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生物体研究的新方向--细胞外基质和细胞粘附因子
多年来细胞一直是生物界的研究重点.而近年来研究者们开始关注将细胞连在一起的细胞外基质(extracellular matrix, ECM)[1~5],并提出单细胞动物的进化论虽未统一,但进化中ECM是必不可少的论点却是一致的.
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人粘膜血管地址素在大肠杆菌中的表达及其抗血清制备
粘膜血管地址素 (mucosal vascular addressin cell adhesion molecule-1, MAdCAM-1)是主要表达于肠道及其相关淋巴组织血管内皮细胞表面的一种粘附分子,系单链跨膜糖蛋白,由N端的配体结合域、近膜的粘蛋白样区及跨膜区和胞浆区组成。通过与淋巴细胞膜上的受体分子α4β7整合素相结合,介导淋巴细胞向肠道粘膜组织定向迁移,因此,它在肠道粘膜免疫中具有重要的作用。
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CNE-1细胞高剂量X线常规分割照射后MDR1与PECAM1表达情况观察
本实验采用体外培养的人鼻咽癌CNE-1细胞系高剂量X线照射后,初步探讨高剂量照射引起血小板内皮细胞黏附分子-1(platelet endothelial cell adhesion molecule-1,PECAM1) 改变与CNE-1细胞产生多药耐药(multiple drug resistance,MDR)的可能的相关性。
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血小板内皮细胞黏附分子-1基因Asn563Ser多态及血浆可溶性血小板内皮细胞黏附分子-1与脑梗死的关系
动脉粥样硬化性脑梗死(atherosclerotic cerebral infarction,ACI)是一种多基因病,其分子机制和致病基因尚不清楚.我们探讨血小板内皮细胞黏附分子-1(platelet endothelial cell adhesion molecule-1,PECAM-1)基因的Asn563Ser多态及血浆可溶性PECAM-1(sPECAM-1)水平与ACI的关系.
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黏附分子在实验性变应性鼻炎鼻黏膜中的表达
变应性鼻炎迟发相反应阶段是以嗜酸粒细胞为代表的大量的炎性细胞的浸润而导致的慢性炎症,血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)、细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)在嗜酸粒细胞等炎性细胞的黏附、浸润到黏膜炎症区域起着重要作用[1].本研究观察实验性变应性鼻炎鼻黏膜中黏附分子的表达.
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慢性根尖周病中细胞粘附分子的表达
以往对根尖周病发病机理的研究多局限于细胞水平[1].现发现,参与免疫反应的实质是一类分子的调节作用[2,3].我们研究了血管细胞粘附分子(Vaascular cell adhesion molecule-1,VCAM-1),细胞间粘附分子( inter cellular adhesion molecule-1,ICAM-1)及内皮细胞白细胞粘附分子(endothelial-leukocyte adnesion molecule-1,ELAM-1)在根尖周病免疫机制中的作用,以期探讨炎性细胞浸润的机制.
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细胞因子在放射诱导的正常组织急性反应中的作用
正常组织的放射损伤按出现症状的时间划分为:急性反应、亚急性反应和晚期迟发反应。急性反应与晚期反应的关系一直不明确,有人认为,急性反应中发生的事件在晚期放射损伤的发病机理中起着重要的作用,提出正常组织放射损伤应按照引发损伤的原始事件、正常组织的病理生理反应和组织细胞动力学划分为:原始事件、修复稳定期和缓慢进展期[1]。因此,研究急性反应发生机理,采取针对性的措施来减轻或延缓晚期损伤的出现就显得很有必要。 1.一般炎症过程中细胞因子的作用。在炎症反应过程中,介导淋巴细胞穿过毛细血管进入组织的分子机理已经有了深入了解,在这一过程中,表达在淋巴细胞和毛细血管内皮细胞上的细胞粘附分子起着关键性的作用。淋巴细胞穿过毛细血管迁移到组织中是炎症反应中不可缺少的一个步骤。在穿过毛细血管之前,淋巴细胞在促炎性细胞因子的作用下,从血流中心开始靠近毛细血管的边缘,经过在毛细血管内皮细胞表面滚动、俘获等过程与毛细血管内皮细胞结合,然后,通过毛细血管内皮间隙穿过毛细血管达到组织中,这一过程需要许多细胞因子的参与,如淋巴细胞功能相关抗原-1(lymphocyte function-associated antigen-1,LFA-1)、选择素(包括P-选择素、E-选择素、L-选择素)、整合素、细胞粘附分子(CAMs)等。细胞粘附分子包括细胞间粘附分子-1(intercellular adhesion molecule-1,ICAM-1,CD54)、血管细胞粘附分子-1(vascular cell adhesion molecule-1,VCAM-1)、血小板-内皮细胞粘附分子-1(platelet-endothelial cell adhesion molecule-1,PECAM-1,CD31)。
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血管细胞黏附分子与肺部疾病
血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)是在1989年首次被发现,是免疫球蛋白超家族中的重要成员之一,对体内单个核白细胞募集到炎症部位起重要作用.随着免疫学和分子生物学的发展,目前对VCAM-1和可溶性VCAM-1(sVCAM-1)的研究不断深入,笔者对VCAM-1与肺部疾病的关系作一综述.
