CCR2与MIP-1在中枢神经系统疾病中作用的研究进展

在炎症反应中,趋化因子（chemokine）在炎症反应局部通过激活和趋化的作用募集炎性细胞参与炎症反应。起初,人们认为趋化因子仅与炎症反应相关,直到发现趋化因子与人类免疫缺陷病毒（HIV）所致的脑白质病有密切关系之后,才逐渐认识到神经系统也是重要的免疫器官,而趋化因子及其受体在神经元、星形胶质细胞、小胶质细胞和少突胶质细胞均有表达,其表达量高低与许多生理和病理过程密切相关。     

RANTES与肾脏疾病

RANTES是一种C C家庭趋化因子 ,它主要由活化的T细胞产生 ,它的主要作用是对单核 /巨噬细胞、T淋巴细胞和嗜酸性粒细胞产生趋化作用 ,从而参与炎症过程。近年来研究发现其与肾脏疾病有着密切关系 ,在肾小球炎症、间质性肾炎、肾移植排斥反应的发现、发展和转归中起着重要作用 ,本文介绍其在肾脏疾病发生中的作用。     

RANTES与肾脏疾病

RANTES是一种C－C家庭趋化因子，它主要由活化的T细胞产生，它的主要作用是对单核／巨噬细胞、T淋巴细胞和嗜酸性粒细胞产生趋化作用，从而参与炎症过程。近年来研究发现其与肾脏疾病有着密切关系，在肾小球炎症、间质性肾炎、肾移植排斥反应的发现、发展和转归中起着重要作用，本文介绍其在肾脏疾病发生中的作用。     

炎症反应在前列腺癌骨转移中的作用研究进展

骨转移是前列腺癌晚期最常见的并发症,而炎症反应在前列腺癌骨转移的发生、发展中扮演着重要的角色,广泛参与骨转移肿瘤微环境的形成和肿瘤细胞的侵袭、转移过程;通过对其作用机制的研究,有望寻找到预防和治疗前列腺癌骨转移的新的药物靶点。本文就骨细胞、肿瘤相关巨噬细胞、肿瘤相关成纤维细胞、趋化因子和趋化因子受体、炎性细胞因子在前列腺癌骨转移过程中的作用及机制的研究进展进行综述。     

趋化因子与人工关节无菌性松动

趋化因子是一类能趋化细胞定向迁移的分泌性蛋白,在多种生理病理过程中起重要作用。在人工关节无菌性松动过程中,趋化因子不仅是人工关节周围炎症反应的主要参与者,还是调节破骨细胞分化成熟的重要因子。深入研究趋化因子与人工关节无菌性松动的关系,有助于为人工关节无菌性松动的防治研究开辟新途径。该文就近年有关趋化因子与人工关节无菌性松动方面的研究作一综述。     

NF-κB信号通路与神经系统损伤关系的研究进展

神经系统损伤相关性疾病可导致患者的学习、认知能力受损,对患者的生活和健康造成很大影响,也是引起患者死亡的主要原因之一[1]。导致神经系统损伤的原因有很多,外伤、缺血缺氧、感染、神经退行性病变、麻醉药物损伤等均可引起神经组织产生炎症反应,并影响神经细胞的增殖、分化和凋亡,从而使神经系统的功能受损[2-4]。核转移因子-κB （NF-κB）作为一类重要的转录因子,参与了神经系统的多种生理病理过程[5-6]。NF-κB 在神经细胞、胶质细胞及血管内皮细胞中均有表达,并与各种原因引起的神经系统损伤密切相关,参与介导神经系统的炎症反应,细胞增殖、分化和凋亡,神经保护等过程[7]。本文综述了近年来关于NF-κB及相关信号通路在神经系统损伤中作用的研究进展。     

中枢肥大细胞对神经系统的双向作用

中枢肥大细胞是脑内重要的免疫细胞之一,其与小胶质细胞、神经元等中枢细胞一起参与多种生理病理过程,在神经系统疾病中起着双向调节作用。文章综述了生理状态下中枢肥大细胞在神经系统中参与调节神经发生及神经保护的可能机制及其异常激活后引起血脑屏障破坏、神经炎症、应激、神经病理性疼痛等病理过程,为治疗神经系统疾病提供新思路。     

趋化因子及其受体与进展性肾病研究新进展

大多数慢性肾脏疾病都存在炎症反应 ,一系列研究发现趋化因子及其受体在肾脏炎症反应中的中心作用 ,对肾脏病的发生发展及其预后起重要作用。本文就有关趋化因子及其受体与进展性肾病的研究作有关介绍。     

