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Growth-associated protein 43 and neural cell adhesion molecule expression following bone marrow-derived mesenchymal stem cell transplantation in a rat model of ischemic brain injury 被引量:18
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作者 Yu Peng Qimei Zhang +3 位作者 Hui You Weihua Zhuang Ying Zhang Chengyan Li 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第13期975-980,共6页
BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated pr... BACKGROUND: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves motor functional recovery, but the mechanisms remain unclear. OBJECTIVE: To investigate expression of growth-associated protein 43 (GAP-43) and neural cell adhesion molecule following BMSC transplantation to the lateral ventricle in rats with acute focal cerebral ischemic brain damage. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment using immunohistochemistry was performed at the laboratories of Department of Neurology, Renmin Hospital of Wuhan University and Doctoral Scientific Research Work Station of C-BONS PHARMA, Hubei Province, China, from January 2007 to December 2008. MATERIALS: Monoclonal mouse anti-rat 5-bromo-2-deoxyuridine and neural cell adhesion molecule antibodies were purchased from Sigma, USA; monoclonal mouse anti-rat GAP-43 antibody was purchased from Wuhan Boster, China. METHODS: Rat models of right middle cerebral artery occlusion were established using the thread method. At 1 day after middle cerebral artery occlusion, 20μL culture solution, containing 5×10^5 BMSCs, was transplanted to the left lateral ventricle using micro-injection. MAIN OUTCOME MEASURES: Scores of neurological impairment were measured to assess neural function. Expression of GAP-43 and neural cell adhesion molecule at the lesion areas was examined by immunohistochemistry. RESULTS: GAP-43 and neural cell adhesion molecule expression was low in brain tissues of the sham-operated group, but expression increased at the ischemic boundary (P 〈 0.05). Transplantation of BMSCs further enhanced expression of GAP-43 and neural cell adhesion molecule (P 〈 0.05) and remarkably improved neurological impairment of ischemic rats (P 〈 0.05). CONCLUSION: BMSC transplantation promoted neurological recovery in rats by upregulating expression of GAP-43 and neural cell adhesion molecule. 展开更多
关键词 growth-associated protein 43 neural cell adhesion molecule bone marrow-derived mesenchymal stem cell brain injury neural regeneration
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Alterations in the polysialylated neural cell adhesion molecule and retinal ganglion cell density in mice with diabetic retinopathy 被引量:2
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作者 Natalia Lobanovskaya Monika Jürgenson +1 位作者 Anu Aonurm-Helm Alexander Zharkovsky 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2018年第10期1608-1615,共8页
AIM:To investigate the impact of polysialylated neural cell adhesion molecule(PSA-NCAM)on the survival of retinal ganglion cells(RGCs)in the experimentally induced diabetes in mice.METHODS:Diabetes was induced i... AIM:To investigate the impact of polysialylated neural cell adhesion molecule(PSA-NCAM)on the survival of retinal ganglion cells(RGCs)in the experimentally induced diabetes in mice.METHODS:Diabetes was induced in 2.5 months old Swiss Webster mice by intraperitoneal injection of streptozotocin(STZ,90 mg/kg)once daily for two consecutive days.Examination of the proteins of interest in the