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    30 April 2016, Volume 11 Issue 4 Previous Issue    Next Issue
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    A novel technique using hydrophilic polymers to promote axonal fusion
    Ravinder Bamba, D. Colton Riley, Nathaniel D. Kelm, Mark D. Does, Richard D. Dortch, Wesley P. Thayer
    2016, 11 (4):  525-528.  doi: 10.4103/1673-5374.180724
    Abstract ( 212 )   PDF (1141KB) ( 554 )   Save

    The management of traumatic peripheral nerve injury remains a considerable concern for clinicians. With
    minimal innovations in surgical technique and a limited number of specialists trained to treat peripheral
    nerve injury, outcomes of surgical intervention have been unpredictable. The inability to manipulate the
    pathophysiology of nerve injury (i.e., Wallerian degeneration) has left scientists and clinicians depending
    on the slow and lengthy process of axonal regeneration (~1 mm/day). When axons are severed, the endings
    undergo calcium-mediated plasmalemmal sealing, which limits the ability of the axon to be primarily repaired.
    Polythethylene glycol (PEG) in combination with a bioengineered process overcomes the inability
    to fuse axons. The mechanism for PEG axonal fusion is not clearly understood, but multiple studies have
    shown that a providing a calcium-free environment is essential to the process known as PEG fusion. The
    proposed mechanism is PEG-induced lipid bilayer fusion by removing the hydration barrier surrounding
    the axolemma and reducing the activation energy required for membrane fusion to occur. This review
    highlights PEG fusion, its past and current studies, and future directions in PEG fusion.

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    Examining the properties and therapeutic potential of glial restricted precursors in spinal cord injury
    Kazuo Hayakawa, Christopher Haas, Itzhak Fischer
    2016, 11 (4):  529-533.  doi: 10.4103/1673-5374.180725
    Abstract ( 225 )   PDF (473KB) ( 775 )   Save

    In the aftermath of spinal cord injury, glial restricted precursors (GRPs) and immature astrocytes offer the
    potential to modulate the inflammatory environment of the injured spinal cord and promote host axon regeneration.
    Nevertheless clinical application of cellular therapy for the repair of spinal cord injury requires
    strict quality-assured protocols for large-scale production and preservation that necessitates long-term
    in vitro expansion. Importantly, such processes have the potential to alter the phenotypic and functional
    properties and thus therapeutic potential of these cells. Furthermore, clinical use of cellular therapies may
    be limited by the inflammatory microenvironment of the injured spinal cord, altering the phenotypic and
    functional properties of grafted cells. This report simulates the process of large-scale GRP production and
    demonstrates the permissive properties of GRP following long-term in vitro culture. Furthermore, we defined
    the phenotypic and functional properties of GRP in the presence of inflammatory factors, and call
    attention to the importance of the microenvironment of grafted cells, underscoring the importance of
    modulating the environment of the injured spinal cord.

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    The choroid plexus-cerebrospinal fluid interface in Alzheimer’s disease: more than just a barrier
    Sriram Balusu, Marjana Brkic, Claude Libert, Roosmarijn E. Vandenbroucke
    2016, 11 (4):  534-537.  doi: 10.4103/1673-5374.180372
    Abstract ( 369 )   PDF (519KB) ( 544 )   Save

    The choroid plexus is a complex structure which hangs inside the ventricles of the brain and consists
    mainly of choroid plexus epithelial (CPE) cells surrounding fenestrated capillaries. These CPE cells not
    only form an anatomical barrier, called the blood-cerebrospinal fluid barrier (BCSFB), but also present an
    active interface between blood and cerebrospinal fluid (CSF). CPE cells perform indispensable functions
    for the development, maintenance and functioning of the brain. Indeed, the primary role of the choroid
    plexus in the brain is to maintain homeostasis by secreting CSF which contains different molecules, such as
    nutrients, neurotrophins, and growth factors, as well as by clearing toxic and undesirable molecules from
    CSF. The choroid plexus also acts as a selective entry gate for leukocytes into the brain. Recent findings have
    revealed distinct changes in CPE cells that are associated with aging and Alzheimer’s disease. In this review,
    we review some recent findings that highlight the importance of the CPE-CSF system in Alzheimer’s disease
    and we summarize the recent advances in the regeneration of brain tissue through use of CPE cells as a
    new therapeutic strategy.

