急性胰腺炎时血脑屏障通透性变化规律及其与胰腺病变的关系

胰性脑病是急性胰腺炎的重要并发症，其临床发生率为3％～27％，而死亡率高达40％以上。血脑屏障是中枢神经系统（CNS）的重要保护机制，它能保护大脑免受外周致病因子的攻击。血脑屏障的损伤和通透性升高是多种CNS炎症及病变的前提。胶质纤维酸性蛋白（GFAP）是星形胶质细胞的标志蛋白，由各种原因引起的CNS损伤均可引起星形胶质细胞活化、GFAP表达增加，因此GFAP表达水平可以作为CNS损伤程度的标志。     

小胶质细胞在中枢神经系统疾病血管新生中的作用

小胶质细胞是中枢神经系统(CNS)的免疫细胞,监视CNS免受损伤在神经发育过程中也起着重要作用.血管新生在缺血性脑卒中和肿瘤等疾病中发挥着重要作用,调控血管新生已成为这些疾病的潜在治疗靶点.在神经发育及CNS疾病的发生、发展过程中,小胶质细胞与血管新生均有着密切联系.然而,目前对于小胶质细胞在CNS疾病血管新生中的作用...     

中枢神经系统损伤修复的若干进展

神经系统损伤后，中枢与末梢损伤的局部微环境不同是造成两者出现再生差异的主要原因。巨噬细胞和小胶质细胞的功能状态决定了免疫应答反应的程度和细胞素释放的水平，从而影响了损伤局部的微环境。此外，神经细胞的凋亡亦是脑缺血损伤后导致神经元死亡的类型之一。一些原癌基因在损伤早期的表达，是抑制凋亡的重要基因。     

中枢神经系统损伤修复的若干进展

神经系统损伤后,中枢与末梢损伤的局部微环境不同是造成两者出现再生差异的主要原因。巨噬细胞和小胶质细胞的功能状态决定了免疫应答反应的程度和细胞素释放的水平,从而影响了损伤局部的微环境。此外,神经细胞的凋亡亦是脑缺血损伤后导致神经元死亡的类型之一。一些原癌基因在损伤早期的表达,是抑制凋亡的重要基因。     

参与小胶质细胞活化的膜受体研究进展

<正>在中枢神经系统(CNS),小胶质细胞(MG)的作用越来越受到重视,MG被认为是CNS中天然免疫和适应性免疫的主要调节者〔1〕,MG以静息和活化两种状态存在,静息的MG对CNS起着支持、营养、保护和修复等作用,而活化的MG一方面营养和保护了CNS,另一方面通过释放促炎症细胞因子、自由基、超氧化物阴离子、一氧化氮(NO)、活性氧、前列腺素E2(PGE2)等多种物质,对CNS产生了更多的损伤作用。研究发现活化的     

小胶质细胞参与间歇低氧对中枢神经系统神经元的损伤

阻塞性睡眠呼吸暂停（obstructivesleepapnea,OsA）是一种以睡眠期间上气道反复发生完全（呼吸暂停）或部分（低通气）阻塞导致低氧血症和夜间反复觉醒为特征的常见慢性疾病。0SA所造成的间歇低氧（IH）可导致中枢神经系统（CNS）结构性神经元损伤与功能障碍,在临床上表现为神经认知与行为障碍,其主要病生理基础在细胞水平上可被归为小胶质细胞为主的氧化应激和炎性损伤。小胶质细胞是CNS中主要的炎症细胞,通过线粒体、NADPH氧化酶以及兴奋性神经毒性递质的释放来引发CNs氧化应激和炎症。小胶质细胞为主的炎症过程是把双刃剑,神经毒性与神经保护之间、炎症与抗炎小胶质细胞细胞因子之间的平衡决定了小胶质细胞在OSAIH暴露后最终扮演的角色。小胶质细胞炎性损伤一旦启动,可能会持续不停并级联放大,最终导致有临床意义的CNs神经元损伤。本文将综述OSAIH对CNS结构性神经元的损伤极其并发的功能障碍,以及在小胶质细胞可能发挥的作用及其可能机制。     

小胶质细胞的活化与调控

小胶质细胞在中枢神经系统 (CNS)中起重要作用 ,与CNS的生理功能和病理过程密切相关。小胶质细胞的活化和调控过程涉及多种因素 ,如细胞因子、某些蛋白质和酶、细胞内外离子和电位的变化等。     

成年大鼠神经元和星形胶质细胞细胞周期蛋白依赖激酶的表达

目的 研究成年大鼠细胞周期蛋白依赖激酶（CDK）在神经元和星型胶质细胞的表达.方法 应用免疫荧光和激光扫描共聚焦显微镜观察成年大鼠生理状态下大脑皮层或海马CA1区神经元和星型胶质细胞CDK1、CDK2、CDK4的表达.结果 成年大鼠大脑皮层和海马CA1区神经元的细胞核和细胞浆均有CDK1、CDK2和CDK4表达,以胞核为主;星形胶质细胞也有CDK1、CDK2和CDK4的表达,但表达细胞数目较少,且表达这些指标的星形胶质细胞多聚集在海马CA1区.结论 成年大鼠大脑皮层和海马区的神经元和星形胶质细胞均表达CDK,而神经元的CDK表达较星形胶质细胞更为普遍.     