retinas from diabetic mice at 2mo after diabetes induction was performed using immunohistochemistry and Western blot analysis.RGCs were counted in the wholemounted retinas,and Brn3a marker was used.RESULTS:Examination of retinas from diabetic mice at 2mo after diabetes induction revealed a considerable reduction in RGC density.Our experiments also demonstrated a redistribution of PSA-NCAM in the retina of diabetic animals.PSA-NCAM immunoreactivity was diminished in the inner part of the retina where RGCs were located.In contrast,an enhanced PSA-NCAM immunoreactivity was detected in the outer layers of the retina.PSA-NCAM signal was co-localized with glial fibrillary acidic protein immunoreactivity in the Müller cell branches.Previous studies have shown that matrix metalloproteinase-9(MMP-9)is responsible for the reduction in PSA-NCAM levels in neuronal cells.The reduced levels of PSA-NCAM in inner layers(nerve fiber layer,ganglion cell layer)were accompanied by the increased expression of MMP-9.In contrast,in the outer retinal layers,the expression of MMP-9 was much less pronounced.CONCLUSION:MMP-9 induces PSA-NCAM shedding in the inner part of the retina and the decreased level of PSA-NCAM in the inner part of the retina might be,at least in part,responsible for the loss of RGCs in diabetic mice. 展开更多
关键词 diabetic retinopathy matrix metalloproteinase-9 polysialylated neural cell adhesion molecule retinal ganglion cells
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Nerve bundle formation during the promotion of peripheral nerve regeneration:collagenⅥ-neural cell adhesion molecule 1 interaction 被引量:2
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作者 Jia-Hui Sun Ming Huang +8 位作者 Zhou Fang Tian-Xiao Li Ting-Ting Wu Yi Chen Da-Ping Quan Ying-Ying Xu Yu-Ming Wang Yi Yang Jian-Long Zou 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第5期1023-1033,共11页
The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how... The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how the extracellular matrix(ECM)microenvironment affects this process.Here,we seeded dorsal root ganglion tissue blocks on different ECM substrates of peripheral nerve ECM-derived matrixgel,Matrigel,laminin 521,collagen I,and collagen IV,and observed well-aligned axon bundles growing in the peripheral nerve ECM-derived environment.We confirmed that NCAM1 is necessary but not sufficient to trigger this phenomenon.A protein interaction assay identified collagen VI as an extracellular partner of NCAM1 in the regulation of axonal fasciculation.Collagen VI interacted with NCAM1 by directly binding to the FNIII domain,thereby increasing the stability of NCAM1 at the axolemma.Our in vivo experiments on a rat sciatic nerve defect model also demonstrated orderly nerve bundle regeneration with improved projection accuracy and functional recovery after treatment with 10 mg/m L Matrigel and 20μg/m L collagen VI.These findings suggest that the collagen VI-NCAM1 pathway plays a regulatory role in nerve bundle formation.This study was approved by the Animal Ethics Committee of Guangzhou Medical University(approval No.GY2019048)on April 30,2019. 展开更多
关键词 axonal fasciculation collagen VI extracellular matrix MICROENVIRONMENT nerve bundle formation nerve projection neural cell adhesion molecule 1 NEUROGENESIS peripheral nerve regeneration
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Cognitive disorder and changes in cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury