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    Repositioning again of zonisamide for nerve regeneration
    Kinji Ohno, Hideki Yagi, Bisei Ohkawara
    2016, 11 (4):  541-542.  doi: 10.4103/1673-5374.180727
    Abstract ( 559 )   PDF (316KB) ( 900 )   Save
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    Local translation of cell adhesion molecules in axons
    Shruti Jain, Kristy Welshhans
    2016, 11 (4):  543-544.  doi: 10.4103/1673-5374.180728
    Abstract ( 315 )   PDF (269KB) ( 563 )   Save
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    Counteraction of Nogo-A and axonal growth inhibitors by green tea polyphenols and other natural products
    Tiffany K. Fan, Usha Gundimeda, William J. Mack, Rayudu Gopalakrishna
    2016, 11 (4):  545-546.  doi: 10.4103/1673-5374.180729
    Abstract ( 239 )   PDF (392KB) ( 610 )   Save
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    Role of pleiotrophin-protein tyrosine phosphatase receptor type Z signaling in myelination
    Akihiro Fujikawa, Masaharu Noda
    2016, 11 (4):  549-551.  doi: 10.4103/1673-5374.180761
    Abstract ( 269 )   PDF (668KB) ( 736 )   Save
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    Toll-like receptor-4 antagonism mediates benefits during neuroinflammation
    Sagar Gaikwad, Challagundla Naveen, Reena Agrawal-Rajput
    2016, 11 (4):  552-553.  doi: 10.4103/1673-5374.180732
    Abstract ( 264 )   PDF (347KB) ( 766 )   Save
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    Laser therapy on points of acupuncture on nerve repair
    Renata F. de Oliveira, Patrícia M. de Freitas
    2016, 11 (4):  557-558.  doi: 10.4103/1673-5374.180734
    Abstract ( 318 )   PDF (163KB) ( 890 )   Save
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    Prevention and protection against cerebral ischemic injury using acupuncture
    Philip V. Peplow, Bridget Martinez
    2016, 11 (4):  559-560.  doi: 10.4103/1673-5374.180735
    Abstract ( 196 )   PDF (252KB) ( 715 )   Save
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    Exploring a need for improved preclinical models of post-stroke depression
    Nitish Mittal, Patricia D. Hurn, Timothy Schallert
    2016, 11 (4):  561-562.  doi: 10.4103/1673-5374.180736
    Abstract ( 204 )   PDF (251KB) ( 546 )   Save
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    Neuroprotective effect of antioxidant compounds
    Rachid Skouta
    2016, 11 (4):  566-567.  doi: 10.4103/1673-5374.180738
    Abstract ( 261 )   PDF (172KB) ( 716 )   Save
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    Autologous bone marrow mononuclear cells as neuroprotective treatment of amyotrophic lateral sclerosis
    Francisco José Ruiz-López, Miguel Blanquer
    2016, 11 (4):  568-569.  doi: 10.4103/1673-5374.180730
    Abstract ( 204 )   PDF (278KB) ( 790 )   Save
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    Paracrine factors for neurodegenerative disorders: special emphasis on Parkinson’s disease
    Stefano Di Santo, Hans Rudolf Widmer
    2016, 11 (4):  570-571.  doi: 10.4103/1673-5374.180739
    Abstract ( 223 )   PDF (550KB) ( 495 )   Save
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    Cell proliferation and apoptosis in optic nerve and brain integration centers of adult trout Oncorhynchus mykiss after optic nerve injury
    Evgeniya V. Pushchina, Sachin Shukla, Anatoly A. Varaksin, Dmitry K. Obukhov
    2016, 11 (4):  578-590.  doi: 10.4103/1673-5374.180742
    Abstract ( 243 )   PDF (3028KB) ( 833 )   Save

