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槲皮素防治神经退行性疾病的机制研究进展
神经退行性疾病(degenerative diseases of the central nervous system,ND)是一组以原发性神经元变性为基础的慢性进行性神经系统疾病.该类疾病主要包括阿尔茨海默氏病( Alzheimer' s disease,AD)、帕金森病( Parkinson's disease,PD)、Huntington舞蹈病(huntington disease,HD)、脑缺血缺氧所致神经元变性等.研究发现,ND由多种不同原因导致,包括神经元或神经胶质细胞不能提供充分的营养、轴突传递功能受损、谷氨酸受体活性过高、活性氧(reactive oxygen species,ROS)水平过高、线粒体能量产生减少、折叠错误的蛋白质形成增加或降解不充分、炎症过程、特殊蛋白质的产生等因素[1].
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神经系统肿瘤病理诊断中新抗体的应用
长期以来,大多数神经系统肿瘤都可以通过常规的HE染色切片得以明确诊断,但仍有一部分疑难病例的确诊需要免疫组织化学技术的帮助.尤其从20世纪70年代发现胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)可作为胶质细胞标志物而应用于胶质瘤的诊断以后,因其较高的特异性和敏感性一直以来已成为中枢神经系统肿瘤诊断中重要的标志物.
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Objective:Blood-brain barrier is the key barrier of brain in the innate immune. It can prevent the harmful substances from the blood into the brain. In order to keep the brain in a relatively stable environment and maintain the normal function of the nervous system, it can also pump harmful substances or excess substances outside the brain selectively. Among them, brain microvascular endothelial cell tissue is a key part in the blood-brain barrier's function. The number of the patients with central nervous system ( CNS) diseases increased year by year. The therapeutic drug is usually inhibited by the blood-brain barrier and is difficult to work. Therefore, how to modify the drug and to make it easier to cross the blood brain barrier is the key point to cure CNS. At present, more than 95% research focus only on how nano drugs can enter the cell, the way and efficiency to enter the cell and the research of effect of nano drug etc. For the process of drug carrier in endocytosis, intracellular transport and release and regulation of research are rarely reported. Clathrin and P-glycoprotein are related protein in endo-cytosis and exocytosis with nano drug. Clathrin is located on the plasma membrane. It participates in endocytosis of some nutrients, and maybe the entry into the cell of some drugs. P-glycoprotein is located in the membrane of cer-ebral capillary endothelial cells. It can efflux drugs relying on ATP. Although there is a certain understanding of the cell in the inner swallow and efflux. But the process of the liposome drug is not clear. To solve the above prob-lems, using colloidal gold liposome nano materials to trace liposome's transport and regulation mechanism in brain microvascular endothelial cells, and study endocytosis, release, distribution and regulation mechanism of nano lipo-somes in brain microvascular. The solution of this problem can guide to construct reasonable drug carrier, and look forward to clarifing the molecular basis and mechanism of nano drug carriers across the BBB. This work has impor-tant theoretical and practical significance for the development and application of liposomes in the future. Results:For untreated cerebral microvascular endothelial cells, the cells incubated with colloidal gold liposomes can uptake of liposome colloidal gold, and with the extension of time, there are gold colloids in the plasma membrane, endo-plasmic reticulum, Golgi apparatus and lysosomes in order, and finally colloidal gold liposome exports out of the cell. For cerebral microvascular endothelial cells treated by sodium azide, compared with untreated cells, the cells incubated with colloidal gold liposomes, cannot be observed liposome colloidal gold in them. For cerebral microvas-cular endothelial cells treated by reserpine, the cells incubated with colloidal gold liposomes, compared with un-treated cells, colloidal gold liposome cannot export out of the cell. Conclusions:The uptake of liposomes in brain microvascular endothelial cells require clathrin's participation. The excretion of liposomes from brain microvascular endothelial cells require P-glycoprotein's participation. After colloidal gold liposome entering brain microvascular endothelial cells, it moves into the endoplasmic reticulum, Golgi apparatus and lysosomes in order. Finally colloi-dal gold liposome exports out of the cell.