趋化因子和肾脏的疾病

趋化因子是一组对白细胞有趋化功能的细胞因子，按其结构被分为Ｃ－Ｘ－Ｃ和Ｃ－Ｃ两个亚族，前者主要作用于中性粒细胞，后者主要作用于革核／巨噬细胞。在炎症等病理条件下，它们可由体内多种细胞分泌，并促使炎症细胞聚积。此外，还有活化多种细胞的功能。许多肾脏细胞均可在ＴＮＦ，ＩＬ－１及ＩＮＦ等刺激下分泌趋化因子。在一些肾脏病变的病人及动物模型的肾组织中，趋化因子及其大量ｍＲＮＡ增多，同时与肾组织内炎症细胞的浸润成正比。用相应的抗趋化因子抗体能减少白细胞的浸润和尿蛋白量。说明这类因子在肾脏病变过程中起到重要作用。     

MCP-1及其受体CCR2在肾脏疾病中的作用

趋化因子参与了肾脏的炎症过程 ,其中单核细胞趋化蛋白 1是重要的一种。本文对单核细胞趋化蛋白 1及其受体CCR2结构和功能以及在肾脏疾病的发生发展中的作用进行综述     

Chronic pain and neuroinflammation

In rheumatology, chronic pain most often sets in after a musculoskeletal injury. Its persistence is not always due to the progression of the initial injury, but in some cases to the onset of central sensitization. Much scientific data suggests that this central sensitization is caused by multiple complex interactions between the nervous system and immune system. Afferent nerve fibers carrying pain information are responsible for peripheral sensitization partly linked to inflammation molecules. These afferent fibers release neurotransmitters in the dorsal root ganglion and dorsal horn of the spinal cord, capable of activating microglia, which are the local immune cells. The activated microglia will produce pro-inflammatory cytokines, chemokines and neuropeptides capable of interacting with the second-order neuron, but also segmental and descending inhibitory neurons. This is referred to as neuroinflammation, which will amplify the hypersensitivity of second-order neurons, otherwise called central sensitization. This neuroinflammation will be able to reach the higher brain structures, which are involved in pain modulation and the emotional and cognitive aspects of pain. The aim of this update is to describe the pathophysiology of chronic pain, incorporating the latest scientific data on neuroplasticity and neuroinflammation.     

急性肾损伤导致远隔器官功能障碍的机制

急性肾损伤( AKI)患者有较高的死亡率。研究显示这种高死亡率与AKI患者并发的肺、心脏、肝脏以及神经系统功能衰竭密切相关。越来越多证据显示,AKI通过产生系统性炎症反应导致机体其他器官功能障碍。这一过程包括：AKI产生肾脏局部炎症信号分子;通过激活嘌呤代谢途径使血尿酸增高,放大炎症反应信号,进一步通过Toll样受体引发第二波炎症级联反应(包括细胞因子、趋化因子、炎症以及抗炎因子的释放);最后形成持续性、系统性炎症反应[以高迁移率旋蛋白1(HMGB1)释放入血为代表]。同时伴随氧化应激损伤、凋亡途径的活化以及白细胞迁移等,最终导致肺、心脏、肝脏以及神经系统功能障碍。本文综述了目前国际上最新的关于AKI及其导致远隔器官损伤作用的临床和实验研究。以便临床工作者更加深入的了解AKI导致远隔器官损伤的病理生理过程,为降低AKI患者的死亡率提供合理的治疗靶点。     

趋化因子在骨癌痛机制中的研究进展

背景 骨癌痛(cancer induced bone pain,CIBP)是中晚期癌症常见的并发症之一,严重影响癌症患者的生活质量,目前尚缺乏有效的治疗手段.趋化因子是有趋化作用的蛋白质,通过趋化白细胞定向移动的方式来参与免疫应答.近几年研究证明,趋化因子在CIBP的发生及维持中起到很重要的作用.目的 了解趋化因子在CIBP发生发展过程中所扮演的角色,从而为CIBP患者提供新的治疗策略.内容 综述近几年相关文献,阐述趋化因子及其受体参与CIBP发生与维持的研究进展.趋向 趋化因子有望成为CIBP治疗的新靶点.     

The immune aspect in neuropathic pain: Role of chemokines

Neuropathic pain is a pathological symptom experienced worldwide by patients suffering with nervous system dysfunction caused by various diseases. Treatment of neuropathic pain is always accompanied by a poor response and undesired adverse effects. Therefore, developing a novel “pain-kill” drug design strategy is critical in this field. Recent evidence demonstrates that neuroinflammation and immune response contributes to the development of neuropathic pain. Nerve damage can initiate inflammatory and immune responses, as evidenced by the upregulation of cytokines and chemokines. In this paper, we demonstrated that different chemokines and chemokine receptors (e.g., CX3CL1/CX3CR1, CCL2/CCR2, CCL3/CCR1, CCL4/CCR5 and CCL5/CCR5) serve as mediators for neuron–glia communication subsequently modulate nociceptive signal transmission. By extensively understanding the role of chemokines in neurons and glial cells in nociceptive signal transmission, a novel strategy for a target-specific drug design could be developed.     

