities and so affect motor function. We propose that microtubule-based transport in the longitudinal bands of Cajal permits internodal Schwann cells to lengthen in response to axonal growth, thus ensuring rapid nerve impulse transmission.     

Nerve regeneration factor promotes nerve regeneration in rat

Nerve regeneration factor (NRF) extracted from an oral liquid of traditional Chinese medicine, as a nerve growth decoction has been reported by previous studies to exert effects of promoting nerve growth and preventing neuron apoptosis. For new insights into the function of NRF on primary cultured neurons, we investigated the neurite outgrowth in cultured rat dorsal root ganglion (DRG) explant treated with NRF by immunofluorescence and the gene and protein expressions of neurofilament-H(NF-H) and growth associated protein 43 (GAP43) in the cultured rat DRG neurons by real-time quantitative RT-PCR and Western blotting, respectively. In addition, we used a rat model of sciatic nerve crush to evaluate the effect of NRF on regeneration of injured sciatic nerve by a combination of walk track analysis, electrophysiological and histological assessments. The in vitro experiments indicated that NRF promoted the neurite growth of DRGs and the expression of NF-H and GAP43 at mRNA and protein levels in DRG neurons, and in vivo experiments showed that NRF improved peripheral nerve regeneration and functional recovery.     

神经营养因子联合治疗促进脊髓轴索再生的研究现状

神经营养因子（neurotrophic factors,NTFs）在急性脊髓损伤（spinal cord injury,SCI）后神经细胞的生长发育、保护和修复的过程中发挥重要作用。然而,单一的治疗尚不足以激活神经元内源性的再生程序;其次,再生抑制因子限制了NTFs对SCI后结构和功能恢复。因此,越来越多的学者选择以联合的方式探索NTFs对再生的促进作用。本文归纳了NTFs以联合的方式治疗轴索再生的基本原理和最新进展,旨在为联合治疗的进一步研究提供科学指导。     

Immunohistochemical localization of endogenous nerve growth factor

Nerve growth factor (NGF) has been proposed as a trophic molecule essential for the development of sympathetic and primary sensory neurones. In newborn mice and rats, administration of nerve growth factor results in an increase in the number of surviving neurones, whereas administration of antiserum to NGF decreases neuronal survival. Thus it has been proposed that the factor is produced and secreted by the relevant target tissues to provide trophic support for the ingrowing nerves. The site of synthesis of nerve growth factor is still unknown, and it has been emphasized that a precise physiological role for the molecule cannot be ascribed until the cell types that produce it are known. I report here the use of immunohistochemistry to localize endogenous NGF in the rat iris, a tissue in which there is sound biochemical evidence for the production of NGF activity. Surprisingly, the results reveal that NGF can be detected readily in Schwann cells, but not in smooth muscle cells of the iris when it is sympathetically denervated or cultured.     

Basic fibroblast growth factor prevents death of lesioned cholinergic neurons in vivo

Cutting the axons of the cholinergic neurons that project to the hippocampal formation results in death of most of these cells. Previous studies have shown that administration of nerve growth factor before or at the same time as the lesion will prevent this cell death. Here we demonstrate that basic fibroblast growth factor (FGF) administered into the brain reduces the death of cholinergic neurons in the medial septum and diagonal band of Broca after transection of their axons, in both young adult and aged rats. Moreover, FGF can partially protect against death of cholinergic neurons even when administered two days after axonal transection. These results indicate a possible function for FGF in the normal support of basal forebrain cholinergic neurons, but its range of activity could be wider, for FGF also supports noncholinergic neurons in vitro, it is localized in many of the central nervous system neurons, and it is found in relatively high concentrations in the brain.