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原发性中枢神经系统淋巴瘤伽玛刀治疗前后的MRI评估
原发性中枢神经系统淋巴瘤(primary central nervous system lymphoma,PCNSL)是发生于中枢神经系统的一种少见的结外恶性淋巴瘤,近几十年其发病率逐年上升[1].目前,影像学对该病的诊断已经积累了较多的经验,尤其MRI 在术前治疗方案的制订中发挥了重要的作用.关于该病的治疗方法,现多采用放化疗结合的综合性治疗手段.伽玛刀作为一种有效的局部放疗方法,近些年已经应用于临床治疗.
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原发中枢神经系统淋巴瘤的诊治进展
原发中枢神经系统淋巴瘤( primary central nervous system lymphoma ,PCNSL)属于结外侵袭性非霍奇金淋巴瘤( NHL)的一种特殊类型,占颅脑肿瘤的1%~6%,在NHL中不足1%。其中96%以上为高度恶性的B细胞淋巴瘤,弥漫大B细胞淋巴瘤是其中常见的亚型,而T细胞淋巴瘤和低度恶性淋巴瘤仅占1%~4%。由于发病时病变仅存在于脑实质(少数可发生于脑脊膜或眼后),病变取材困难,影像学特征性缺乏特异性,因此诊断有一定难度,而治疗也不靠手术,因此临床医生需提高对本病的认识。
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自发缓解复发的原发性中枢神经系统淋巴瘤
原发性中枢神经系统淋巴瘤( primary central nervous system lymphoma,PCNSL)为非霍奇金淋巴瘤侵入脑、脑膜、脊髓、脑和脊髓的神经根及眼(玻璃体,脉络膜,视网膜)和视神经;中枢神经系统以外部位,包括淋巴结,没有淋巴瘤的证据.PCNSL非常少见,占颅内原发肿瘤的3.1%,占全部非霍奇金淋巴瘤的2%~3%[1,2],而自发缓解的PCNSL更加少见[3,4],国内尚未见报道.我们报道一例临床和影像学自发缓解的PCNSL,结合文献复习,丰富对PCNSL的认识.
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Objective To investigate the diagnostic value of brain magnetic resonance imaging in detecting central nervous system diseases among AIDS patients of different levels of T cells. Methods Total of 164 AIDS patients who did not receive antiviral treatment were divided into 2 groups according to their baseline CD4+T cell counts. Group A had CD4+T cell below or equal to 50 cells/μl (n=81) and group B had CD4+T cells over 50 cells/μl (n=83). All patients underwent brain MRI scan. Imaging analysis and the prevalence of the central nervous system disorders were compared between two groups. Results Among them 48 cases were found of abnormal brain MRI, group A was higher than group B (35.8%vs. 22.9%) although without statistical significance (P = 0.065). Altogether 48 cases were diagnosed as AIDS related central nervous system disorders based on clinical symptoms, signs and laboratory findings. The prevalence of CNS disorders was higher in group A than in group B (41.9%vs. 16.8%) with statistical significance (P<0.01). Conclusions The patients with CD4+T cell count less than or equal to 50 cells/μl had high prevalence of CNS diseases. Brain MRI plays an important role in the diagnosis and differentiation of CNS diseases in advanced AIDS patients. This study suggests patients with low CD4+T cell count (≤ 50/μl) should routinely undergo MRI examination.
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AIDS合并原发性中枢神经系统淋巴瘤一例
原发性中枢神经系统淋巴瘤(primary central nervous system lymphoma,PCNSL)是艾滋病晚期的并发症之一,起病通常较急,进展快,预后不佳。其临床表现、影像学检查均无显著特点,易被误诊误治。临床医师需要提高认识,在条件许可下及早进行脑活检明确诊断对治疗极为重要。本科室收治一例AIDS合并原发性中枢神经系统淋巴瘤,现报道如下。
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胎儿中枢神经系统的超声检查操作指南
1 简介中枢神经系统(CNS )畸形是常见的先天性畸形之一.神经管缺陷在CNS 畸形中为常见,其发生率为1/1000~2 /1000 .有些胎儿颅内CNS 畸形但神经管完整,只有在出生后才逐渐显现出来,因此其发生率并不确定.不过长期随访研究显示其发病率高达1/100[1].