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作者 Weiliang Zhao Dezhi Kang Yuanxiang Lin 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第3期305-308,共4页
BACKGROUND: Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated... BACKGROUND: Learning and memory damage is one of the most permanent and the severest symptoms of traumatic brain injury; it can seriously influence the normal life and work of patients. Some research has demonstrated that cognitive disorder is closely related to nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor. OBJECTIVE: To summarize the cognitive disorder and changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury. RETRIEVAL STRATEGY: A computer-based online search was conducted in PUBMED for English language publications containing the key words "brain injured, cognitive handicap, acetylcholine, N-methyl-D aspartate receptors, neural cell adhesion molecule, brain-derived neurotrophic factor" from January 2000 to December 2007. There were 44 papers in total. Inclusion criteria: ① articles about changes in nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor following brain injury; ② articles in the same researching circle published in authoritative journals or recently published. Exclusion criteria: duplicated articles. LITERATURE EVALUATION: References were mainly derived from research on changes in these four factors following brain injury. The 20 included papers were clinical or basic experimental studies. DATA SYNTHESIS: After craniocerebral injury, changes in these four factors in brain were similar to those during recovery from cognitive disorder, to a certain degree. Some data have indicated that activation of nicotine cholinergic receptors, N-methyl-D aspartate receptors, neural cell adhesion molecule, and brain-derived neurotrophic factor could greatly improve cognitive disorder following brain injury. However, there are still a lot of questions remaining; for example, how do these factors change at different time points after brain injury, and what is the relationship between associated factors and cognitive disorder. CONCLUSION: It is necessary to comprehensively study some associated factors, to analyze their changes and their relationship with cognitive disorder following brain injury, and to investigate their effects at different time points after brain injury. 展开更多
关键词 brain injured cognitive handicap ACETYLCHOLINE N-methyl-D aspartate receptors neural cell adhesion molecule brain-derived neurotrophic factor
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Expression changes of nerve cell adhesion molecules L1 and semaphorin 3A after peripheral nerve injury 被引量:1
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作者 Qian-ru He Meng Cong +5 位作者 Qing-zhong Chen Ya-feng Sheng Jian Li Qi Zhang Fei Ding Yan-pei Gong 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第12期2025-2030,共6页
The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peri... The expression of nerve cell adhesion molecule L1 in the neuronal growth cone of the central nervous system is strongly associated with the direction of growth of the axon, but its role in the regeneration of the peripheral nerve is still unknown. This study explored the problem in a femoral nerve section model in rats. L1 and semaphorin 3A m RNA and protein expressions were measured over the 4-week recovery period. Quantitative polymerase chain reaction showed that nerve cell adhesion molecule L1 expression was higher in the sensory nerves than in motor nerves at 2 weeks after