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皮肌炎/多发性肌炎病人血清CD106和CD62E的表达
研究表明,可溶性血管细胞粘附分子1(soluble vascular cell adhesion molecule-1,sVCAM-1,CD106)和E选择素(sE-selectin,CD62E)在多种自身免疫性疾病和炎性疾病中表达异常[1-4].有关皮肌炎/多发性肌炎(dermatomyositis/polymyositis,DM/PM)病人CD106和CD62E研究国内未见报道.本研究旨在检测DM/PM病人血清CD106和CD62E的表达水平,并与临床症状及其他实验室指标进行比较,探讨其在DM/PM发病中的作用和意义.
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血管细胞黏附分子-1与脑缺血再灌注损伤研究进展
近年来,黏附分子在脑缺血再灌注损伤中的作用已成为研究的热点之一[1].血管细胞黏附分子-1(vascular cell adhesion molecule-1,VCAM-1)是一种重要的黏附分子,现就其与脑缺血再灌注损伤的关系做一综述.
关键词: 血管 细胞黏附分子 脑缺血再灌注损伤 Cell Adhesion 综述 -
VCAM-1的表达与乳癌血管生成、生长、转移的关系研究
肿瘤的生长和转移是极为复杂的多阶段过程,粘附分子在此过程中起着极为重要的作用,每一步都有多种粘附分子的参与.血管细胞粘附分子(vascular cell adhesion molecule-1, VCAM-1,CD106)是其中作用较强的粘附分子之一.我们对手术切除的乳癌瘤体标本进行VCAM-1及血管染色,探讨乳癌瘤体VCAM-1的表达与乳癌的血管生成、生长、转移的关系.
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Effects of Molecular Length, Ortientation and Amino Acid Mutation on Kinetics of Selectin/Ligand Interactions
Receptor/ligand interactions are basic issues to cell adhesion, which are important to many physiological and pathological processes such as lymphocyte-mediated cytotoxicity ,tumor metastasis and inflammatory reactionl.
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Mechano- Chemical Coupling at Molecular Level: Forced Dissociation of Selectin/Ligand Binding
Mechano - chemical coupling is a common phenomenon that exists in various biological processes at different physiological levels. Bone tissue remodeling strongly depends on the local mechanical load. Leukocytes are sheared to form the transient aggregates with platelets or other leukocytes in the circulation. Flow pattern affects the signal transduction pathways in endothelial cells. Receptor/ligand interactions are important to cell adhesion since they supply the physical linkages among cells. How external forces influence the biological function has little been known, and nowadays attract more and more attentions. Here the forced dissociation of selectin/ligand binding is used to test mechano - chemical coupling at molecular level.
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长期吸入糖皮质激素对支气管哮喘患儿粘附分子系统的影响
支气管哮喘(简称哮喘)是儿科常见慢性肺部疾病.其发病机制十分复杂,是由多种炎性细胞参与的慢性气道炎症性疾病.在炎症细胞向气道炎症区跨内皮转移和浸润过程中,细胞粘附分子(cell adhesion molecules,CAMs)发挥了重要作用,是介导炎症过程的关键分子[1].粘附分子种类繁多,与哮喘关系密切的有细胞间粘附分子-1(intercellular adhesion molecule-1,ICAM-1)和血管内皮细胞粘附分子-1(vascular cell adhesion molecule-1,VCAM-1).近年来,吸入糖皮质激素(IGS)防治儿童哮喘,其效果得到充分肯定[2].本研究检测了对照组与哮喘患儿IGS治疗前及治疗后(3、6、12个月)血清ICAM-1(sICAM-1)及血清VCAM-1(sVCAM-1)水平的变化,旨在探讨sICAM-1和sVCAM-1在哮喘发病中的作用,为预防、诊断及治疗哮喘提供理论依据.
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血小板内皮细胞粘附分子-1与心血管疾病关系研究
血小板内皮细胞粘附分子-1(platelet-endothelial cell adhesion molecule-1, PECAM-1),又称CD31,是免疫球蛋白(Ig)超家族的主要成员之一,其相对分子质量(Mr)为130 kDa,由6个细胞外的Ig折叠而成.PECAM-1早是由Newman教授及其同事[1]发现,该分子除在血小板上表达外,还表达于内皮细胞连接处、NK细胞、T细胞亚群和绝大部分粒白细胞,在整个造血干细胞的发育过程中均有表达[2].