少突胶质细胞与缺血性脑损伤

少突胶质细胞是中枢神经系统的成髓鞘胶质细胞，在许多神经系统疾病中对损伤具有易损性。与神经元一样，少突胶质细胞对缺血性损伤有高度敏感性，其损伤机制包括氧化应激、兴奋性氨基酸和凋亡通路激活。了解少突胶质细胞的死亡机制有可能为白质缺血损伤后结构和功能的保存与修复提供新的治疗策略。     

胶质细胞源性神经营养因子与缺血性脑血管病的研究进展

胶质细胞源性神经营养因子是近年来发现的对神经系统有较强营养作用的因子，对神经元发育、生长、分化、修复和再生有其他神经营养因子不可替代的作用，对中枢和周围神经具有相同的作用，已成为当今神经科学领域研究的热点。文章阐述了胶质细胞源性神经营养因子及其受体在脑缺血后的表达以及在减轻缺血后自由基损伤、钙超载、脑水肿、缩小梗死体积及对迟发性神经元坏死的保护等方面的作用。     

Nano neuro knitting: peptide nanofiber scaffold for brain repair and axon regeneration with functional return of vision

Nanotechnology is often associated with materials fabrication, microelectronics, and microfluidics. Until now, the use of nanotechnology and molecular self assembly in biomedicine to repair injured brain structures has not been explored. To achieve axonal regeneration after injury in the CNS, several formidable barriers must be overcome, such as scar tissue formation after tissue injury, gaps in nervous tissue formed during phagocytosis of dying cells after injury, and the failure of many adult neurons to initiate axonal extension. Using the mammalian visual system as a model, we report that a designed self-assembling peptide nanofiber scaffold creates a permissive environment for axons not only to regenerate through the site of an acute injury but also to knit the brain tissue together. In experiments using a severed optic tract in the hamster, we show that regenerated axons reconnect to target tissues with sufficient density to promote functional return of vision, as evidenced by visually elicited orienting behavior. The peptide nanofiber scaffold not only represents a previously undiscovered nanobiomedical technology for tissue repair and restoration but also raises the possibility of effective treatment of CNS and other tissue or organ trauma.     

Fibrinogen inhibits neurite outgrowth via beta 3 integrin-mediated phosphorylation of the EGF receptor

Changes in the molecular and cellular composition of the CNS after injury or disease result in the formation of an inhibitory environment that inhibits the regeneration of adult mammalian CNS neurons. Although a dramatic change in the CNS environment after traumatic injury or disease is hemorrhage because of vascular rupture or leakage of the blood-brain barrier, the potential role for blood proteins in repair processes remains unknown. Here we show that the blood protein fibrinogen is an inhibitor of neurite outgrowth that is massively deposited in the spinal cord after injury. We show that fibrinogen acts as a ligand for beta3 integrin and induces the transactivation of EGF receptor (EGFR) in neurons. Fibrinogen-mediated inhibition of neurite outgrowth is reversed by blocking either beta3 integrin or phoshorylation of EGFR. Inhibition of Src family kinases that mediate the cross-talk between integrin and growth factor receptors rescue the fibrinogen-induced phosphorylation of EGFR. These results identify fibrinogen as the first blood-derived inhibitor of neurite outgrowth and suggest fibrinogen-induced EGFR transactivation on neuronal cells as a molecular link between vascular and neuronal damage in the CNS after injury.     

Complex bile duct injuries: management

BACKGROUND: Laparoscopic cholecystectomy is the present treatment of choice for patients with gallbladder stones, despite its being associated with a higher incidence of biliary injuries compared with the open procedure. Injuries occurring during the laparoscopic approach seem to be more complex. A complex biliary injury is a disease that is difficult to diagnose and treat. We considered complex injuries: 1) injuries that involve the confluence; 2) injuries in which repair attempts have failed; 3) any bile duct injury associated with a vascular injury; 4) or any biliary injury in association with portal hypertension or secondary biliary cirrhosis. The present review is an evaluation of our experience in the treatment of these complex biliary injuries and an analysis of the international literature on the management of patients.     