    Fishes have remarkable ability to effectively rebuild the structure of nerve cells and nerve fibers after central
    nervous system injury. However, the underlying mechanism is poorly understood. In order to address this
    issue, we investigated the proliferation and apoptosis of cells in contralateral and ipsilateral optic nerves,
    after stab wound injury to the eye of an adult trout Oncorhynchus mykiss. Heterogenous population of
    proliferating cells was investigated at 1 week after injury. TUNEL labeling gave a qualitative and quantitative
    assessment of apoptosis in the cells of optic nerve of trout 2 days after injury. After optic nerve injury,
    apoptotic response was investigated, and mass patterns of cell migration were found. The maximal concentration
    of apoptotic bodies was detected in the areas of mass clumps of cells. It is probably indicative of
    massive cell death in the area of high phagocytic activity of macrophages/microglia. At 1 week after optic
    nerve injury, we observed nerve cell proliferation in the trout brain integration centers: the cerebellum and
    the optic tectum. In the optic tectum, proliferating cell nuclear antigen (PCNA)-immunopositive radial
    glia-like cells were identified. Proliferative activity of nerve cells was detected in the dorsal proliferative
    (matrix) area of the cerebellum and in parenchymal cells of the molecular and granular layers whereas local
    clusters of undifferentiated cells which formed neurogenic niches were observed in both the optic tectum
    and cerebellum after optic nerve injury. In vitro analysis of brain cells of trout showed that suspension cells
    compared with monolayer cells retain higher proliferative activity, as evidenced by PCNA immunolabeling.
    Phase contrast observation showed mitosis in individual cells and the formation of neurospheres which
    gradually increased during 1–4 days of culture. The present findings suggest that trout can be used as a
    novel model for studying neuronal regeneration.

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    Nerve growth factor promotes in vitro proliferation of neural stem cells from tree shrews
    Liu-lin Xiong, Zhi-wei Chen, Ting-hua Wang
    2016, 11 (4):  591-596.  doi: 10.4103/1673-5374.180743
    Abstract ( 191 )   PDF (1241KB) ( 823 )   Save

    Neural stem cells promote neuronal regeneration and repair of brain tissue after injury, but have limited resources and proliferative ability
    in vivo. We hypothesized that nerve growth factor would promote in vitro proliferation of neural stem cells derived from the tree shrews, a
    primate-like mammal that has been proposed as an alternative to primates in biomedical translational research. We cultured neural stem
    cells from the hippocampus of tree shrews at embryonic day 38, and added nerve growth factor (100 μg/L) to the culture medium. Neural
    stem cells from the hippocampus of tree shrews cultured without nerve growth factor were used as controls. After 3 days, fluorescence microscopy
    after DAPI and nestin staining revealed that the number of neurospheres and DAPI/nestin-positive cells was markedly greater in
    the nerve growth factor-treated cells than in control cells. These findings demonstrate that nerve growth factor promotes the proliferation
    of neural stem cells derived from tree shrews.

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    Denervated hippocampus provides a favorable microenvironment for neuronal differentiation of endogenous neural stem cells
    Lei Zhang, Xiao Han, Xiang Cheng, Xue-feng Tan, He-yan Zhao, Xin-hua Zhang
    2016, 11 (4):  597-603.  doi: 10.4103/1673-5374.180744
    Abstract ( 245 )   PDF (843KB) ( 796 )   Save

    Fimbria-fornix transection induces both exogenous and endogenous neural stem cells to differentiate into neurons in the hippocampus.
    This indicates that the denervated hippocampus provides an environment for neuronal differentiation of neural stem cells. However, the
    pathways and mechanisms in this process are still unclear. Seven days after fimbria fornix transection, our reverse transcription polymerase
    chain reaction, western blot assay, and enzyme linked immunosorbent assay results show a significant increase in ciliary neurotrophic
    factor mRNA and protein expression in the denervated hippocampus. Moreover, neural stem cells derived from hippocampi of fetal (embryonic
    day 17) Sprague-Dawley rats were treated with ciliary neurotrophic factor for 7 days, with an increased number of microtubule
    associated protein-2-positive cells and decreased number of glial fibrillary acidic protein-positive cells detected. Our results show that ciliary
    neurotrophic factor expression is up-regulated in the denervated hippocampus, which may promote neuronal differentiation of neural
    stem cells in the denervated hippocampus.