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神经影像学检查在小儿危重症脑功能评价中的应用
中枢神经系统包括脑和脊髓,深藏在被骨骼包围的颅腔和椎管内,一般物理学检查不易达到,因此影像学检查具有重要意义.近30年来,随着数字X线、CT、磁共振成像(MRI)设备的不断改进和完善,检查技术和方法也在不断地创新,中枢神经系统的影像学诊断已从单一依靠形态变化进行诊断发展成为集形态、功能和代谢改变为一体的综合诊断体系.
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中枢神经系统感染患儿脑脊液中IGF-Ⅱ及IGFBP-3水平变化的研究
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北京市儿童与肠道病毒71型感染有关的手足口病伴中枢神经系统症状一例
ASE REPORTA 9-year-and-8-month-old girl experienced intermittent headache of 2 d, fever of 1 d and convulsion of 2 h and was sent to the emergency room (ER). Two days before admission, the girl presented with intermittent headache of obscure cause, which had no fixed site and was tolerable, accompanied by dizziness; she had no change in vision, nor vertigo, nausea, vomiting, cough, nasal discharge or otalgia. One day before hospitalization, the girl became feverish, with the highest body temperature of 38. 8℃ while she had convulsions two hours before the visit to the ER, presenting with binocular gazing, trismus, loss of consciousness, initially noncyanotic face, unaccompanied by extremities rigidity or clonus. Her convulsion could not be controlled after intramuscular injection of 6 mg valium at the local clinic and was transferred to a neighboring secondary hospital 20 min later, where she began to develop extremities clonus, irregular respiration and cyanosis.
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原发性中枢神经系统恶性淋巴瘤
原发性中枢神经系统恶性淋巴瘤(primary central nervous system malignant lymphoma,PCNSL或CNSPML)是一种病变局限于中枢神经系统而颅外无淋巴瘤证据的罕见的恶性肿瘤。于1929年由Bailey首次报道。其发生率占恶性淋巴瘤的0.9%~2%,约占颅内肿瘤的0.3%~1.5%,占淋巴结外恶性淋巴瘤的1.6%。由于本病临床……
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Non-invasive brain stimulations mainly consist of repetitive transcranial magnetic stimulation and transcranial direct current stimulation. Repetitive transcranial magnetic stimulation exhib-its satisfactory outcomes in improving multiple sclerosis, stroke, spinal cord injury and cerebral palsy-induced spasticity. By contrast, transcranial direct current stimulation has only been studied in post-stroke spasticity. To better validate the effcacy of non-invasive brain stimulations in im-proving the spasticity post-stroke, more prospective cohort studies involving large sample sizes are needed.
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The accumulation of myelin debris may be a major contributor to the inlfammatory response after diffuse axonal injury. In this study, we examined the accumulation and clearance of myelin debris in a rat model of diffuse axonal injury. Oil Red O staining was performed on sections from the cerebral cortex, hippocampus and brain stem to identify the myelin debris. Seven days after diffuse axonal injury, many Oil Red O-stained particles were observed in the cerebral cortex, hippocampus and brain stem. In the cerebral cortex and hippocampus, the amount of myelin debris peaked at 14 days after injury, and decreased signiifcantly at 28 days. In the brain stem, the amount of myelin debris peaked at 7 days after injury, and decreased signiifcantly at 14 and 28 days. In the cortex and hippocampus, some myelin debris could still be observed at 28 days after diffuse axonal injury. Our ifndings suggest that myelin debris may persist in the rat central ner-vous system after diffuse axonal injury, which would hinder recovery.
