Role of the extracellular matrix in neural crest cell migration

Development of the neural crest involves a remarkable feat of coordinated cell migration in which cells detach from the neural tube, take varying routes of migration through the embryonic tissues and then differentiate at the end of their journey to participate in the formation of a number of organ systems. In general, neural crest cells appear to migrate without the guidance of long-range physical or chemical cues, but rather they respond to heterogeneity in the extracellular matrix that forms their migration substrate. Molecules such as fibronectin and laminin act as permissive substrate components, encouraging neural crest cell attachment and spreading, whereas chondroitin sulphate proteoglycans are nonpermissive for migration. A balance between permissive and nonpermissive substrate components seems to be necessary to ensure successful migration, as indicated by a number of studies in mouse mutant systems where nonpermissive molecules are over-expressed, leading to inhibition of neural crest migration. The neural crest expresses cell surface receptors that permit interaction with the extracellular matrix and may also modify the matrix by secretion of proteases. Thus the principles that govern the complex migration of neural crest cells are beginning to emerge.     

Human neural transplantation

Great advances in neurobiology have resulted from 100 years of neural transplantation research. In the last 20 years, there has been a focus on using neural transplantation to repair the damaged central nervous system (CNS) utilising experimental animal models of various human neurodegenerative disease and CNS injury. Since 1985, there has been a rapid proliferation of adrenal medullary autograft transplantation to the caudate nucleus of humans with Parkinson's disease. However, this operation proved to be unsuccessful and was associated with unacceptable morbidity. Implantation of human fetal mesencephalon into patients with severe parkinsonism has supplanted the adrenal operation and has produced promising results, with some patients reported to improve markedly and some evidence of graft survival noted on positron emission tomography (PET). Host tissue recovery appears to be an important mechanism for this clinical improvement. The optimal technique is to use three to four fetuses from induced abortions of 6.5 to 8 weeks gestation, with multiple stereotactic implants into the putamen and caudate nucleus. Many biological questions still remain and the community remains troubled by the ethical problems of using fetal tissue obtained from abortions. This procedure is still experimental and should be restricted to a few centres with excellence in cell and molecular biology. A multicentre study is needed to more carefully evaluate CNS transplantation. Cloned neural precursor cells or immortalized embryonic cell lines genetically modified to manufacture selected growth factors or neurotransmitters may offer an alternative to the use of human fetal tissue. Much more experimental animal research is necessary before transplantation can be used to treat other CNS maladies.     

Intraparenchymal fetal striatal transplants and recovery in kainic acid lesioned rats

Striatal kainic acid (KA) lesions induce behavioral and biochemical deficits which resemble symptoms encountered in patients suffering from Huntington's disease. In rats with KA lesions, fetal striatal transplants have shown to reverse the pervasive nocturnal hyperactivity induced by the lesion. In the present study 4.6 mm3 of fetal striatal tissue were delivered bilaterally into the anterodorsal portion of the lesioned caudate nucleus. Care was taken to deliver the transplant within the host parenchyma and away from the lateral ventricles. Locomotor behavior analyzed using the Digiscan animal activity monitors before and after the transplants demonstrated a reversal of the hyperactivity following transplants in 70% of lesioned animals. Microinjections of horseradish peroxidase delivered into the globus pallidus and substantia nigra of a small group of functionally recovered transplanted animals, did not reveal evidence for reinnervation between host nigra or pallidum and the transplant at 10 weeks post-transplantation. Other laboratories have reported anatomical connections by 6 months post-transplantation. Ventricular/brain ratios demonstrated that intraparenchymal transplants significantly reduced the ventricular dilation following KA lesion. These results suggest that functional recovery can be obtained when the transplant is immersed into the host's striatal parenchyma regardless of the existence of long-range anatomical connections.     

新生大鼠脊髓神经干细胞的分离培养及鉴定

目的　从新生大鼠的脊髓中分离培养神经干细胞并观察其增殖和分化能力。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　分离的细胞生长旺盛 ,单克隆化生成的细胞团 ,BrdU掺入呈强阳性。分离培养获得的细胞团呈Nestin强阳性 ,至今已在体外连续传代 8个月。培养的细胞团经 1%小牛血清诱导可分化为神经元和星形胶质细胞。结论　成功分离培养了新生大鼠脊髓神经干细胞     

噪声中EP信号的提取算法及研究进展

诱发电位的提取是脑电信号处理领域的前沿课题近年来 ,通过少次甚至单次试验提取诱发电位已经成为研究的主流。本文对近年来提取诱发电位的信号处理方法进行了简要的回顾 ,并分别从小波变换、神经网络、高阶累积量、独立分量分析等四个方面对算法进行了介绍     