injury, but vice versa for the expression of semaphorin 3A. Western blot assay results demonstrated that nerve cell adhesion molecule L1 expression was higher in motor nerves than in the sensory nerves at the proximal end after injury, but its expression was greater in the sensory nerves at 2 weeks. Semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 3 days and 1 week after injury. Nerve cell adhesion molecule L1 and semaphorin 3A expressions at the distal end were higher in the motor nerves than in the sensory nerves at 3 days, 1 and 2 weeks. Immunohistochemical staining results showed that nerve cell adhesion molecule L1 expression at the proximal end was greater in the sensory nerves than in the motor nerves; semaphorin 3A expression was higher in the motor nerves than in the sensory nerves at 2 weeks after injury. Taken together, these results indicated that nerve cell adhesion molecules L1 and semaphorin 3A exhibited different expression patterns at the proximal and distal ends of sensory and motor nerves, and play a coordinating role in neural chemotaxis regeneration. 展开更多
关键词 nerve regeneration neural cell adhesion molecule L1 semaphorin 3A sensory nerve motor nerve peripheral nerve injury chemotaxis regeneration neural regeneration
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Molecular and cellular changes in the post-traumatic spinal cord remodeling after autoinfusion of a genetically-enriched leucoconcentrate in a mini-pig model 被引量:2
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作者 Maria Aleksandrovna Davleeva Ravil Rasimovich Garifulin +9 位作者 Farid Vagizovich Bashirov Andrei Aleksandrovich Izmailov Leniz Faritovich Nurullin Ilnur Ildusovich Salafutdinov Dilara Zilbarovna Gatina Dmitrij Nikolaevich Shcherbinin Andrei Aleksandrovich Lysenko Irina Leonidovna Tutykhina Maksim Mikhailovich Shmarov Rustem Robertovich Islamov 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第7期1505-1511,共7页
Post-traumatic spinal cord remodeling includes both degenerating and regenerating processes,which affect the potency of the functional recovery after spinal cord injury(SCI).Gene therapy for spinal cord injury is prop... Post-traumatic spinal cord remodeling includes both degenerating and regenerating processes,which affect the potency of the functional recovery after spinal cord injury(SCI).Gene therapy for spinal cord injury is proposed as a promising therapeutic strategy to induce positive changes in remodeling of the affected neural tissue.In our previous studies for delivering the therapeutic genes at the site of spinal cord injury,we developed a new approach using an autologous leucoconcentrate transduced ex vivo with chimeric adenoviruses(Ad5/35)carrying recombinant cDNA.In the present study,the efficacy of the intravenous infusion of an autologous genetically-enriched leucoconcentrate simultaneously producing recombinant vascular endothelial growth factor(VEGF),glial cell line-derived neurotrophic factor(GDNF),and neural cell adhesion molecule(NCAM)was evaluated with regard to the molecular and cellular changes in remodeling of the spinal cord tissue at the site of damage in a model of mini-pigs with moderate spinal cord injury.Experimental animals were randomly divided into two groups of 4 pigs each:the therapeutic(infused with the leucoconcentrate simultaneously transduced with a combination of the three chimeric adenoviral vectors Ad5/35‐VEGF165,Ad5/35‐GDNF,and Ad5/35‐NCAM1)and control groups(infused with intact leucoconcentrate).The