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    Electroacupuncture at Baihui (DU20) acupoint up-regulates mRNA expression of NeuroD molecules in the brains of newborn rats suffering in utero fetal distress
    Lu Chen, Yan Liu, Qiao-mei Lin, Lan Xue, Wei Wang, Jian-wen Xu
    2016, 11 (4):  604-609.  doi: 10.4103/1673-5374.180745
    Abstract ( 283 )   PDF (743KB) ( 699 )   Save

    NeuroD plays a key regulatory effect on differentiation of neural stem cells into mature neurons in the brain. Thus, we assumed that
    electroacupuncture at Baihui (DU20) acupoint in newborn rats exposed to in utero fetal distress would influence expression of NeuroD.
    Electroacupuncture at Baihui was performed for 20 minutes on 3-day-old (Day 3) newborn Sprague-Dawley rats exposed to in utero fetal
    distress; electroacupuncture parameters consisted of sparse and dense waves at a frequency of 2–10 Hz. Real-time fluorescent quantitative
    PCR results demonstrated that mRNA expression of NeuroD, a molecule that indicates NeuroD, increased with prolonged time in brains
    of newborn rats, and peaked on Day 22. The level of mRNA expression was similar between Day 16 and Day 35. These findings suggest that
    electro acupuncture at Baihui acupoint could effectively increase mRNA expression of molecules involved in NeuroD in the brains of newborn
    rats exposed to in utero fetal distress.

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    Moxibustion upregulates hippocampal progranulin expression
    Tao Yi, Li Qi, Ji Li, Jing-jing Le Lei Shao, Xin Du, Jing-cheng Dong
    2016, 11 (4):  610-616.  doi: 10.4103/1673-5374.180746
    Abstract ( 362 )   PDF (696KB) ( 858 )   Save

    In China, moxibustion is reported to be useful and has few side effects for chronic fatigue syndrome, but its mechanisms are largely unknown.
    More recently, the focus has been on the wealth of information supporting stress as a factor in chronic fatigue syndrome, and
    largely concerns dysregulation in the stress-related hypothalamic-pituitary-adrenal axis. In the present study, we aimed to determine the
    effect of moxibustion on behavioral symptoms in chronic fatigue syndrome rats and examine possible mechanisms. Rats were subjected to
    a combination of chronic restraint stress and forced swimming to induce chronic fatigue syndrome. The acupoints Guanyuan (CV4) and
    Zusanli (ST36, bilateral) were simultaneously administered moxibustion. Untreated chronic fatigue syndrome rats and normal rats were
    used as controls. Results from the forced swimming test, open field test, tail suspension test, real-time PCR, enzyme-linked immunosorbent
    assay, and western blot assay showed that moxibustion treatment decreased mRNA expression of corticotropin-releasing hormone in
    the hypothalamus, and adrenocorticotropic hormone and corticosterone levels in plasma, and markedly increased progranulin mRNA and
    protein expression in the hippocampus. These findings suggest that moxibustion may relieve the behavioral symptoms of chronic fatigue
    syndrome, at least in part, by modulating the hypothalamic-pituitary-adrenal axis and upregulating hippocampal progranulin.