神经干细胞的端粒酶活性与其增殖分化的关系

目的探讨体外培养的神经干细胞端粒酶活性与细胞增殖、分化的关系,以及细胞分化后端粒酶逆转录酶的表达情况。方法采用无血清培养法从新生大鼠脑皮质分离培养神经干细胞；通过免疫荧光细胞染色鉴定神经干细胞；细胞计数法检测细胞的增殖情况；TRAP-ELISA法测定神经干细胞的端粒酶活性：RT-PCR法和Western-blot法测定细胞分化前后的端粒酶逆转录酶的表达。结果从新生大鼠脑皮质分离培养的神经干细胞具有端粒酶活性；体外培养12周内,神经干细胞的端粒酶活性未见变化,细胞的增殖速率亦未见明显不同；神经干细胞分化后端粒酶活性丧失,端粒酶逆转录酶的mRNA和蛋白质也均未见表达。结论在体外培养过程中,大鼠脑神经干细胞的端粒酶活性和细胞增殖速率未见变化；神经干细胞分化后端粒酶活性丧失,可能是由于端粒酶逆转录酶停止表达所致。     

人胚脑与脊髓神经干细胞体外生物学特性的差异

目的:探讨人胚脑源性神经干细胞和脊髓源性神经干细胞的体外培养和分化的差异。方法:从人胚脑组织和脊髓组织中分离培养神经干细胞,分为EGF组、bFGF组、EGF±bFGF组,在连续传代过程中观察并比较神经干细胞体外培养特性的差异:用血清诱导神经干细胞分化,观察其分化状况的不同。结果:从人胚脑组织分离的细胞在bFGF 单独存在时无法形成神经球,在EGF或EGF±bFGF存在时形成大量具有连续增殖能力的神经球;从人胚脊髓组织分离的细胞在EGF单独存在时无法形成神经球,在bFGF单独存在时只形成少量神经球,在EGF±bFGF存在时形成大量具有连续增殖能力的神经球。同样在EGF±bFGF存在的情况下,脑源性于细胞的增殖速度较快。经血清诱导后,脑组织来源的干细胞分化为NSE阳性细胞数明显多于脊髓组织来源的干细胞,二者之间的差异具有显著性(P<0．05)。结论:脑源性和脊髓源性神经干细胞在生长和分化方面有明显差别:脑源性神经干细胞可在bFGF或EGF士bFGF存在的情况下长期传代,而脊髓源性神经干细胞只能在EGF±bFGF存在的情况下长期传代,脑源性干细胞的增殖能力明显高于脊髓源性干细胞;脑源性干细胞较脊髓源性干细胞更易分化为神经元。     

室管膜细胞在大鼠脊髓损伤后的反应性增生

目的旨在探讨成年大鼠脊髓损伤后室管膜细胞的增殖反应,为进一步促进脊髓损伤后自身修复提供理论依据。方法应用动脉瘤夹压迫建立大鼠脊髓压迫损伤模型,通过组织病理学及免疫组织化学方法检测不同时段室管膜细胞的反应性增生和神经外胚层多潜能细胞特异性抗原巢蛋白(nestin)的表达。结果常规病理学检查显示损伤模型类似于临床常见的脊髓横贯伤,损伤后24h可以观察到室管膜细胞nestin表达明显升高,增殖细胞核抗原(PCNA)呈阳性;1周后见室管膜细胞显著增生;nestin的表达随时间进展呈向下调节。结论静止的室管膜细胞有潜在的增殖能力,在脊髓损伤后表现出明显的分裂增生,可能在结构和功能重塑过程中起作用。     

神经网络分析方法用于心脏病诊断的研究

神经网络可以很好的拟合任意的非线性函数。我们从 QRS波群的高频三维频谱中提取出一些定量的特征参数 ,用神经网络的方法对这些参数进行有监督的学习训练 ,最终能在由这些特征参数张成的 m维空间中构建出一个 m维的曲面来区分病人和健康人的 QRS波群高频三维频谱 ,从而使得训练后的网络能基于 QRS波群的高频三维频谱自行诊断出病人和健康人     

人胚神经干细胞的体外培养及鉴定

目的 探讨人胚神经干细胞的体外培养和诱导分化的条件。方法 从药物流产的12周到16周的人胚胎海马组织中分离神经干细胞，在EGF、bFGF和LIF联合作用下使其稳定增殖，并用10％的胎牛血清诱导其贴壁分化，应用免疫荧光染色方法行Nestin、NSE、MAP-2、GFAP和GalC免疫荧光染色，对神经干细胞及其分化的细胞进行鉴定。结果 体外培养的神经干细胞增殖成神经干细胞球并传代，鉴定为Nestin染色阳性细胞，并可诱导分化为神经细胞、星形胶质细胞和少突胶质细胞。结论 利用无血清培养技术和特定生长因子，可培养出在体外稳定增殖并有多向分化潜能的人胚神经干细胞。