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| 1 | 脊髓神经干细胞的培养和鉴定显示文摘目的 研究脊髓源性神经干细胞的培养和体外分化情况 .方法 采用细胞培养技术结合间接免疫荧光细胞化学法 .结果 1在只有 EGF存在的情况下 ,没有干细胞团的生成 ;而在只有 b FGF存在的情况下 ,有少量干细胞团生成 ;在EGF和 b FGF同时存在时 ,有大量神经干细胞团生成 . 2体外存活时间越长 ,培养中的干细胞成分越多 ,分化后成分越少 . 3随诱导分化时间的加长 ,分化的细胞类型开始出现并增多 ,干细胞比率下降 .结论 脊髓神经干细胞的存活有赖于 EGF和 b FGF的共同作用 ,体外培养 4wk以上的细胞 ,所含的前体细胞的成分较少 。 | 孟晋宏 Udo Bartsch Melitta Schachner 鞠躬 | 2000 | 第四军医大学学报2000，21，8： | 20 |
| 2 | A Surgery Protocol for Adult Zebrafish Spinal Cord Injury显示文摘成年 zebrafish 有一个显著能力从针的绳索损害恢复,提供为学习 neuroregeneration 的一个优秀模型。这里,我们列出设备和试剂,并且为成年 zebrafish 的完全的横断给一个详细协议针的绳索。在这个协议,潜在的问题和他们的答案被描述以便 zebrafish 针的绳索损害模型能更容易并且 reproducibly 被执行。另外,二个评价被介绍监视外科和功能的恢复的成功:估计免费游泳能力的一测试和另外的测试到估计 neuroregeneration 的程度由在跟踪的 vivo anterograde axonal。在游泳行为测试,成功的完全的针的绳索横断被 zebrafish 的无能监视在针的绳索损害以后自由地游泳 1 个星期,在损害以后在 6 个星期以内由全部的运动能力的渐渐的获得列在后面。作为 morphometric 相互关联,跟踪的 anterograde axonal 允许调查者监视改革轴突的能力穿过损害地点并且逐渐地在损害以后与时间延续到灰色、白的事,证实功能的恢复。这个 zebrafish 模型从针的绳索损害为恢复提供一个范例,启用小径的鉴定和 neuroregeneration 的部件。 | Ping Fang Jin-Fei Lin Hong-Chao Pan Yan-Qin Shen Melitta Schachner | 2012 | Journal of Genetics and Genomics2012，39，9： | 7 |
| 3 | A mimetic peptide of α2,6-sialyllactose promotes neuritogenesis显示文摘Oxidative stress contributes to the pathogenesis of neurodegenerative diseases.With the aim to find reagents that reduce oxidative stress,a phage display library was screened for peptides mimicking a2,6-sialyllactose(6'-SL),which is known to beneficially influence neural functions.Using Sambucus nigra lectin,which specifically binds to 6'-SL,we screened a phage display library and found a peptide comprising identical sequences of 12 amino acids.Mimetic peptide,reverse peptide and scrambled peptide were tested for inhibition of 6'-SL binding to the lectin.Indeed,lectin binding to 6'-SL was inhibited by the most frequently identified mimetic peptide,but not by the reverse or scrambled peptides,showing that this peptide mimics 6'-SL.Functionally,mimetic peptide,but not the reverse or scrambled peptides,increased viability and expression of neural cell adhesion molecule L1 in SK-N-SH human neuroblastoma cells,and promoted survival and neurite outgrowth of cultured mouse cerebellar granule neurons challenged by H_20_2-induced oxidative stress.The combined results indicate that the 6'-SL mimetic peptide promotes neuronal survival and neuritogenesis,thus raising hopes for the treatment of neurodegenerative diseases.This study was approved by the Medical Ethics Committee of Shantou University Medical College,China(approval No.SUMC 2014-004)on February 20,2014. | Shuang-Xi Chen Jia-Hui He Yong-Jian Mi Hui-Fan Shen Melitta Schachner Wei-Jiang Zhao | 2020 | Neural Regeneration Research2020，15，6： | 2 |
| 4 | Neural recognition molecules of the immunoglobulin superfamily: signaling transducers of axon guidance and neuronal migration显示文摘 | Patricia F Maness Melitta Schachner | 2007 | Nat Neurosci2007，10，1： | 1 |