morphometric and immunofluorescence analysis of the spinal cord regeneration in the rostral and caudal segments according to the epicenter of the injury in the treated animals compared to the control mini-pigs showed:(1)higher sparing of the grey matter and increased survivability of the spinal cord cells(lower number of Caspase-3-positive cells and decreased expression of Hsp27);(2)recovery of synaptophysin expression;(3)prevention of astrogliosis(lower area of glial fibrillary acidic protein-positive astrocytes and ionized calcium binding adaptor molecule 1-positive microglial cells);(4)higher growth rates of regeneratingβIII-tubulin-positive axons accompanied by a higher number of oligodendrocyte transcription factor 2-positive oligodendroglial cells in the lateral corticospinal tract region.These results revealed the efficacy of intravenous infusion of the autologous genetically-enriched leucoconcentrate producing recombinant VEGF,GDNF,and NCAM in the acute phase of spinal cord injury on the positive changes in the post-traumatic remodeling nervous tissue at the site of direct injury.Our data provide a solid platform for a new ex vivo gene therapy for spinal cord injury and will facilitate further translation of regenerative therapies in clinical neurology. 展开更多
关键词 autologous genetically-enriched leucoconcentrate chimeric adenoviral vector gene therapy glial cell line-derived neurotrophic factor MINI-PIG neural cell adhesion molecule spinal cord contusion injury vascular endothelial growth factor
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ADAM10 facilitates rapid neural stem cell cycling and proper positioning within the subventricular zone niche via JAMC/RAP1Gap signaling
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作者 Nadia McMillan Gregory W.Kirschen +3 位作者 Sanket Desai Emma Xia Stella E.Tsirka Adan Aguirre 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第11期2472-2483,共12页
The mechanisms that regulate neural stem cell(NSC)lineage progression and maintain NSCs within diffe rent domains of the adult neural stem cell niche,the subventricular zone are not well defined.Quiescent NSCs are arr... The mechanisms that regulate neural stem cell(NSC)lineage progression and maintain NSCs within diffe rent domains of the adult neural stem cell niche,the subventricular zone are not well defined.Quiescent NSCs are arranged at the apical ventricular wall,while mitotically activated NSCs are found in the basal,vascular region of the subventricular zone.Here,we found that ADAM 10(a disintegrin and metalloproteinase 10)is essential in NSC association with the ventricular wall,and via this adhesion to the apical domain,ADAM10 regulates the switch from quiescent and undiffe rentiated NSC to an actively prolife rative and differentiating cell state.Processing of JAMC(junctional adhesion molecule C)by ADAM 10 increases Rap1 GAP activity.This molecular machinery promotes NSC transit from the apical to the basal compartment and subsequent lineage progression.Understanding the molecular mechanisms responsible for regulating the proper positioning of NSCs within the subventricular zone niche and lineage progression of NSCs could provide new targets for drug development to enhance the regenerative prope rties of neural tissue. 展开更多
关键词 ADAM10 adhesion junctional adhesion molecule C neural stem cells NEUROGENESIS olfactory bulb Rap1Gap sub-ventricular zone
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宁夏无果枸杞芽提取物对自然衰老小鼠SOD、MDA及NCAM的影响 被引量:12
