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    15 April 2013, Volume 8 Issue 11 Previous Issue    Next Issue
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    Chondroitinase ABC plus bone marrow mesenchymal stem cells for repair of spinal cord injury
    Chun Zhang, Xijing He, Haopeng Li, Guoyu Wang
    2013, 8 (11):  965-974.  doi: 10.3969/j.issn.1673-5374.2013.11.001
    Abstract ( 178 )   PDF (347KB) ( 844 )   Save

    As chondroitinase ABC can improve the hostile microenvironment and cell transplantation is proven to be effective after spinal cord injury, we hypothesized that their combination would be a more effective treatment option. At 5 days after T8 spinal cord crush injury, rats were injected with bone marrow mesenchymal stem cell suspension or chondroitinase ABC 1 mm from the edge of spinal cord damage zone. Chondroitinase ABC was first injected, and bone marrow mesenchymal stem cell suspension was injected on the next day in the combination group. At 14 days, the mean Basso, Beattie and Bresnahan score of the rats in the combination group was higher than other groups. Hematoxylin-eosin staining showed that the necrotic area was significantly reduced in the combination group compared with other groups. Glial fibrillary acidic protein-chondroitin sulfate proteoglycan double staining showed that the damage zone of astrocytic scars was significantly reduced without the cavity in the combination group. Glial fibrillary acidic protein/growth associated protein-43 double immunostaining revealed that positive fibers traversed the damage zone in the combination group. These results suggest that the combination of chondroitinase ABC and bone marrow mesenchymal stem cell transplantation contributes to the repair of spinal cord injury.

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    Chondroitinase ABC plus bone marrow mesenchymal stem cells for repair of spinal cord injury
    Murat Karaman, Arzu Tuncel, Shahrouz Sheidaei, Mehmet Güney Şenol, Murat Hakan Karabulut, Ildem Deveci, Nihan Karaman
    2013, 8 (11):  975-982.  doi: 10.3969/j.issn.1673-5374.2013.11.002
    Abstract ( 205 )   PDF (348KB) ( 953 )   Save

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    Extracts from rabbit skin inflamed by the vaccinia virus attenuate bupivacaine-induced spinal neurotoxicity in pregnant rats
    Rui Cui, Shiyuan Xu, Liang Wang, Hongyi Lei, Qingxiang Cai, Hongfei Zhang, Dongmei Wang
    2013, 8 (11):  983-990.  doi: 10.3969/j.issn.1673-5374.2013.11.003
    Abstract ( 229 )   PDF (249KB) ( 1522 )   Save

    Extracts from rabbit skin inflamed by the vaccinia virus can relieve pain and promote repair of nerve injury. The present study intraperitoneally injected extracts from rabbit skin inflamed by the vaccinia virus for 3 and 4 days prior to and following intrathecal injection of bupivacaine into pregnant rats. The pain threshold test after bupivacaine injection showed that the maximum possible effect of tail-flick latency peaked 1 day after intrathecal injection of bupivacaine in the extract-pretreatment group, and gradually decreased, while the maximum possible effect in the bupivacaine group continued to increase after intrathecal injection of bupivacaine. Histological observation showed that after 4 days of intrathecal injection of bupivacaine, the number of shrunken, vacuolated, apoptotic and caspase-9-positive cells in the dorsal root ganglion in the extract-pretreatment group was significantly reduced compared with the bupivacaine group. These findings indicate that extracts from rabbit skin inflamed by the vaccinia virus can attenuate neurotoxicity induced by intrathecal injection of bupivacaine in pregnant rats, possibly by inhibiting caspase-9 protein expression and suppressing nerve cell apoptosis.

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    Divalent cation tolerance protein binds to β-secretase and inhibits the processing of amyloid precursor protein
    Runzhong Liu, Haibo Hou, Xuelian Yi, Shanwen Wu, Huan Zeng
    2013, 8 (11):  991-999.  doi: 10.3969/j.issn.1673-5374.2013.11.004
    Abstract ( 215 )   PDF (264KB) ( 733 )   Save