| 5 | L1 is a potential marker for poorly-differentiated pancreatic neuroendocrine carcinoma显示文摘瞄准:在胰腺的神经内分泌肿瘤决定 L1 的表示并且相关它与这个肿瘤的分类。方法:我们回顾地在原发性瘤或转移的石蜡节上由免疫组织化学在胰腺的神经内分泌肿瘤的 63 种情况中分析了 L1 表示。染色被过氧化物酶技术对人的 L1 与单音的同种细胞的抗体 UJ127.11 执行。所有肿瘤被分类根据分类同样区分得好的神经内分泌肿瘤和癌或糟糕区分的神经内分泌癌。结果:L1 在 5 被检测(7.9%) 63 个胰腺的神经内分泌肿瘤。(44.4%) 四 9 糟糕区分的癌表示了 L1。相反,仅仅(1.9%) 1 为 L1 54 个区分得好的肿瘤或癌是积极的。没有表示在正常胰腺的织物的 Langerhans 小岛房间被发现。生气桌子分析显示出在 L1 表示和胰(P<0.01 ) 的神经内分泌肿瘤的分类之间的一个重要协会。结论:L1 明确地在被知道有最糟的预后的糟糕区分的胰腺的神经内分泌癌被表示。L1 可能是为与胰腺的神经内分泌癌诊断的病人的风险预言的一个标记。 | Jussuf T Kaifi Ulrich Zinnkann Emre F Yekebas Paulus G Schurr Uta Reichelt Robin Wachowiak Henning C Fiegel Susann Petri Melitta Schachner Jakob RIzbicki | 2006 | World Journal of Gastroenterology2006，12，1： | 1 |
| 6 | Ethological analysis of the senescenceaccelerated P/8 mouse显示文摘 | Joerg Brandewiede Melitta Schachner Fabio Morellini | 2005 | Behav Brain Res2005，15，8： | 1 |
| 7 | Major vault protein promotes locomotor recovery and regeneration after spinal cord injury in adult zebrafish显示文摘 | Hong‐Chao Pan Jin‐Fei Lin Li‐Ping Ma Yan‐Qin Shen Melitta Schachner | 2012 | Eur J Neurosci2012，，2： | 1 |
| 8 | 朗飞结处神经突起生长抑制因子(英文)显示文摘朗飞结以及结侧区是有鞘轴突上的一些极化区域,越来越多的证据表明胶质细胞分泌的某些抑制中枢神经系统损伤后轴突再生过程中神经突起生长的分子如粘蛋白(tenascins)、硫酸软骨素蛋白聚糖(chondroitin sulphate pro-teoglycans)、髓鞘相关糖蛋白(myelin-associated glycopro-tein,MAG)、轴突生长抑制因子(Nogo)以及少突胶质细胞髓鞘糖蛋白(OMGP)等非常特异性的富集于朗飞结区域。这些分子在体外组织培养过程中显示出强烈的神经突起生长抑制作用。在一些基因无义突变的动物模型,能够观察到朗飞结处轴突的生长,表明这些抑制分子能够生理性地保持轴突的完整性并且阻止轴突间随机和错误的联结,然而,大部分的基因无义突变动物模型显示不出明显的中枢神经系统再生改善。这些被称为抑制因子的分子是否是神经再生失败的真正元凶这些抑制因子体内体外实验结果的不一致以及它们特异的定位分布让我们有理由对它们在其他生理作用和功能方面进行重新评价。考虑到轴突-胶质细胞相互作用的双向特性,本综述认为这些抑制因子不仅通过神经元上的受体信号通路调节轴突的极化、离子通道的功能以及轴突的分枝,另一方面轴突产生的化学分子也能反馈性的通过朗飞结区域寡突胶质细胞上的胶质细胞受体信号通路影响寡突胶质细胞的发育。 | Du-Yu Nie Qi-Dong Hu Quan-Hong Ma Melitta Schachner Zhi-Cheng Xiao | 2008 | 神经疾病与精神卫生2008，8，1： | 1 |
| 9 | Neuregulin 1 Enhances Cell Adhesion Molecule L1 Expression in Human Glioma Cells and Promotes Their Migration as a Function of Malignancy显示文摘 | Wei-Jiang Zhao Melitta Schachner | 2013 | Journal of Neuropathology & Experimental Neurology2013，，3： | 1 |
| 10 | Differences in the regenerative response of neuronal cell populations and indications for plasticity in intraspinal neurons after spinal cord transection in adult zebrafish显示文摘 | Thomas Becker Bettina C. Lieberoth Catherina G. Becker Melitta Schachner | 2005 | Molecular and Cellular Neuroscience2005，，： | 1 |
| 11 | Prion protein as trans-interacting partner for neurons is involved in neurite outgrowth and neuronal survival显示文摘 | Suzhen Chen Alain Mangé Ling Dong Sylvain Lehmann Melitta Schachner | 2003 | Molecular and Cellular Neuroscience2003，，2： | 1 |
| 12 | HMGB1 in Development and Diseases of the Central Nervous System显示文摘 | Ping Fang Melitta Schachner Yan-Qin Shen | 2012 | Molecular Neurobiology2012，，3： | 1 |
| 13 | Mice lacking perforin have improved regeneration of the injured femoral nerve显示文摘The role that the immune system plays after injury of the peripheral nervous system is still not completely understood.Perforin,a natural killer cell-and T-lymphocyte-derived enzyme that mediates cytotoxicity,plays important roles in autoimmune diseases,infections and central nervous system trauma,such as spinal cord injury.To dissect the roles of this single component of the immune response to injury,we tested regeneration after femoral nerve injury in