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作者 张莲香 陈海军 +6 位作者 胡嘉航 马江波 贾桦 秦毅 朱佳新 王瑞 王凡 《宁夏医科大学学报》 2012年第12期1265-1268,F0002,共5页
目的观察宁夏无果枸杞芽醇提取物(FLE)对老年小鼠学习、记忆功能、血浆和脑组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及神经细胞黏附分子(NCAM)在海马和皮质表达的影响。方法将60只13个月龄自然衰老KM小鼠分为老年对照组和FLE低... 目的观察宁夏无果枸杞芽醇提取物(FLE)对老年小鼠学习、记忆功能、血浆和脑组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及神经细胞黏附分子(NCAM)在海马和皮质表达的影响。方法将60只13个月龄自然衰老KM小鼠分为老年对照组和FLE低剂量组(FLE1组)、FLE中剂量组(FLE2组)、FLE高剂量组(FLE3组),每组15只;另将15只6个月龄KM小鼠做为成年对照组。FLE1、FLE2、FLE3组分别用质量/体积百分比为5%、10%、20%FLE灌胃,0.2mL.(10g.d)-1,老年对照组和成年对照组灌胃等量生理盐水,连续8周。用Morris水迷宫实验检测各组小鼠学习记忆能力;黄嘌呤氧化酶法测定血清和脑组织SOD活性,硫代巴比妥酸法测定MDA水平;免疫组化SP法检测小鼠脑组织中NCAM的表达。结果与成年对照组比较,老年对照组小鼠的空间搜索平台停留时间百分比降低,血清SOD活性降低,MDA水平提高(P<0.01),脑组织中NCAM表达下调(P<0.01)。与老年对照组比较,FLE2、FLE3组的学习记忆能力均提高、血清和脑组织中SOD活性均增加,MDA水平降低,脑组织中NCAMs表达均上调(P<0.05)。结论 FLE能够改善自然衰老KM小鼠的学习记忆能力,其机制可能与FLE的抗氧化和上调脑组织中NCAM表达有关。 展开更多
关键词 衰老 无果枸杞芽 神经细胞粘附分子 学习 记忆
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坐骨神经结扎大鼠脊髓背根神经节GDNF和NCAM表达的变化 被引量:4
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作者 胡玉萍 胡益民 +2 位作者 王昱 杨建军 李伟彦 《临床麻醉学杂志》 CAS CSCD 北大核心 2010年第5期427-429,共3页
目的 观察坐骨神经结扎大鼠脊髓背根神经节(隙G)胶质细胞源性神经营养因子(GD-NF)和神经细胞黏附分子(NCAM)表达的变化.方法 成年SD大鼠42只,随机均分为疼痛组(CCI组)和对照组(C组).CCI组行左侧坐骨神经结扎术,建立慢性限制... 目的 观察坐骨神经结扎大鼠脊髓背根神经节(隙G)胶质细胞源性神经营养因子(GD-NF)和神经细胞黏附分子(NCAM)表达的变化.方法 成年SD大鼠42只,随机均分为疼痛组(CCI组)和对照组(C组).CCI组行左侧坐骨神经结扎术,建立慢性限制性损伤模型;C组行假手术.分别于术前1d和术后1、3、5、7、14、21 d测机械痛阈(MWT)和热痛阈(TWL).采用免疫组织化学染色和适时PCR技术检测DRG中GDNF和NCAM的表达.结果 CCI组术后3、5、7、14 d MWT明显低于、TWL短于C组(P〈0.01),而GDNF和NCAM表达明显高于C组(P〈0.05或P〈0.01).结论 坐骨神经结扎大鼠术后可出现痛阈下降,同时伴有DRG中GDNF和NCAM的表达增高. 展开更多
关键词 坐骨神经 背根神经节 胶质细胞源性神经营养因子 神经细胞黏附分子
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PGP9.5及NCAM在阻塞性睡眠呼吸暂停低通气综合征患者软腭末梢神经表达的研究 被引量:4
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作者 王干 罗伟 +6 位作者 郝红 李桂梅 曹晓卉 王旭平 王佩杰 张佳 何飞 《安徽医科大学学报》 CAS 北大核心 2014年第7期988-991,共4页
目的研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者软腭组织中蛋白基因产物9.5(PGP9.5)和神经细胞黏附因子(NCAM)的表达及末梢神经在软腭各层组织中分布,探讨OSAHS患者软腭末梢神经分布特点及调节的变化。方法选取30例OSAHS患者作为... 目的研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者软腭组织中蛋白基因产物9.5(PGP9.5)和神经细胞黏附因子(NCAM)的表达及末梢神经在软腭各层组织中分布,探讨OSAHS患者软腭末梢神经分布特点及调节的变化。方法选取30例OSAHS患者作为实验组,10例排除OSAHS的单纯慢性扁桃体炎患者作为对照组。通过HE染色检测软腭组织中末梢神经的分布,免疫组化检测软腭组织中PGP9.5和NCAM的表达。结果 1实验组软腭不同层次组织中末梢神经的分布不同,末梢神经主要分布在黏膜下层、腺体、血管周围,肌肉组织周围少量分布;2实验组OSAHS患者软腭组织中PGP9.5及NCAM表达明显高于对照组,差异有统计学意义(P<0.05);3 PGP9.5、NCAM的表达水平与呼吸暂停低通气指数(AHI)呈正相关(r=0.706,P=0.01;r=0.636,P=0.01)。结论 OSAHS患者软腭组织中末梢神经的分布及支配异常,且与病情严重程度密切相关。 展开更多
关键词 阻塞性睡眠呼吸暂停低通气综合征 软腭 末梢神经 蛋白基因产物9 5 神经细胞黏附因子
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S-100和NCAM在腺样囊性癌组织中的表达及意义 被引量:2
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作者 杜咏梅 郭煜 +1 位作者 骆树瑜 李蕊 《中国肿瘤临床》 CAS CSCD 北大核心 2012年第10期670-673,共4页
目的:分析腺样囊性癌(adenoid cystic carcinoma,ACC)的临床病理特点,观察雪旺细胞标记物S-100和神经细胞粘附分子(neural cell adhesion molecule,NCAM)在ACC中的表达,探讨S-100和NCAM与ACC嗜神经侵袭性的关系。方法:对天津医科大学口... 目的:分析腺样囊性癌(adenoid cystic carcinoma,ACC)的临床病理特点,观察雪旺细胞标记物S-100和神经细胞粘附分子(neural cell adhesion molecule,NCAM)在ACC中的表达,探讨S-100和NCAM与ACC嗜神经侵袭性的关系。方法:对天津医科大学口腔医院42例ACC病例应用免疫组织化学方法检测S-100和NCAM在ACC中的表达,并探讨其相关性。结果:S-100在ACC嗜神经组阳性表达率80.0%明显高于非嗜神经组33.3%(P=0.011)。NCAM在嗜神经和非嗜神经侵袭组ACC中的阳性表达差异无统计学意义。S-100与NCAM在ACC中的阳性表达无明显相关性(P>0.05)。结论:S-100蛋白的表达与ACC的嗜神经现象密切相关,在管状型中的表达明显高于充实型,与肿瘤细胞分化具有一定相关性。NCAM蛋白的表达与ACC的嗜神经现象无统计学相关性,与S-100蛋白的表达亦无明显相关。 展开更多
关键词 腺样囊性癌 神经侵袭 S-100蛋白 神经细胞粘附分子 免疫组织化学
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海马脑片LTP产生中NO对NCAM蛋白合成的影响 被引量:2
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作者 胡志安 陈伯成 +1 位作者 黎海蒂 罗峻 《第三军医大学学报》 CAS CSCD 北大核心 2004年第1期43-46,共4页