    The deposition of amyloid-beta is a pathological hallmark of Alzheimer’s disease. Amyloid-beta is derived from amyloid precursor protein through sequential proteolytic cleavages by β-secretase (beta-site amyloid precursor protein-cleaving enzyme 1) and γ-secretase. To further elucidate the roles of beta-site amyloid precursor protein-cleaving enzyme 1 in the development of Alzheimer’s disease, a yeast two-hybrid system was used to screen a human embryonic brain cDNA library for proteins directly interacting with the intracellular domain of beta-site amyloid precursor protein-cleaving enzyme 1. A potential beta-site amyloid precursor protein-cleaving enzyme 1- interacting protein identified from the positive clones was divalent cation tolerance protein. Immunoprecipitation studies in the neuroblastoma cell line N2a showed that exogenous divalent cation tolerance protein interacts with endogenous beta-site amyloid precursor protein-cleaving enzyme 1. The overexpression of divalent cation tolerance protein did not affect beta-site amyloid precursor protein-cleaving enzyme 1 protein levels, but led to increased amyloid precursor protein levels in N2a/APP695 cells, with a concomitant reduction in the processing product amyloid precursor protein C-terminal fragment, indicating that divalent cation tolerance protein inhibits the processing of amyloid precursor protein. Our experimental findings suggest that divalent cation tolerance protein negatively regulates the function of beta-site amyloid precursor protein-cleaving enzyme 1. Thus, divalent cation tolerance protein could play a protective role in Alzheimer’s disease.

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    Diazoxide preconditioning antagonizes cytotoxicity induced by epileptic seizures
    Qingxi Fu, Zhiqing Sun, Jinling Zhang, Naiyong Gao, Faying Qi, Fengyuan Che, Guozhao Ma
    2013, 8 (11):  1000-1006.  doi: 10.3969/j.issn.1673-5374.2013.11.005
    Abstract ( 184 )   PDF (197KB) ( 872 )   Save

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    Wall shear stress in intracranial aneurysms and adjacent arteries
    Fuyu Wang, Bainan Xu, Zhenghui Sun, Chen Wu, Xiaojun Zhang
    2013, 8 (11):  1007-1015.  doi: 10.3969/j.issn.1673-5374.2013.11.006
    Abstract ( 186 )   PDF (276KB) ( 684 )   Save

    Hemodynamic parameters play an important role in aneurysm formation and growth. However, it is difficult to directly observe a rapidly growing de novo aneurysm in a patient. To investigate possible associations between hemodynamic parameters and the formation and growth of intracranial aneurysms, the present study constructed a computational model of a case with an internal carotid artery aneurysm and an anterior communicating artery aneurysm, based on the CT angiography findings of a patient. To simulate the formation of the anterior communicating artery aneurysm and the growth of the internal carotid artery aneurysm, we then constructed a model that virtually removed the anterior communicating artery aneurysm, and a further two models that also progressively decreased the size of the internal carotid artery aneurysm. Computational simulations of the fluid dynamics of the four models were performed under pulsatile flow conditions, and wall shear stress was compared among the different models. In the three aneurysm growth models, increasing size of the aneurysm was associated with an increased area of low wall shear stress, a significant decrease in wall shear stress at the dome of the aneurysm, and a significant change in the wall shear stress of the parent artery. The wall shear stress of the anterior communicating artery remained low, and was significantly lower than the wall shear stress at the bifurcation of the internal carotid artery or the bifurcation of the middle cerebral artery. After formation of the anterior communicating artery aneurysm, the wall shear stress at the dome of the internal carotid artery aneurysm increased significantly, and the wall shear stress in the upstream arteries also changed significantly. These findings indicate that low wall shear stress may be associated with the initiation and growth of aneurysms, and that aneurysm formation and growth may influence hemodynamic parameters in the local and adjacent arteries.

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    Activin A prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation
    Guihua Xu, Jinting He, Hongliang Guo, Chunli Mei, Jiaoqi Wang, Zhongshu Li, Han Chen, Jing Mang, Hong Yang, Zhongxin Xu
    2013, 8 (11):  1016-1024.  doi: 10.3969/j.issn.1673-5374.2013.11.007
    Abstract ( 190 )   PDF (180KB) ( 889 )   Save

    In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth factor, and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous Activin A. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous Activin A significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in Activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the Activin A/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous Activin A plays an anti-apoptotic role and protects neurons by means of activating the Activin A/Smads signaling pathway.

