内脏平滑肌Cajal间质细胞起搏功能(英文)

胃肠道的大部分区域都存在着一种特殊的间质细胞——Cajal间质细胞(interstitial cells of Cajal,ICCs)。尽管在100多年前它们的存在就已被发现,但是直到最近几十年的研究才逐渐揭示了它们的功能。在胃肠道,ICCs被认为是平滑肌自发性节律性电活动,即"基本电节律"(又称"慢波")的起搏细胞,并介导神经至平滑肌的神经信号传递活动。除胃肠道外,ICC样细胞同样存在于其它内脏平滑肌,如泌尿、生殖系统以及血管平滑肌等。本文仅就这些内脏平滑肌ICCs的功能做一简单综述。     

试论神经科学发展的几个特点

近年来神经科学的急剧发展,显著地改写着人们对正常和异常神经活动本质的认识。当我们回顾20世纪,特别是第二次世界大战后神经科学研究所走过的道路和取得的重大进展时,有几个特点给人印象特别深刻。首先,作为一门实验科学,对神经系统的研究在很大程度上有赖于研究手段的发展和完善。在19世纪末叶,尽管显微镜已具备了足够的空间分辨的能力,但是如果没有Golgi染色法的发明,神经细胞在显微镜的视野中只是一团乱麻,Cajal不可能作出关于神经元的几个     

胚胎小肠Cajal细胞的发育研究

目的研究人胚胎小肠cajal细胞的发育变化规律。方法采用全层铺片结合切片的免疫细胞化学技术。结果Cajal细胞呈酪氨酸激酶受体(Kit)和波形蛋白(vinlentin)免疫反应阳性。在胚胎发育早期,cajal细胞较少,为单层,稀疏分布于肌间神经丛周围,细胞为梭形,可见两个短而小的突起,未见分支;随着胎龄的增加,Cajal细胞数量增多,胞体增大,突起伸长,并出现分支。此时,肌间神经丛周围的Cajal细胞出现两层,其长轴彼此垂直,分别平行于环行肌和纵行肌。与此同时环行肌层内亦可见少许Cajal细胞;出生前,肌间神经丛部位的Cajal细胞接近成熟,两层细胞的突起进一步增多、伸长,彼此间形成与成人相似的完整的细胞网络。此时深肌丛附近亦可见少量Cajal细胞。结论人的小肠Cajal细胞发育有一定的时间顺序,即肌间神经丛周围最先出现,肌内次之,深肌丛较晚,出生前肌间神经丛周围的Cajal细胞已经接近成熟。这种发育演变若发生异常,可能导致某些胃肠动力障碍性疾病。     

Cajal间质细胞与慢性假性结肠肠梗阻关系的研究进展

Cajal间质细胞(interstitial cells of cajal,ICC)主要分布在胃肠道平滑肌细胞与神经纤维之间,是一类特殊的间质细胞,它是胃肠运动的起搏细胞,具有产生、传导慢波,调节胃肠道平滑肌运动的功能。而慢性假性肠梗阻是由于胃肠神经抑制,毒素刺激或肠壁平滑肌本身病变,导致的肠壁肌肉运动功能减弱,临床上具有肠梗阻的症状和体征,但无肠内外机械性肠梗阻因素存在,故又称动力性肠梗阻,按病程有急性和慢性之分,麻痹性肠梗阻和痉挛性肠梗阻属于急性假性肠梗阻,深入研究Cajal间质细胞,对进一步认识胃肠运动的生理及胃肠动力疾病的发生机制有重要意义。     

小鼠小肠Cajal间质细胞和氮能与胆碱能神经元的数量和形态生后发育特征

目的观察出生后至成年小鼠小肠Cajal间质细胞(interstitial cells of Cajal,ICC)、氮能神经元、胆碱能神经元的发育情况。方法取出生后7d、28d和60d小鼠小肠制作全层铺片,利用(免疫)组织化学等技术分别显示ICC、氮能神经元、胆碱能神经元的数量和形态。结果小鼠生后小肠ICC的数量明显增多,但单位面积细胞数量随小肠长度和面积的增加而降低,在生后28d达到成体水平。而氮能神经元和胆碱能神经元的数量生后即达成体水平,随年龄增加仅见神经突起增长、神经纤维增粗以及神经网络的密度变疏等改变。结论小鼠小肠ICC和胃肠壁内的肠神经系统(enteric nervous system,ENS)神经元的发育并非同步,ICC的发育成熟明显晚于ENS,提示出生后早期局部微环境更易影响ICC的发育与成熟,可能与部分婴幼儿胃肠运动功能障碍疾病的发生发展有关。     