perforin-deficient(Pfp^(-/-))and wild-type control mice.Single frame motion analysis showed better motor recovery in Pfp^(-/-)mice compared with control mice at 4 and 8 weeks after injury.Retrograde tracing of the motoneuron axons regrown into the motor nerve branch demonstrated more correctly projecting motoneurons in the spinal cord of Pfp^(-/-)mice compared with wild-types.Myelination of regrown axons measured by g-ratio was more extensive in Pfp^(-/-)than in wild-type mice in the motor branch of the femoral nerve.Pfp^(-/-)mice displayed more cholinergic synaptic terminals around cell bodies of spinal motoneurons after injury than the injured wild-types.We histologically analyzed lymphocyte infiltration 10 days after surgery and found that in Pfp^(-/-)mice the number of lymphocytes in the regenerating nerves was lower than in wild-types,suggesting a closed blood-nerve barrier in Pfp^(-/-)mice.We conclude that perforin restricts motor recovery after femoral nerve injury owing to decreased survival of motoneurons and reduced myelination. | Igor Jakovčevski Monika von Düring David Lutz Maja Vulović Mohammad Hamad Gebhard Reiss Eckart Förster Melitta Schachner | 2022 | Neural Regeneration Research2022，17，8： | 0 |
| 14 | Induction of clusterin Expression by Neuronal Cell Death in Zebrafish显示文摘Clusterin,a protein associated with multiple functions,is expressed in a wide variety of mammalian tissues.Although clusterin is known to be involved in neurodegenerative diseases,ageing,and tumorigenesis,a detailed analysis of the consequences of gain- or loss-offunction approaches has yet to be performed to understand the underlying mechanisms of clusterin functions.Since clusterin levels change in neurological diseases,it is likely that clusterin contributes to cell death and degeneration in general.Zebrafish was investigated as a model system to study human diseases.During development,zebrafish clusterin was expressed in the notochord and nervous system.Embryonic overexpression of clusterin by mRNA microinjection did not affect axis formation,whereas its knock-down by anti-sense morpholino treatment resulted in neuronal cell death.To analyze the function of clusterin in neurodegeneration,a transgenic zebrafish was investigated,in which nitroreductase expression is regulated under the control of a neuron-specific huC promoter which is active between the stages of early neuronal precursors and mature neurons.Nitroreductase turns metronidazole into a cytotoxic agent that induces cell death within 12 h.After metronidazole treatment,transgenic zebrafish showed neuron-specific cell death.Interestingly,we also observed a dramatic induction of clusterin expression in the brain and spinal cord in these fish,suggesting a direct or indirect role of clusterin in neuronal cell death and thus,more generally,in neurodegeneration. | Yun-Mi Jeong Tae-Eun Jin Jung-Hwa Choi Mi-Sun Lee Hyun-Taek Kim Kyu-Seok Hwang Doo-Sang Park Hyun-Woo Oh Joong-Kook Choi Vladimir Korzh Melitta Schachner Kwan-Hee You Cheol-Hee Kim | 2014 | Journal of Genetics and Genomics2014，41，11： | 0 |
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