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奥扎格雷钠对急性脑梗死患者血清白细胞介素-6和可溶性细胞间黏附分子-1的影响
近年来,脑血管疾病逐年增多,尤其是缺血性脑血管病发病率有上升趋势[1].有研究显示,急性脑梗死的患者血清可溶性细胞间黏附分子-1(intercellular cell adhesion molecule-1 solubility,sICAM1)、白细胞介素-6(interleukin-6,IL-6)的水平明显升高;而sICAM-1、IL-6的浓度水平与脑梗死的体积呈正相关[2].本研究旨在观察奥扎格雷对急性缺血性脑卒中患者血清IL-6和sICAM-1浓度水平和神经功能改善的影响.
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牛磺酸对糖尿病大鼠早期肾损伤与肾脏凝集素样氧化低密度脂蛋白受体1和胞间黏附分子1表达的影响
儿童期糖尿病(DM)是青少年发生动脉粥样硬化(AS)的危险预测因子,早期易并发血管病变,从而导敛肾功能不全.凝集素样氧化低密度脂蛋白(oxLDL)受体1(LOX-1)通过与oxLDL在内皮的结合,上调胞间黏附分子1(ICAM-1)在内皮及系膜细胞的表达,诱导炎性反应[1].牛磺酸(TAU)作为一种内源性的抗氧化剂,具有稳定细胞膜、抑制脂质过氧化、平衡细胞内外渗透浓度及调节血管内皮活性物质合成等多种作用[2].本研究通过检测肾组织LOX-1和ICAM-1蛋白及基因的表达水平,观察牛磺酸对DM早期肾功能的保护作用,并探讨其可能机制.
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INTRODUCTIONS Cell adhesion is crucial to many pathophysiological processes, such as inflammatory reaction and tumor metastasis. It is mediated by specific interactions between receptors and ligands, and provides the physical linkages among cells. For example, interactions between selectins and glycoconjugate ligands mediate leukocyte initially tethering to and subsequently rolling on vascular surfaces in sites of inflammation or injury, which is determined by their fast kinetic rates. To mediate cell adhesion, the interacting receptors and ligands must anchor to apposing surfaces of two cells or a cell and the substratum, i.e. , the so-called two-dimensional (2D) binding, which differs from interactions in the fluid phase, i.e. , the three-dimensional (3D) binding. How structural variations and surface environments of interacting molecules affect their 2D kinetics, and how external forces manipulate their dissociation has little been known quantitatively, and nowadays attracts more and more attentions.
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细胞间粘附分子-1和血管细胞间粘附分子-1的结构与功能
细胞粘附分子(cell adhesion molecule, CAM)是一类调节细胞与细胞、细胞与细胞外基质(extracellular matrix, ECM)间相互结合、起粘附作用的膜表面糖蛋白.细胞间粘附分子-1(intercellular adhesion molecular-1, ICAM-1)和血管细胞间粘附分子-1(vascular cell adhesion molecular-1, VCAM-1)均属于CAM中免疫球蛋白超家族(immunoglobulin superfamily, IGSF)中的成员,是目前研究多的粘附分子.本文拟就目前有关这两种粘附分子的结构及功能的研究进展作一综述.
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于福興實驗室研究計劃
1 Molecular regulation of corneal wound healing Rapid healing of the corneal epithelium in response to injury is essential for maintenance of its barrier function. The long-term goal of this project is to obtain basic information about the molecular and cell biology of corneal wound healing. The project will test the hypotheses that amyloid β/A4 precursor-like protein controls serine proteinase activity, mediates cell adhesion, and promotes cell migration during corneal reepithelialization. This study should provide the basis to begin constructing a detailed nap of the molecular pathways and interconnecting networks of proteins functioning in wound repair and to develop therapeutics for treatment of corneal diseases like recurrent erosions and persistent defects of the epithelium.2 Developing an ex vivo model for ocular irritation testThe objective of this project is to develop an ex vivo assay system to predict ocular irritation potential of test chemicals and consumer products. Our hypothesis has been that activation of these transcription factors and disruption of corneal integrity can be used as endpoints/ markers for evaluating ocular toxicity in organ culture. Our goal is to develop a sensitive, efficient, economical and reliable ex vivo model for predicting irritation potential of a chemical or consumer product with mechanistic basis.3 Modulation of epithelial barrier function during corneal infectionThe long-term goal of this project is to understand the mechanisms underlying the induction of the inflammatory reaction and breakdown of the epithelial barrier in the cornea upon infection. We will test the hypothesis that in the cornea TLRs confer responsiveness of HCE cells to pathogens, and PA challenge-induced TLR signaling, through activation of NF-?B and/ or mitogen-activated protein kinase (MAPK), contributes to infection-induced epithelial barrier breakdown. The following studies will be carried out. An understanding of how TLRs transmit signals that lead to epithelial response, including modulation of barrier function,may allow the development of therapeutic agents that prevent breakdown or enhance recovery of barrier function during infection and, as an adjuvant therapy, eliminate the corneal scarring and vision loss associated with bacterial keratitis.4 Developing an adjuvant therapy to reduce inflammatory response induced by bacterial infection of the cornea (bacterial keratitis).