神经威武

Rodolfo Llinas采用大胆的方法研究神经生理学，彻底改变了人们对神经元个体的理解，以及对神经元产生运动和意识的过程的认识。     

新生小鼠小肠Cajal间质细胞增殖的实验研究

Cajal间质细胞（interstitial cells of Cajal,ICC）是胃肠道运动的起搏细胞,本研究拟探讨在新生小鼠小肠的发育过程中ICC是否出现增殖。采用新生2d（P2d）,14d（P14d）和24d（P24d）的小鼠小肠,采用BrdU腹腔注射,24h后取材,Kit和BrdU免疫荧光染色。Kit免疫荧光显示,Kit阳性的ICC在肌间神经丛周围呈网络状分布,     

膀胱Cajal样细胞的研究现状与展望

Cajal间质细胞(ICCs)是胃肠道的起搏者,在消化系统中具有重要的起搏功能.目前在膀胱中发现了形态学和免疫学上和ICCs相似的细胞,被称为膀胱Cajal样细胞.这类细胞既具有某些起搏细胞的特征,同时又与膀胱逼尿肌细胞紧密相连.这类细胞在膀胱活动中所起的作用就成为广大科研人员关注的问题,本文就膀胱Cajal样细胞的结构、形态、分布特点及其在信号传导中的作用进行了综述.     

综述与专论: 神经胶质细胞转分化为神经元的研究进展

细胞转分化是通过基因重编程，诱导某种细胞直接转变为另一种细胞，而不经过其他中间状态的过程。神经元丢失是神经系统疾病中常见的病理过程，神经元丢失通常不可逆转，且造成运动、感觉、精神症状。而由于人中枢神经系统神经元再生能力十分有限，仅有部分区域在神经损伤的刺激下能够新生少量神经元。在这样的背景下，将神经胶质细胞（星形胶质细胞、小胶质细胞和少突胶质前体细胞）在神经元丢失处原位转分化为功能性神经元并整合进神经网络的治疗性策略，受到了广泛关注。近年来，学者通过在神经胶质细胞中将神经元命运决定的重要转录因子过表达或敲减等手段，成功实现其向神经元的转分化，取得多项重大进展，但由于目前研究手段的局限性、判断标准的分歧性、结果和结论间较难自洽等问题，部分研究成果的结论仍存在很大的争议。本文系统地回顾了神经胶质细胞转分化为神经元的发现与发展历程，总结了神经胶质细胞转分化为神经元的重要发现，并进行讨论与展望。     

豚鼠膀胱内Cajal样间质细胞的分布情况研究

目的:观察Cajal样间质细胞(ICCs)在成年豚鼠膀胱的分布情况.方法:取5只成年豚鼠膀胱,制作全层冰冻切片,行ICCs特异性标志物c-kit免疫荧光染色,按粘膜层、粘膜下层和肌层进行统计分析.结果:豚鼠膀胱内可见c-kit免疫阳性细胞,胞体呈梭形,两端伸出长的突起,其形态与肠壁肌层Cajal细胞相似.且肌层和粘膜下层多于粘膜层.结论:豚鼠膀胱存在Cajal样间质细胞,并在肌层高表达,可能参与膀胱自主节律性运动的调控,调节逼尿肌的运动,为"神经-Cajal样间质细胞-肌肉"单元的形成提供组织学基础.     

激光对花生诱变效果的研究

Ｈｅ－ＮｅＹＡＧ和ＣＯ２激光对花生Ｌ１代幼苗期有刺激生长的作用,ＣＯ２激光对花生Ｌ１代的株高有较明显的抑制作用,ＣＯ２,Ｈｅ－Ｎｅ和ＹＡＧ激光对花生Ｌ１代植株的总果数,饱果数有一定的增多作用,且前者最明显,但Ｎ２激光对花生Ｌ１代植株的总果数,饱果数均有明显的减少作用;Ｈｅ－ＮｅＹＡＧ,Ｎ２和ＣＯ２激光均能诱发药生根尖细胞染色体畸变,且畸变率随辐照剂量的增大而上升,以上四种激光所诱发发生的变异性状是     

Failure of CD4 T-cells to respond to liver-derived antigen and to provide help to CD8 T-cells

