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    05 June 2013, Volume 8 Issue 16 Previous Issue    Next Issue
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    How does the motor relearning program improve neurological function of brain ischemia monkeys?
    Yong Yin, Zhen Gu, Lei Pan, Lu Gan, Dongdong Qin, Bo Yang, Jin Guo, Xintian Hu, Tinghua Wang, Zhongtang Feng
    2013, 8 (16):  1445-1454.  doi: 10.3969/j.issn.1673-5374.2013.16.001
    Abstract ( 289 )   PDF (214KB) ( 965 )   Save

    The motor relearning program can significantly improve various functional disturbance induced by ischemic cerebrovascular diseases. However, its mechanism of action remains poorly understood. In injured brain tissues, glial fibrillary acidic protein and neurofilament protein changes can reflect the condition of injured neurons and astrocytes, while vascular endothelial growth factor and basic fibroblast growth factor changes can indicate angiogenesis. In the present study, we induced ischemic brain injury in the rhesus macaque by electrocoagulation of the M1 segment of the right middle cerebral artery. The motor relearning program was conducted for 60 days from the third day after model establishment. Immunohistochemistry and single-photon emission CT showed that the numbers of glial fibrillary acidic protein-, neurofilament protein-, vascular endothelial growth factor- and basic fibroblast growth factor-positive cells were significantly increased in the infarcted side compared with the contralateral hemisphere following the motor relearning program. Moreover, cerebral blood flow in the infarcted side was significantly improved. The clinical rating scale for stroke was used to assess neurological function changes in the rhesus macaque following the motor relearning program. Results showed that motor function was improved, and problems with consciousness, self-care ability and balance function were significantly ameliorated. These findings indicate that the motor relearning program significantly promoted neuronal regeneration, repair and angiogenesis in the surroundings of the infarcted hemisphere, and improve neurological function in the rhesus macaque following brain ischemia.

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    Novel nanometer scaffolds regulate the biological behaviors of neural stem cells
    Jihui Zhou, Fuge Sui, Meng Yao, Yansong Wang, Yugang Liu, Feipeng Tian, Qiang Li, Xiaofeng He, Lin Shao, Zhiqiang Liu
    2013, 8 (16):  1455-1464.  doi: 10.3969/j.issn.1673-5374.2013.16.002
    Abstract ( 286 )   PDF (317KB) ( 1135 )   Save

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    Role of Toll-like receptor 4 in inflammatory reactions of hippocampal neurons
    Yae Hu, Jiahui Mao, Yu Zhang, Ailing Zhou
    2013, 8 (16):  1465-1472.  doi: 10.3969/j.issn.1673-5374.2013.16.003
    Abstract ( 205 )   PDF (273KB) ( 870 )   Save

    Lipopolysaccharide stimulates Toll-like receptor 4 on immune cells to produce immune mediators. Toll-like receptor 4 is also expressed by non-immune cells, which can be stimulated by lipopolysaccharide. However, whether Toll-like receptor 4 is expressed by primary cultured hippocampal neurons and its specific role in lipopolysaccharide-induced neuroinflammation is currently undefined. In this study, Toll-like receptor 4 antibody blocking was used to analyze the Toll-like receptor 4 signaling pathway and changes in inflammation of lipopolysaccharide stimulated hippocampal neurons. Immunofluorescence showed that Toll-like receptor 4 protein was mainly located in the membrane of hippocampal neurons. Quantitative reverse transcription-PCR and western blot assay showed that after stimulation of lipopolysaccharide, the mRNA and protein levels of Toll-like receptor 4 and the mRNA levels of interleukin-1β and tumor necrosis factor-α were significantly increased. In addition, there was increased phosphorylation and degradation of kappa B α inhibitor in the cytosol and increased nuclear factor-κB p65 expression in the nuclei. Pretreatment with Toll-like receptor 4 antibody could almost completely block this increase. These experimental findings indicate that lipopolysaccharide participates in neuroinflammation by stimulating Toll-like receptor 4/nuclear factor-κB pathway in hippocampal neurons, which may be both “passive victims” and “activators” of neuroinflammation.