Evoked potentials and brain stem reflexes

Summary The recording of evoked potentials (EPs) has become one of the most useful functional diagnostic techniques in the neurosciences during recent years. In combination with the neurophysiological investigation of brain stem reflexes (BSRs) EPs provide good information concerning circumscribed and diffuse brain and brain stem lesions. In this article the role of EPs and BSRs will be pointed out with special regard to their use in neurosurgery concerning awake and comatose patients as well. Pathological findings caused by extracerebral factors or due to neurological (systemic) and otological diseases will be discussed from the aspect of differential diagnosis only.Evoked potentials described in this paper are short latency potentials which are related to more or less defined generators in the peripheral and central nervous system. EPs of long latency seem to play a role in cognitive, affective and integrative functions of the central nervous system and they will not be dealt with in this article.In recent years an increasing number of review articles and monographs dealing with several aspects of evoked potentials has appeared [16, 17, 18, 25, 69, 80, 84, 122, 123, 124, 127, 130].     

Calcium signaling pathways in the enteric nervous system

The intracellular calcium level is an important regulator of cellular functioning, and its tight regulation occurs at several levels. Influx of extracellular calcium occurs via voltage-gated channels in response to a depolarization, and "capacitative" extracellular calcium occurs with cellular calcium depletion. Intracellular release of calcium also occurs through both the inositol trisphosphate- and ryanodine-sensitive stores of calcium. The following will detail these events and recent discoveries in Ca2+ signaling, and will specifically focus on their role in the functioning of the enteric nervous system.     

Central toxicity of local anesthetics. New data

The central nervous toxicity of local anaesthetics has long been thought to be limited to the generalized tonicoclonic convulsions which follow the appearance of such symptoms as sleepiness, tingling of the lips, slurred speech, numbness, etc. Also the central nervous system was considered to be more sensitive than the cardiovascular system. However, recent experimental studies would seem to indicate that at least the more potent local anaesthetics, such as bupivacaine, have deleterious effects on parts of the brain other than the cerebral hemispheres. This may point to an involvement of the central nervous system (the amygdala and vasopressor areas of the floor of the fourth ventricle) in the pathogenesis of the hypotension and arrhythmias which may be seen at the same time as central nervous system signs of systemic toxicity. This is important for the treatment of such accidents: should a convulsion occur alone, sodium thiopentone, a muscle relaxant and a benzodiazepine, with oxygen and assisted breathing, will be the treatment; should an arrhythmia occur, its treatment should also include an anticonvulsant drug, such as a benzodiazepine. The prophylactic use of benzodiazepines should also be encouraged.     

Die gesunde und kranke wirbelsäule im röntgenbild: Pathological-anatomical investigations by Geh. Med.-Rat Prof. Dr. Georg Schmorl. With the roentgenological cooperation of Dr. Med. Herbert Junghanns. Vol. 23, Supplements to the Fortschritte auf dem Gebiete der Röntgenstrahlen. Ed. by Prof. Dr. Grashey,Köln. Leipzig,Georg Thieme, 1932.

A brief review of the recent advances in the surgery of the sympathetic nervous system is presented in the hope that further interest will be aroused that will tend to a more complete knowledge of this mechanism, which undoubtedly holds the key to many unsolved problems. In such a limited survey of this field many valuable references have been omitted and it is with regret that all worthwhile contributions cannot be listed. However it is obvious that careful and deliberate selection of patient and operation will be of distinct advantage in many apparently hopeless cases, with a minimal mortality in skilled hands.     

Neurotransplantation: lux et veritas, fiction or reality?

Neurotransplantation remains a much-debated frontier in contemporary neurosurgery and neuroscience, with roots dating to the late 19th century. Contemporary applications are far-reaching, and ongoing laboratory research and clinical trials seek to define the mechanisms at play in neurotransplant engraftment and growth, while advancing the field forward into the 21st century. Neural transplantation therapy remains an attractive idea for treating central nervous system (CNS) and peripheral nervous system (PNS) pathologies. Phase I and phase II clinical trials assessing safety and efficacy are currently underway for various disorders. The remainder of this review will focus on ongoing clinical trials and more recent research advances involving neural transplantation therapy for neuronal death, axonal injury, peripheral nerve lesions, and cancer. The field of neural transplantation, while promising, is not without ethical and scientific dilemmas; this review will conclude with a discussion of the challenges researchers and clinicians face as the field of neural transplantation moves forward.     

钙黏蛋白在突触发育和突触可塑性调节中的作用

背景 钙黏蛋白（cadherin）是一类存在于细胞表面的跨膜糖蛋白,最初被认为是一种钙离子依赖性的细胞黏附分子,主要参与调节细胞黏附、促进细胞增殖、维持细胞极性等过程.近几年对cadherin调节突触发育和突触可塑性的研究取得了较大进展. 目的 围绕cadherin在突触发育和突触可塑性过程中的作用及其相关分子机制简要作一综述,旨在为神经系统疾病的治疗提供理论依据. 内容 Cadherin的概述,cadherin在突触发育和突触可塑性调节中的作用以及相关分子机制,cadherin与神经疾病. 趋向 随着cadherin在调节突触发育和突触可塑性过程中的研究不断深入,cadherin将成为治疗神经疾病的一个新型的靶点.