CD4 T-cell help is required for the induction of efficient CD8 T-cells responses and the generation of memory cells. Lack of CD4 T-cell help may contribute to an exhausted CD8 phenotype and viral persistence. Little is known about priming of CD4 T-cells by liver-derived antigen. We used TF-OVA mice expressing ovalbumin in hepatocytes to investigate CD4 T-cell priming by liver-derived antigen and the impact of CD4 T-cell help on CD8 T-cell function. Naïve and effector CD4 T-cells specific for ovalbumin were transferred into TF-OVA mice alone or together with naïve ovalbumin-specific CD8 T-cells. T-cell activation and function were analyzed. CD4 T-cells ignored antigen presented by liver antigen-presenting cells (APCs) in vitro and in vivo but were primed in the liver-draining lymph node and the spleen. No priming occurred in the absence of bone-marrow derived APCs capable of presenting ovalbumin in vivo. CD4 T-cells primed in TF-OVA mice displayed defective Th1-effector function and caused no liver damage. CD4 T-cells were not required for the induction of hepatitis by CD8 T-cells. Th1-effector but not naïve CD4 T-cells augmented the severity of liver injury caused by CD8 T-cells. Our data demonstrate that CD4 T-cells fail to respond to liver-derived antigen presented by liver APCs and develop defective effector function after priming in lymph nodes and spleen. The lack of CD4 T-cell help may be responsible for insufficient CD8 T-cell function against hepatic antigens.     

Ability of human T lymphocytes to adhere to vascular endothelial cells and to augment endothelial permeability to macromolecules is linked to their state of post-thymic maturation

The accumulation of mononuclear cells at sites of chronic inflammation is dependent on a number of factors including localized adherence of lymphocytes to vascular endothelial cells (EC), cytokine-mediated increased adhesiveness of endothelium, chemotactic factors and endothelial permeability. The present study investigates two of the above attributes of lymphocyte-EC interaction: namely, the ability of maturationally distinct subpopulations of human T lymphocytes to adhere to vascular EC and to increase vascular endothelial permeability to macromolecules in an in vitro model. Thus, human T lymphocytes were separated into CD4+ CD8-helper/inducer, CD4- CD8+ cytotoxic/suppressor, CD29+ CD45RA- CD45RO+ memory, and CD29- CD45RA+ CD45RO- naive/virgin T subpopulations, were activated with PHA and PMA, and then examined for their adherence to EC and also for their effect on endothelial permeability. Upon activation, cells within each of the above four subpopulations exhibited increased adherence to EC. In contrast, resting CD29+ CD45RA- CD45RO+ memory T lymphocytes exhibited two to three times greater ability to adhere to EC than their CD29- CD45RA+ CD45RO- naive/virgin counterparts. Consistent with their increased adherence to EC, CD29+ CD45RO+ memory T lymphocytes, when activated, significantly increased endothelial permeability to albumin. Although activated CD45RA+ naive T lymphocytes exhibited increased adherence to EC, these cells failed to increase significantly endothelial permeability. Similar to their polyclonal counterparts, Ag-specific CD4+ CD29+ CD45RO+ T cell clones, but not their actively released mediators, also increased endothelial permeability via a noncytolytic mechanism(s). This ability of CD29+ CD45RO+ memory T lymphocytes to augment endothelial permeability may facilitate their transendothelial migration into extravascular space. These observations may provide additional insights into molecular mechanism(s) underlying pathophysiology of localized chronic inflammatory responses in general and more specifically selective accumulation of CD29+/CD45RO+ memory T lymphocytes at sites of chronic inflammation such as rheumatoid synovium.     

Multi-level regulation of cellular glycosylation: from genes to transcript to enzyme to structure

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Working together to respond to the challenges of EU policy to replace animal testing

This paper presents a personal perspective on efforts during the past 15 years to replace animal testing for assessing the safety of chemicals and products. It is based on an invited lecture--the FRAME Annual Lecture--given in October 2005, with the theme of "making progress by working together" (government-industry-academia-NGOs). Where we have achieved some successes, these have clearly been due to effective cooperation and collaboration between the relevant stakeholders. In recent times, there has not been this same level of active commitment and coordination. This needs to change, since, if we are to make good progress in the years to come in responding to the new challenges of the EU policy to replace animal testing, this will undoubtedly require us to work together, hopefully facilitated by effective leadership and coordination from the EU policy-makers themselves.