目的 观察NMDA受体和一氧化氮 (NO)对海马脑片突触传递长时程增强 (LTP)产生中神经细胞粘附分子 (NCAM)合成的影响。方法 采用胞外记录方法检测LTP产生和维持。Westernblot技术检测NCAM合成变化。结果 条件刺激 10min后 ,LTP产生 ,N... 目的 观察NMDA受体和一氧化氮 (NO)对海马脑片突触传递长时程增强 (LTP)产生中神经细胞粘附分子 (NCAM)合成的影响。方法 采用胞外记录方法检测LTP产生和维持。Westernblot技术检测NCAM合成变化。结果 条件刺激 10min后 ,LTP产生 ,NCAM合成显著增加。条件刺激 60min后 ,LTP稳定维持 ,NCAM蛋白水平持续增高。NMDA受体阻断剂AP 5和NO合酶抑制剂N硝基精氨酸在抑制LTP产生的同时 ,也显著抑制NCAM合成。 展开更多
关键词 长时程增强 一氧化氮 神经细胞粘附分子 海马 大鼠
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慢传输型便秘大鼠结肠组织GFRα1、RET、NCAM的表达以及外源性GDNF的影响 被引量:3
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作者 金曼 范一宏 +3 位作者 张高松 李延玲 吕宾 张璐 《胃肠病学》 2011年第11期658-661,共4页
背景:研究证实胶质细胞源性神经营养因子(GDNF)既可抗神经元凋亡,又可阻止神经细胞胞体萎缩,从而改善肠道动力,但其具体机制目前仍未完全明了。目的:研究慢传输型便秘(STC)大鼠结肠组织中GFRα1、RET、NCAM的表达以及外源性GDNF对其的影... 背景:研究证实胶质细胞源性神经营养因子(GDNF)既可抗神经元凋亡,又可阻止神经细胞胞体萎缩,从而改善肠道动力,但其具体机制目前仍未完全明了。目的:研究慢传输型便秘(STC)大鼠结肠组织中GFRα1、RET、NCAM的表达以及外源性GDNF对其的影响,从而探讨GDNF保护STC大鼠结肠神经元的途径及其信号转导机制。方法:44只大鼠随机分为对照组和模型组,以大黄灌胃建立STC模型。造模成功后,对照组进一步分为正常对照组和GDNF组,模型组分为STC组和STC+GDNF组。GDNF组和STC+GDNF组大鼠尾静脉注射rhGDNF,其余两组注射0.9%NaC1溶液。1周后处死大鼠,采用免疫组化法检测结肠组织中GFRα1、RET、NCAM表达。结果:STC组GFRα1、NCAM表达较正常对照组显著减弱(P<0.05);STC组大鼠以GDNF干预后,GFRα1、NCAM表达较STC组显著增强(P<0.05);GDNF组GFRα1、NCAM表达亦较STC组、正常对照组显著增强(P<0.05)。RET仅在正常对照组结肠组织少量表达,其余各组均无表达。结论:长期使用大黄可减弱结肠组织中CFRα1、NCAM的表达,外源性GDNF可能通过GDNF-GFRα1-NCAM途径而非GDNF-GFRα1-RET途径进行信号转导,从而保护结肠神经元。 展开更多
关键词 慢传输型便秘 胶质细胞源性神经营养因子 胶质细胞源性神经营养因子受体 RET 神经细胞黏附分子类
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大鼠脑损伤后ChAT、NCAM表达及其与认知障碍变化的关系 被引量:3
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作者 康德智 赵卫良 王灯亮 《福建医科大学学报》 2010年第5期320-323,共4页
目的观察大鼠在脑损伤后额叶皮层、海马、伏隔核乙酰胆碱转移酶(ChAT)和神经细胞黏附因子(NCAM)的变化,探讨ChAT、NCAM变化与脑损伤后认知障碍的关系。方法以自由落体打击建立轻型和中型脑损伤大鼠模型,以"假手术"大鼠的脑组... 目的观察大鼠在脑损伤后额叶皮层、海马、伏隔核乙酰胆碱转移酶(ChAT)和神经细胞黏附因子(NCAM)的变化,探讨ChAT、NCAM变化与脑损伤后认知障碍的关系。方法以自由落体打击建立轻型和中型脑损伤大鼠模型,以"假手术"大鼠的脑组织为对照。水迷宫检测伤后认知障碍变化,应用分光光度法测定额叶皮层、海马、伏隔核ChAT含量,应用ELISA法测定额叶皮层、海马、伏隔核NCAM含量。结果轻、中型脑损伤组大鼠于伤后2 d认知障碍最严重;伤后ChAT及NCAM含量均呈现先降后升的趋势,均于伤后2 d达到最低水平。结论脑损伤后认知障碍变化趋势同额叶皮层、海马、伏隔核ChAT和NCAM含量变化趋势有相似性。 展开更多
关键词 脑损伤 认知障碍 胆碱O-乙酰转移酶 神经细胞黏附分子类
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1800MHz电磁波出生前暴露对大鼠海马NCAM表达的影响 被引量:2
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作者 木云珍 张嫒 +3 位作者 武慧欣 周浩 赵丽娟 吴锡南 《昆明医学院学报》 2011年第10期4-9,共6页
目的了解1 800 MHz电磁波出生前暴露对大鼠海马NCAM表达的影响.方法 7周龄SD雌性大鼠32只,雄性16只,适应环境1周后以雌:雄=2:1交配,受孕后雌鼠随机分为四组(两个实验组和两个对照组);实验组采用1 800 MHz射频电磁波对大鼠于孕0~20 d进... 目的了解1 800 MHz电磁波出生前暴露对大鼠海马NCAM表达的影响.方法 7周龄SD雌性大鼠32只,雄性16只,适应环境1周后以雌:雄=2:1交配,受孕后雌鼠随机分为四组(两个实验组和两个对照组);实验组采用1 800 MHz射频电磁波对大鼠于孕0~20 d进行21 d连续全身暴露,每天12 h,功率密度为0.5 mW/cm2和1.0 mW/cm2,各实验组分别设置虚拟暴露作为对照组.暴露期间的温度、湿度、背景噪声等环境条件稳定.暴露完成后在F1代子鼠长至3周龄和7周龄,每组随机抽取8只子鼠采用免疫组织化学方法分别对海马NCAM进行染色,然后采用图像分析系统分析海马CA1、CA3和DG区(齿状回)NCAM的表达.结果 1.0 mW/cm2暴露组未发现对3周龄、7周龄F1代大鼠海马各区NCAM表达有影响,其表达与对照组无统计学意义;0.5 mW/cm2暴露组3周龄F1代大鼠海马各区NCAM表达和对照组差异无统计学意义(P>0.05),0.5mW/cm2暴露组7周龄F1代大鼠海马各区NCAM表达出现了下调,其表达与对照组相比有统计学意义(P<0.05).结论 1 800 MHz功率密度0.5 mW/cm2电磁波出生前暴露使7周龄大鼠NCAM在海马各区表达下调. 展开更多
关键词 电磁波 出生前暴露 海马 神经细胞粘附分子
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周围神经端侧缝合后再生轴突PSA-NCAM的表达及对趋化性的影响 被引量:1
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作者 虞庆 蒋良福 +5 位作者 丁健 李志杰 王安远 陈一衡 李士 林康 《中国现代医生》 2015年第7期14-16,共3页
目的观察端侧缝合后再生轴突表面唾液酸-神经细胞黏附分子(polysialic acid-neural cell adhesion molecule,PSA-NCAM)分子的表达,及其对趋化性的影响。方法雌性清洁级SD大鼠24只,分4组,正常对照组、端侧缝合组、电刺激组和PSA拮抗剂组... 目的观察端侧缝合后再生轴突表面唾液酸-神经细胞黏附分子(polysialic acid-neural cell adhesion molecule,PSA-NCAM)分子的表达,及其对趋化性的影响。方法雌性清洁级SD大鼠24只,分4组,正常对照组、端侧缝合组、电刺激组和PSA拮抗剂组。3个月后进行电生理检测,免疫组化检测再生轴突PSA-NCAM表达,肌肉组织学检测,神经元逆行荧光示踪观察运动神经元比例。结果正常组不表达PSA-NCAM,电刺激组明显高于端侧组(P<0.05),拮抗剂组与端侧组无显著差异。端侧组运动神经元比例为16.54%,短暂电刺激后运动神经元比例上升至29.25%(P<0.05)。拮抗剂组运动神经元比例与端侧组无显著差异。结论端侧缝合再生的神经趋化性与再生轴突表面PSA-NCAM表达量相关,提高轴突PSA-NCAM的表达有助于改善再生神经的趋化性。 展开更多