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    Application of sodium alginate microspheres in ischemic stroke modeling in miniature pigs
    Yongchun Cui, Yi Tian1, Yue Tang, Liujun Jia, Aili Wu, Peng Peng, Jianzhong Yang, Hong Du, Xiaojuan Wang, Like Wu
    2013, 8 (16):  1473-1480.  doi: 10.3969/j.issn.1673-5374.2013.16.004
    Abstract ( 272 )   PDF (299KB) ( 831 )   Save

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    Diffusion tensor imaging fiber tracking with reliable tracking orientation and flexible step size
    Xufeng Yao, Manning Wang, Xinrong Chen, Shengdong Nie, Zhexu Li, Xiaoping Xu, Xuelong Zhang, Zhijian Song
    2013, 8 (16):  1481-1490.  doi: 10.3969/j.issn.1673-5374.2013.16.005
    Abstract ( 277 )   PDF (474KB) ( 908 )   Save

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    JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury
    Jiang Long, Li Cai, Jintao Li, Lei Zhang, Haiyang Yang, Tinghua Wang
    2013, 8 (16):  1491-1499.  doi: 10.3969/j.issn.2095-4344.2012.33.027
    Abstract ( 173 )   PDF (211KB) ( 1017 )   Save

    Increasing evidence has revealed that the activation of the JNK pathway participates in apoptosis of nerve cells and neurological function recovery after traumatic brain injury. However, which genes in the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in cell apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1, 3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.

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    Artifact suppression and analysis of brain activities with electroencephalography signals
    Md. Rashed-Al-Mahfuz, Md. Rabiul Islam, Keikichi Hirose, Md. Khademul Islam Molla
    2013, 8 (16):  1500-1513.  doi: 10.3969/j.issn.1673-5374.2013.16.007
    Abstract ( 185 )   PDF (2777KB) ( 911 )   Save

    Brain-computer interface is a communication system that connects the brain with computer (or other devices) but is not dependent on the normal output of the brain (i.e., peripheral nerve and muscle). Electro-oculogram is a dominant artifact which has a significant negative influence on further analysis of real electroencephalography data. This paper presented a data adaptive technique for artifact suppression and brain wave extraction from electroencephalography signals to detect regional brain activities. Empirical mode decomposition based adaptive thresholding approach was employed here to suppress the electro-oculogram artifact. Fractional Gaussian noise was used to determine the threshold level derived from the analysis data without any training. The purified electroencephalography signal was composed of the brain waves also called rhythmic components which represent the brain activities. The rhythmic components were extracted from each electroencephalography channel using adaptive wiener filter with the original scale. The regional brain activities were mapped on the basis of the spatial distribution of rhythmic components, and the results showed that different regions of the brain are activated in response to different stimuli. This research analyzed the activities of a single rhythmic component, alpha with respect to different motor imaginations. The experimental results showed that the proposed method is very efficient in artifact suppression and identifying individual motor imagery based on the activities of alpha component.

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    Delayed gait recovery in a stroke patient
    Jeong Pyo Seo, Mi Young Lee, Yong Hyun Kwon, Sung Ho Jang
    2013, 8 (16):  1514-1518.  doi: 10.3969/j.issn.1673-5374.2013.16.008
    Abstract ( 228 )   PDF (234KB) ( 1012 )   Save

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    Delayed gait recovery in a stroke patient
    Danheng Mo, Hongwei Xu, Wensheng Zhou, Qiming Yang, Jianwen Yang, Bo Xiao, Qidong Yang
    2013, 8 (16):  1519-1527. 
    Abstract ( 189 )   PDF (198KB) ( 1007 )   Save

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    Evaluation of vitamin D level in patients from neurosurgical intensive care unit
    Ho Jun Yi, Je Hoon Jeong, Eun-Sun Jin, Il Young Shin, Hyung Sik Hwang, Seung-Myung Moon
    2013, 8 (16):  1528-1534.  doi: 10.3969/j.issn.1673-5374.2013.16.010
    Abstract ( 172 )   PDF (417KB) ( 893 )   Save

    Vitamin D plays an important role in maintaining normal bone metabolism. Recent studies have suggested that vitamin D influences many other physiological processes, including muscle function, cardiovascular homeostasis, nerve function, and immune response. Furthermore, accumulated evidence suggests that vitamin D also mediates the immune system response to infection. Critical neurosurgical patients have higher infection and mortality rates. To correlate vitamin D deficiency to the immunological status of neurosurgical intensive care unit patients, we detected serum vitamin D level in 15 patients with clinically suspected infection and 10 patients with confirmed infection. Serum level of 25-hydroxyvitamin D, the primary circulating form of vitamin D, was significantly decreased in patients with confirmed infection after a 2-week neurosurgical intensive care unit hospitalization, while serum level of 1,25-dihydroxyvitamin D, the active form of vitamin D, was significantly decreased in patients after a 4-week neurosurgical intensive care unit hospitalization. Levels of both 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were in the deficient state after 7 and 14 days in the neurosurgical intensive care unit, respectively, in patients with clinically suspected infection. These findings suggest that vitamin D deficiency is linked to the immunological status of neurosurgical intensive care unit patients and vitamin D supplementation can improve patient’s immunological status.

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