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    Adolescent social isolation influences cognitive function in adult rats
    Feng Shao, Xiao Han, Shuang Shao, Weiwen Wang
    2013, 8 (11):  1025-1030.  doi: 10.3969/j.issn.1673-5374.2013.11.008
    Abstract ( 192 )   PDF (105KB) ( 785 )   Save

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    Construction of a eukaryotic expression plasmid for human retina-derived neurotrophin-3
    Chunxia Peng, Xiaobei Yin, Mengda Li, Ting He, Genlin Li
    2013, 8 (11):  1031-1040.  doi: 10.3969/j.issn.1673-5374.2013.11.009
    Abstract ( 156 )   PDF (586KB) ( 950 )   Save

    Neurotrophin-3 (NT-3) can promote the repair of central nervous system and retinal damage. In previous reports, NT-3 has been expressed by viral vectors. However, plasmid vectors have a safer profile compared with viral vectors in clinical studies. This study recombined amplified human retinal NT-3 with a eukaryotic expression plasmid containing green fluorescent protein (GFP) to construct an NT-3 expression plasmid, pEGFP-N1-NT-3. The transfection efficiency 48 hours after pEGFP-N1-NT-3 transfection to 293T cells was 50.06 ± 2.78%. Abundant NT-3-GFP was expressed in 293T cells as observed by fluorescence microscopy, suggesting the construct pEGFP-N1-NT-3 effectively expressed and secreted NT-3-GFP. Secretory vesicles containing NT-3-GFP were observed in a constant location in cells by laser scan confocal microscopy, indicating the expression and secretion processes of NT-3 in eukaryotic cells were in accordance with the physical synthesis processes of secreted proteins. Western blot assay showed that pro-NT-3-GFP had a molecular weight of 56 kDa, further confirming NT-3-GFP expression. At 48 hours after transfection, the concentration of NT-3 in culture medium was 22.3 ng/mL, suggesting NT-3 produced by pEGFP-N1-NT-3 was efficiently secreted. This study constructed a human retinal-derived NT-3 eukaryotic expression plasmid that efficiently expressed and secreted NT-3.

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    Changes in nerve microcirculation following peripheral nerve compression
    Yueming Gao, Changshui Weng, Xinglin Wang
    2013, 8 (11):  1041-1047.  doi: 10.3969/j.issn.1673-5374.2013.11.010
    Abstract ( 235 )   PDF (103KB) ( 1087 )   Save

    Following peripheral nerve compression, peripheral nerve microcirculation plays important roles in regulating the nerve microenvironment and neurotrophic substances, supplying blood and oxygen and maintaining neural conduction and axonal transport. This paper has retrospectively analyzed the articles published in the past 10 years that addressed the relationship between peripheral nerve compression and changes in intraneural microcirculation. In addition, we describe changes in different peripheral nerves, with the aim of providing help for further studies in peripheral nerve microcirculation and understanding its protective mechanism, and exploring new clinical methods for treating peripheral nerve compression from the perspective of neural microcirculation.

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    Is transcranial direct current stimulation a potential method for improving response inhibition?
    Yong Hyun Kwon, Jung Won Kwon
    2013, 8 (11):  1048-1054.  doi: 10.3969/j.issn.1673-5374.2013.11.011
    Abstract ( 192 )   PDF (107KB) ( 829 )   Save

    Inhibitory control of movement in motor learning requires the ability to suppress an inappropriate action, a skill needed to stop a planned or ongoing motor response in response to changes in a variety of environments. This study used a stop-signal task to determine whether transcranial direct-current stimulation over the pre-supplementary motor area alters the reaction time in motor inhibition. Forty healthy subjects were recruited for this study and were randomly assigned to either the transcranial direct-current stimulation condition or a sham-transcranial direct-current stimulation condition. All subjects consecutively performed the stop-signal task before, during, and after the delivery of anodal transcranial direct-current stimulation over the pre-supplementary motor area (pre-transcranial direct-current stimulation phase, transcranial direct-current stimulation phase, and post-transcranial direct-current stimulation phase). Compared to the sham condition, there were significant reductions in the stop-signal processing times during and after transcranial direct-current stimulation, and change times were significantly greater in the transcranial direct-current stimulation condition. There was no significant change in go processing-times during or after transcranial direct-current stimulation in either condition. Anodal transcranial direct-current stimulation was feasibly coupled to an interactive improvement in inhibitory control. This coupling led to a decrease in the stop-signal process time required for the appropriate responses between motor execution and inhibition. However, there was no transcranial direct-current stimulation effect on the no-signal reaction time during the stop-signal task. Transcranial direct-current stimulation can adjust certain behaviors, and it could be a useful clinical intervention for patients who have difficulties with response inhibition.

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