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The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory be-haviors and structural changes in related brain regions, in a mouse model of Alzheimer’s disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged (4-month-old) or elderly (7-month-old) senescence-accelerated mouse prone 8 (SAMP8) mice. When the middle-aged mice reached 8 months (middle-aged group 1) or 11 months (middle-aged group 2), and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learn-ing and memory were performed, and the cholinergic system was examined in the hippocampus (Nissl staining and acetylcholinesterase histochemistry) and basal forebrain (choline acetyltrans-ferase immunohistochemistry). In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic ifbers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no signiifcant differences in histology or be-havior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present ifndings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer’s disease, and indicate that tooth extraction should be avoided in these populations.
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CD93 and GAIP-interacting protein, C termius (GIPC) have been shown to interactively alter phagocytic processes of immune cells. CD93 and GIPC expression and localization during cen-tral nervous system inflammation have not yet been reported. In this study, we established a rat model of brain inlfammation by lipopolysaccharide injection to the lateral ventricle. In the brain of rats with inlfammation, western blots showed increased CD93 expression that decreased over time. GIPC expression was unaltered. Immunohistochemistry demonstrated extensive distribution of CD93 expression mainly in cell membranes in the cerebral cortex. After lipopoly-saccharide stimulation, CD93 expression increased and then reduced, with distinct staining in the cytoplasm and nucleus. Double immunolfuorescence staining in cerebral cortex of normal rats showed that CD93 and GIPC widely expressed in resting microglia and neurons. CD93 was mainly expressed in microglial and neuronal cell membranes, while GIPC was expressed in both cell membrane and cytoplasm. In the cerebral cortex at 9 hours after model establishment, CD93-immunoreactive signal diminished in microglial membrane, with cytoplasmic transloca-tion and aggregation detected. GIPC localization was unaltered in neurons and microglia. These results are the ifrst to demonstrate CD93 participation in pathophysiological processes of central nervous system inlfammation.
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In this review, we outline the major neural plasticity mechanisms that have been identiifed in the adult central nervous system (CNS), and offer a perspective on how they regulate CNS function. In particular we examine how myelin plasticity can operate alongside neurogenesis and synaptic plasticity to inlfuence information processing and transfer in the mature CNS.
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Paired immunoglobulin-like receptor B (PirB) is a functional receptor of myelin-associated in-hibitors for axonal regeneration and synaptic plasticity in the central nervous system, and thus suppresses nerve regeneration. The regulatory effect of PirB on injured nerves has received a lot of attention. To better understand nerve regeneration inability after spinal cord injury, this study aimed to investigate the distribution of PirB (via immunolfuorescence) in the central nervous system and peripheral nervous system 10 days after injury. Immunoreactivity for PirB increased in the dorsal root ganglia, sciatic nerves, and spinal cord segments. In the dorsal root ganglia and sciatic nerves, PirB was mainly distributed along neuronal and axonal membranes. PirB was found to exhibit a diffuse, intricate distribution in the dorsal and ventral regions. Immunore-activity for PirB was enhanced in some cortical neurons located in the bilateral precentral gyri. Overall, the ifndings suggest a pattern of PirB immunoreactivity in the nervous system after uni-lateral spinal transection injury, and also indicate that PirB may suppress repair after injury.
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Because neurons are susceptible to oxidative damage and thioredoxin reductase 1 is extensively distributed in the central nervous system and has antioxidant properties, we speculated that the enzyme may be involved in the pathogenesis of Parkinson’s disease. A Parkinson’s disease model was produced by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into C57BL/6 mice. Real-time reverse transcription-PCR, western blot analysis and colorimetric assay showed that the levels of thioredoxin reductase 1 mRNA and protein were decreased, along with a significant reduction in thioredoxin reductase activity, in the midbrain of Parkinson’s disease mice compared with normal mice. Immunohistochemical staining revealed that the number of thioredoxin reductase 1-positive neurons in the substantia nigra pars compacta of Parkinson’s disease mice was significantly decreased compared with normal mice. These experimental findings suggest that the expression of thioredoxin reductase 1 in the substantia nigra pars compacta of Parkinson’s disease mice is significantly decreased, and that the enzyme may be associated with disease onset.