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    Non-viral liposome-mediated transfer of brain-derived neurotrophic factor across the blood-brain barrier
    Ying Xing, Chun-yan Wen, Song-tao Li, Zong-xin Xia
    2016, 11 (4):  617-622.  doi: 10.4103/1673-5374.180747
    Abstract ( 280 )   PDF (1861KB) ( 804 )   Save

    Brain-derived neurotrophic factor (BDNF) plays an important role in the repair of central nervous system injury, but cannot directly traverse
    the blood-brain barrier. Liposomes are a new type of non-viral vector, able to carry macromolecules across the blood-brain barrier
    and into the brain. Here, we investigate whether BDNF could be transported across the blood-brain barrier by tail-vein injection of liposomes
    conjugated to transferrin (Tf) and polyethylene glycol (PEG), and carrying BDNF modified with cytomegalovirus promoter (pCMV)
    or glial fibrillary acidic protein promoter (pGFAP) (Tf-pCMV-BDNF-PEG and Tf-pGFAP-BDNF-PEG, respectively). Both liposomes were
    able to traverse the blood-brain barrier, and BDNF was mainly expressed in the cerebral cortex. BDNF expression in the cerebral cortex was
    higher in the Tf-pGFAP-BDNF-PEG group than in the Tf-pCMV-BDNF-PEG group. This study demonstrates the successful construction
    of a non-virus targeted liposome, Tf-pGFAP-BDNF-PEG, which crosses the blood-brain barrier and is distributed in the cerebral cortex.
    Our work provides an experimental basis for BDNF-related targeted drug delivery in the brain.

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    Neuroprotective effect of Cerebralcare Granule after cerebral ischemia/reperfusion injury
    Xiao-xiao Zhang, Fen-fen He, Gui-lin Yan, Ha-ni Li, Dan Li, Yan-ling Ma, Fang Wang, Nan Xu, Fei Cao
    2016, 11 (4):  623-629.  doi: 10.4103/1673-5374.180748
    Abstract ( 385 )   PDF (1480KB) ( 696 )   Save

    Cerebralcare Granule (CG) improves cerebral microcirculation and relieves vasospasm, but studies investigating its therapeutic effect on
    cerebral ischemia/reperfusion injury are lacking. In the present study, we administered CG (0.3, 0.1 and 0.03 g/mL intragastrically) to rats
    for 7 consecutive days. We then performed transient occlusion of the middle cerebral artery, followed by reperfusion, and administered CG
    daily for a further 3 or 7 days. Compared with no treatment, high-dose CG markedly improved neurological function assessed using the
    Bederson and Garcia scales. At 3 days, animals in the high-dose CG group had smaller infarct volumes, greater interleukin-10 expression,
    and fewer interleukin-1β-immunoreactive cells than those in the untreated model group. Furthermore, at 7 days, high-dose CG-treated
    rats had more vascular endothelial growth factor-immunoreactive cells, elevated angiopoietin-1 and vascular endothelial growth factor expression,
    and improved blood coagulation and flow indices compared with untreated model animals. These results suggest that CG exerts
    specific neuroprotective effects against cerebral ischemia/reperfusion injury.

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    A mouse model of weight-drop closed head injury: emphasis on cognitive and neurological deficiency
    Igor Khalin, Nor Laili Azua Jamari, Nadiawati Bt Abdul Razak, Zubaidah Bt Hasain, Mohd Asri bin Mohd Nor, Mohd Hakimi bin Ahmad Zainudin, Ainsah Bt Oma1, Renad Alyautdin
    2016, 11 (4):  630-635.  doi: 10.4103/1673-5374.180749
    Abstract ( 405 )   PDF (932KB) ( 800 )   Save

    Traumatic brain injury (TBI) is a leading cause of death and disability in individuals worldwide. Producing
    a clinically relevant TBI model in small-sized animals remains fairly challenging. For good screening
    of potential therapeutics, which are effective in the treatment of TBI, animal models of TBI should be
    established and standardized. In this study, we established mouse models of closed head injury using the
    Shohami weight-drop method with some modifications concerning cognitive deficiency assessment and
    provided a detailed description of the severe TBI animal model. We found that 250 g falling weight from
    2 cm height produced severe closed head injury in C57BL/6 male mice. Cognitive disorders in mice with
    severe closed head injury could be detected using passive avoidance test on day 7 after injury. Findings
    from this study indicate that weight-drop injury animal models are suitable for further screening of brain
    neuroprotectants and potentially are similar to those seen in human TBI.