关键词 周围神经 神经再生 端侧缝合 唾液酸-神经细胞黏附分子
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pHBAd-MCMV-GFP-NCAM1真核表达质粒的构建和鉴定 被引量:1
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作者 李永明 陈立强 +3 位作者 张东东 赵勇 李晓涛 李艳君 《解剖学研究》 CAS 2015年第1期22-25,共4页
目的将目的基因NCAM1与质粒载体p HBAd-MCMV-GFP进行连接,得到重组质粒p HBAd-MCMV-GFPNCAM1。方法对目的基因和质粒载体分别用内切酶Not I和Nsil进行双酶切,产物回收后进行连接、转化,得到重组质粒p HBAd-MCMV-GFP-NCAM1。转化后的菌... 目的将目的基因NCAM1与质粒载体p HBAd-MCMV-GFP进行连接,得到重组质粒p HBAd-MCMV-GFPNCAM1。方法对目的基因和质粒载体分别用内切酶Not I和Nsil进行双酶切,产物回收后进行连接、转化,得到重组质粒p HBAd-MCMV-GFP-NCAM1。转化后的菌液进行PCR阳性克隆鉴定,并对阳性样本进行测序。结果首先对NCAM1进行扩增,从实验结果看符合预期效果,在双酶切、连接和转化实验后,对构建完成的重组质粒进行鉴定,PCR阳性克隆鉴定结果显示重组质粒构建成功,NCAM1已连接进入重组质粒中,测序的结果进一步印证阳性鉴定结果。结论带有目的基因NCAM1的重组质粒构建成功。 展开更多
关键词 神经细胞黏附分子1 质粒载体 重组质粒
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儿童青少年精神分裂症与NCAM1基因的关联研究 被引量:1
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作者 陈星 唐剑 +5 位作者 刘金同 张燕 栾萌 周鹏 刘文敏 陈刚 《精神医学杂志》 2011年第2期81-85,共5页
目的对通过Affymetrix Genome-W ide SNP Array 6.0全基因组芯片扫描发现,国外曾经报道与精神分裂症关联的NCAM1基因在儿童青少年精神分裂症家系中进行验证。方法选择了100例儿童青少年发病的精神分裂症患者及其父母,通过5个NCAM1基因... 目的对通过Affymetrix Genome-W ide SNP Array 6.0全基因组芯片扫描发现,国外曾经报道与精神分裂症关联的NCAM1基因在儿童青少年精神分裂症家系中进行验证。方法选择了100例儿童青少年发病的精神分裂症患者及其父母,通过5个NCAM1基因内的单核甘酸多态性位点(rs10891495,rs1245133,rs1821693,rs686050,rs12794326)经高分辨率溶解曲线(H igh ResolutionMelting,HRM)进行基因分型后,用HaploV iew 4.1软件进行统计分析。结果未证实上述位点及所构建的单倍型与精神分裂症关联(P>0.05)。结论 (1)不支持NCAM1基因与精神分裂症病因关联;(2)Affymetrix6.0全基因组SNP芯片关联分析产生的假阳性结果可经家系连锁不平衡分析验证。 展开更多
关键词 精神分裂症神经细胞黏附分子1 基因 单核苷酸多态 关联分析
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TPO、CD56、Galectin-3辅助诊断甲状腺乳头状癌的价值分析
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作者 朱彦刘莹 马玉花 +3 位作者 刁兆杰 梁飞 何丽 任丽娟 《中国社区医师》 2024年第14期106-108,共3页
目的:分析甲状腺过氧化物酶(TPO)、神经细胞黏附分子56(CD56)和β-半乳糖凝集素-3(Galectin-3)辅助诊断甲状腺乳头状癌的价值。方法:选取2018年3月—2020年12月于克拉玛依市中心医院接受手术切除的PTC患者104例作为研究对象,分析患者PT... 目的:分析甲状腺过氧化物酶(TPO)、神经细胞黏附分子56(CD56)和β-半乳糖凝集素-3(Galectin-3)辅助诊断甲状腺乳头状癌的价值。方法:选取2018年3月—2020年12月于克拉玛依市中心医院接受手术切除的PTC患者104例作为研究对象,分析患者PTC癌变组织及距离癌灶>2 cm的癌旁组织TPO、CD56、Galectin-3表达情况,评估TPO、CD56、Galectin-3单项及联合检测辅助诊断PTC的效能。结果:TPO、CD56、Galectin-3单项及联合诊断PTC的特异度比较,差异无统计学意义(P>0.05);三项联合诊断PTC的准确度高于TPO、CD56,Galectin-3及TPO均高于CD56,差异有统计学意义(P<0.05);Galectin-3、三项联合诊断PTC的灵敏度高于TPO、CD56,TPO高于CD56,差异有统计学意义(P<0.05)。结论:TPO、CD56、Galectin-3三项联合检测可用于辅助诊断PTC。 展开更多
关键词 甲状腺乳头状癌 甲状腺过氧化物酶 神经细胞黏附分子56 β-半乳糖凝集素-3
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探索学习对局灶性脑梗死大鼠PSA-NCAM、nACHR表达的影响
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作者 张东 槐雅萍 +1 位作者 闫桂芳 贾子善 《中国康复医学杂志》 CAS CSCD 北大核心 2010年第2期123-126,共4页
目的:通过建立局灶性脑梗死大鼠模型,给予探索学习环境干预,观察探索学习环境对脑梗死大鼠海马齿状回区多唾液酸神经细胞黏附因子(polysialylated neural cell adhesion molecule,PSA-NCAM)、烟碱型乙酰胆碱受体(nicotinicacetylcholine... 目的:通过建立局灶性脑梗死大鼠模型,给予探索学习环境干预,观察探索学习环境对脑梗死大鼠海马齿状回区多唾液酸神经细胞黏附因子(polysialylated neural cell adhesion molecule,PSA-NCAM)、烟碱型乙酰胆碱受体(nicotinicacetylcholine receptor,nACHR)表达的影响,进一步阐明康复环境对神经系统损伤恢复的作用机制。方法:健康雄性SD大鼠120只,随机选取80只采用电凝右侧大脑中动脉法(MCAO)制造局灶性脑梗死模型,40只仅开颅不电凝大脑中动脉。手术组大鼠随机分为:社交组(n=40)、探索学习组(n=40),假手术组(n=40)。各组大鼠于术后第1天、3天、7天、14天、28天随机选取5只处死,利用免疫组化技术观察大鼠海马颗粒细胞层nACHR、PSA-NCAM表达情况。结果:MCAO术后第1天模型组较假手术组PSA-NCAM阳性细胞数明显增多(P<0.05),MCAO术后第14、28天探索学习组较社交组PSA-NCAM、nACHR阳性细胞数明显增多(P<0.05);MCAO术后第1天假手术组大鼠颗粒细胞层nACHR阳性细胞数明显多于手术组大鼠。结论:探索学习对于局灶性脑梗死大鼠海马齿状回区颗粒细胞层PSA-NCAM、nACHR表达均有促进作用。 展开更多
关键词 探索学习 脑梗死 记忆 多唾液酸神经细胞黏附因子 烟碱型乙酰胆碱受体
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