Therapeutic potential of melatonin in traumatic central nervous system injury

Abstract:  A vast literature extolling the benefits of melatonin has accumulated during the past four decades. Melatonin was previously considered of importance to seasonal reproduction and circadian rhythmicity. Currently, it appears to be a versatile anti-oxidative and anti-nitrosative agent, a molecule with immunomodulatory actions and profound oncostatic activity, and also to play a role as a potent neuroprotectant. Nowadays, melatonin is sold as a dietary supplement with differential availability as an over-the-counter aid in different countries. There is a widespread agreement that melatonin is nontoxic and safe considering its frequent, long-term usage by humans at both physiological and pharmacological doses with no reported side effects. Endeavors toward a designated drug status for melatonin may be enormously rewarding in clinics for treatment of several forms of neurotrauma where effective pharmacological intervention has not yet been attained. This mini review consolidates the data regarding the efficacy of melatonin as an unique neuroprotective agent in traumatic central nervous system (CNS) injuries. Well-documented actions of melatonin in combating traumatic CNS damage are compiled from various clinical and experimental studies. Research on traumatic brain injury and ischemia/reperfusion are briefly outlined here as they have been recently reviewed elsewhere, whereas the studies on different animal models of the experimental spinal cord injury have been extensively covered in this mini review for the first time.     

The potential of mesenchymal stromal cells as a novel cellular therapy for multiple sclerosis

Multiple sclerosis (MS) is an inflammatory neurodegenerative disease of the CNS for which only partially effective therapies exist. Intense research defining the underlying immune pathophysiology is advancing both the understanding of MS as well as revealing potential targets for disease intervention. Mesenchymal stromal cell (MSC) therapy has the potential to modulate aberrant immune responses causing demyelination and axonal injury associated with MS, as well as to repair and restore damaged CNS tissue and cells. This article reviews the pathophysiology underlying MS, as well as providing a cutting-edge perspective into the field of MSC therapy based upon the experience of authors intrinsically involved in MS and MSC basic and translational science research.     

Immune Mechanisms in Hypertension

Inflammation plays an important role in the pathogenesis of hypertension. Innate and adaptive immune response may contribute to this process. The mechanisms implicating immune response in hypertension are still elusive. To date, the evidence originates in three major areas of data: cytokine production, central nervous system (CNS) stimulation, and kidney damage. The cytokine microenvironment can become proinflammatory and propagate low-grade inflammation, which may contribute to vascular injury and end-organ damage in hypertension. In addition, stimulation of the CNS by some stimuli (e.g., angiotensin II) causes mild hypertension that may modulate peripheral immune responses leading to aggravation of blood pressure elevation. The immune response can induce kidney injury and also interfere with sodium excretion, further contributing to elevation of blood pressure. The purpose of this review is to discuss recent data regarding the contribution of the different immune cell subsets and their response and mechanism of action in promoting hypertension and target-organ damage.     

Use of polysialic acid in repair of the central nervous system

Polysialic acid (PSA), a large cell-surface carbohydrate that regulates cell interactions, is used during vertebrate development to promote precursor cell migration and axon path-finding. The induction of PSA expression in damaged adult CNS tissues could help them to rebuild by creating conditions permissive for architectural remodeling. This possibility has been explored in two contexts, the regeneration of axons and the recruitment of endogenous neural precursors to a lesion. Glial scars that form at CNS injury sites block axon regeneration. It has been found that transfection of scar astrocytes by a viral vector encoding polysialyltransferase leads to sustained expression of high levels of PSA. With this treatment, a substantial portion of severed corticospinal tract axon processes were able to grow through a spinal injury site. In the studies of precursor cell migration to a cortical lesion, it was found that induced PSA expression in a path extending from the subventricular zone to a lesion near the cortical surface increased recruitment of BrdU/nestin-positive cells along the path and into the injury site. These displaced precursors were able to differentiate in a regionally appropriate manner. These findings suggest that induced PSA expression can be used as a strategy for promoting tissue repair involving both replacement of cells and rebuilding of neural connections.     

钝性外伤后结肠损伤的外科诊治分析

目的总结钝性外伤后结肠损伤的临床特点,探讨结肠损伤的诊断和治疗方法。方法回顾性评估62例钝性腹部外伤后结肠损伤患者的临床表现、检查、诊断方法、相关损伤以及手术方法等临床资料。结果62例中41例急诊剖腹探查明确诊断,Ⅰ期肠修补或切除吻合术47例,Ⅱ期肠造瘘术或肠外置术15例,发生肠瘘2例,死亡6例。结论早期诊断、及早手术是结肠损伤治疗的关键。结肠损伤Ⅰ期手术安全可靠,但须掌握其适应证。     

Immune interactions in hepatic fibrosis

Liver cirrhosis is caused by iterative cycles of tissue injury, inflammation, and repair. Although most causes of acute hepatitis resolve without scarring, chronic hepatitis is associated with persistent inflammation and matrix remodeling, which leads to fibrosis and, eventually, cirrhosis. The mechanisms that govern wound healing involve interactions between the innate and adaptive immune systems and stromal cells within a microenvironment composed of cytokines, growth factors, and modified matricellular proteins. The immune system plays a central role in the regulation of fibrosis, tissue repair, and recovery that is vital for the maintenance of tissue homeostasis. Chronic inflammation and fibrosis are inextricably linked and the cellular interactions between immune effector cells, local fibroblasts, and tissue macrophages at sites of scar formation determine the outcome of liver injury and the development of scarring.