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    Anti-inflammatory properties of lipoxin A4 protect against diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury
    Jiang-quan Han, Cheng-ling Liu, Zheng-yuan Wang, Ling Liu, Ling Cheng, Ya-dan Fan
    2016, 11 (4):  636-640.  doi: 10.4103/1673-5374.180750
    Abstract ( 328 )   PDF (626KB) ( 777 )   Save

    Lipoxin A4 can alleviate cerebral ischemia/reperfusion injury by reducing the inflammatory reaction, but it is currently unclear whether
    it has a protective effect on diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury. In this study, we established rat
    models of diabetes mellitus using an intraperitoneal injection of streptozotocin. We then induced focal cerebral ischemia/reperfusion
    injury by occlusion of the middle cerebral artery for 2 hours and reperfusion for 24 hours. After administration of lipoxin A4 via the lateral
    ventricle, infarction volume was reduced, the expression levels of pro-inflammatory factors tumor necrosis factor alpha and nuclear factor-
    kappa B in the cerebral cortex were decreased, and neurological functioning was improved. These findings suggest that lipoxin A4 has
    strong neuroprotective effects in diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury and that the underlying mechanism
    is related to the anti-inflammatory action of lipoxin A4.

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    Ischemic postconditioning protects against ischemic brain injury by up-regulation of acid-sensing ion channel 2a
    Wang-sheng Duanmu, Liu Cao, Jing-yu Chen, Hong-fei Ge, Rong Hu, Hua Feng
    2016, 11 (4):  641-645.  doi: 10.4103/1673-5374.180751
    Abstract ( 331 )   PDF (621KB) ( 544 )   Save

    Ischemic postconditioning renders brain tissue tolerant to brain ischemia, thereby alleviating ischemic brain injury. However, the exact
    mechanism of action is still unclear. In this study, a rat model of global brain ischemia was subjected to ischemic postconditioning treatment
    using the vessel occlusion method. After 2 hours of ischemia, the bilateral common carotid arteries were blocked immediately for
    10 seconds and then perfused for 10 seconds. This procedure was repeated six times. Ischemic postconditioning was found to mitigate
    hippocampal CA1 neuronal damage in rats with brain ischemia, and up-regulate acid-sensing ion channel 2a expression at the mRNA and
    protein level. These findings suggest that ischemic postconditioning up-regulates acid-sensing ion channel 2a expression in the rat hippocampus
    after global brain ischemia, which promotes neuronal tolerance to ischemic brain injury.

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    A cascade model of information processing and encoding for retinal prosthesis
    Zhi-jun Pei, Guan-xin Gao, Bo Hao, Qing-li Qiao, Hui-jian Ai
    2016, 11 (4):  646-651.  doi: 10.4103/1673-5374.180752
    Abstract ( 433 )   PDF (1721KB) ( 652 )   Save

    Retinal prosthesis offers a potential treatment for individuals suffering from photoreceptor degeneration diseases. Establishing biological
    retinal models and simulating how the biological retina convert incoming light signal into spike trains that can be properly decoded by
    the brain is a key issue. Some retinal models have been presented, ranking from structural models inspired by the layered architecture
    to functional models originated from a set of specific physiological phenomena. However, Most of these focus on stimulus image compression,
    edge detection and reconstruction, but do not generate spike trains corresponding to visual image. In this study, based on stateof-
    the-art retinal physiological mechanism, including effective visual information extraction, static nonlinear rectification of biological
    systems and neurons Poisson coding, a cascade model of the retina including the out plexiform layer for information processing and the
    inner plexiform layer for information encoding was brought forward, which integrates both anatomic connections and functional computations
    of retina. Using MATLAB software, spike trains corresponding to stimulus image were numerically computed by four steps:
    linear spatiotemporal filtering, static nonlinear rectification, radial sampling and then Poisson spike generation. The simulated results
    suggested that such a cascade model could recreate visual information processing and encoding functionalities of the retina, which is
    helpful in developing artificial retina for the retinally blind.

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    Human umbilical cord blood-derived stem cells and brain-derived neurotrophic factor protect injured optic nerve: viscoelasticity characterization
    Xue-man Lv, Yan Liu, Fei Wu, Yi Yuan, Min Luo
    2016, 11 (4):  652-656.  doi: 10.4103/1673-5374.180753
    Abstract ( 278 )   PDF (1186KB) ( 775 )   Save

    The optic nerve is a viscoelastic solid-like biomaterial. Its normal stress relaxation and creep properties enable the nerve to resist constant
    strain and protect it from injury. We hypothesized that stress relaxation and creep properties of the optic nerve change after injury. Moreover,
    human brain-derived neurotrophic factor or umbilical cord blood-derived stem cells may restore these changes to normal. To validate
    this hypothesis, a rabbit model of optic nerve injury was established using a clamp approach. At 7 days after injury, the vitreous body received
    a one-time injection of 50 μg human brain-derived neurotrophic factor or 1 × 106 human umbilical cord blood-derived stem cells.
    At 30 days after injury, stress relaxation and creep properties of the optic nerve that received treatment had recovered greatly, with pathological
    changes in the injured optic nerve also noticeably improved. These results suggest that human brain-derived neurotrophic factor or
    umbilical cord blood-derived stem cell intervention promotes viscoelasticity recovery of injured optic nerves, and thereby contributes to
    nerve recovery.

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    Senegenin inhibits neuronal apoptosis after spinal cord contusion injury
    Shu-quan Zhang, Min-fei Wu, Rui Gu, Jia-bei Liu, Ye Li, Qing-san Zhu, Jin-lan Jiang
    2016, 11 (4):  657-663.  doi: 10.4103/1673-5374.180754
    Abstract ( 308 )   PDF (876KB) ( 723 )   Save

    Senegenin has been shown to inhibit neuronal apoptosis, thereby exerting a neuroprotective effect. In the present study, we established a rat
    model of spinal cord contusion injury using the modified Allen’s method. Three hours after injury, senegenin (30 mg/g) was injected into
    the tail vein for 3 consecutive days. Senegenin reduced the size of syringomyelic cavities, and it substantially reduced the number of apoptotic
    cells in the spinal cord. At the site of injury, Bax and Caspase-3 mRNA and protein levels were decreased by senegenin, while Bcl-2
    mRNA and protein levels were increased. Nerve fiber density was increased in the spinal cord proximal to the brain, and hindlimb motor
    function and electrophysiological properties of rat hindlimb were improved. Taken together, our results suggest that senegenin exerts a
    neuroprotective effect by suppressing neuronal apoptosis at the site of spinal cord injury.

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    Combined use of Y-tube conduits with human umbilical cord stem cells for repairing nerve bifurcation defects
    Aikeremujiang•Muheremu, Jun-gang Sun, Xi-yuan Wang, Fei Zhang, Qiang Ao, Jiang Peng
    2016, 11 (4):  664-669.  doi: 10.4103/1673-5374.180755
    Abstract ( 322 )   PDF (1084KB) ( 552 )   Save

    Given the anatomic complexity at the bifurcation point of a nerve trunk, enforced suturing between stumps can lead to misdirection of
    nerve axons, thereby resulting in adverse consequences. We assumed that Y-tube conduits injected with human umbilical cord stem cells
    could be an effective method to solve such problems, but studies focused on the best type of Y-tube conduit remain controversial. Therefore,
    the present study evaluated the applicability and efficacy of various types of Y-tube conduits containing human umbilical cord stem
    cells for treating rat femoral nerve defects on their bifurcation points. At 12 weeks after the bridging surgery that included treatment with
    different types of Y-tube conduits, there were no differences in quadriceps femoris muscle weight or femoral nerve ultrastructure. However,
    the Y-tube conduit group with longer branches and a short trunk resulted in a better outcome according to retrograde labeling and electrophysiological
    analysis. It can be concluded from the study that repairing a mixed nerve defect at its bifurcation point with Y-tube conduits,
    in particular those with long branches and a short trunk, is effective and results in good outcomes.

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    Supplementary motor area deactivation impacts the recovery of hand function from severe peripheral nerve injury
    Ye-chen Lu, Han-qiu Liu, Xu-yun Hua, Yun-dong Shen, Wen-dong Xu, Jian-guang Xu, Yu-dong Gu
    2016, 11 (4):  670-675.  doi: 10.4103/1673-5374.180756
    Abstract ( 274 )   PDF (1164KB) ( 626 )   Save

    Although some patients have successful peripheral nerve regeneration, a poor recovery of hand function often occurs after peripheral
    nerve injury. It is believed that the capability of brain plasticity is crucial for the recovery of hand function. The supplementary motor area
    may play a key role in brain remodeling after peripheral nerve injury. In this study, we explored the activation mode of the supplementary
    motor area during a motor imagery task. We investigated the plasticity of the central nervous system after brachial plexus injury, using the
    motor imagery task. Results from functional magnetic resonance imaging showed that after brachial plexus injury, the motor imagery task
    for the affected limbs of the patients triggered no obvious activation of bilateral supplementary motor areas. This result indicates that it is
    difficult to excite the supplementary motor areas of brachial plexus injury patients during a motor imagery task, thereby impacting brain
    remodeling. Deactivation of the supplementary motor area is likely to be a serious problem for brachial plexus injury patients in terms of
    preparing, initiating and executing certain movements, which may be partly responsible for the unsatisfactory clinical recovery of hand
    function.

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    Electrical stimulation of dog pudendal nerve regulates the excitatory pudendal-to-bladder reflex
    Yan-he Ju, Li-min Liao
    2016, 11 (4):  676-681.  doi: 10.4103/1673-5374.180757
    Abstract ( 356 )   PDF (1741KB) ( 1207 )   Save

    Pudendal nerve plays an important role in urine storage and voiding. Our hypothesis is that a neuroprosthetic device placed in the pudendal
    nerve trunk can modulate bladder function after suprasacral spinal cord injury. We had confirmed the inhibitory pudendal-to-bladder
    reflex by stimulating either the branch or the trunk of the pudendal nerve. This study explored the excitatory pudendal-to-bladder reflex
    in beagle dogs, with intact or injured spinal cord, by electrical stimulation of the pudendal nerve trunk. The optimal stimulation frequency
    was approximately 15–25 Hz. This excitatory effect was dependent to some extent on the bladder volume. We conclude that stimulation of
    the pudendal nerve trunk is a promising method to modulate bladder function.

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    Complement components of nerve regeneration conditioned fluid influence the microenvironment of nerve regeneration
    Guang-shuai Li, Qing-feng Li, Ming-min Dong, Tao Zan, Shuang Ding, Lin-bo Liu
    2016, 11 (4):  682-686.  doi: 10.4103/1673-5374.180758
    Abstract ( 418 )   PDF (441KB) ( 590 )   Save

    Nerve regeneration conditioned fluid is secreted by nerve stumps inside a nerve regeneration chamber. A better understanding of the proteinogram
    of nerve regeneration conditioned fluid can provide evidence for studying the role of the microenvironment in peripheral nerve
    regeneration. In this study, we used cylindrical silicone tubes as the nerve regeneration chamber model for the repair of injured rat sciatic
    nerve. Isobaric tags for relative and absolute quantitation proteomics technology and western blot analysis confirmed that there were more
    than 10 complement components (complement factor I, C1q-A, C1q-B, C2, C3, C4, C5, C7, C8β and complement factor D) in the nerve
    regeneration conditioned fluid and each varied at different time points. These findings suggest that all these complement components have
    a functional role in nerve regeneration.

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