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15 May 2015, Volume 10 Issue 5 Previous Issue    Next Issue

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Active zone stability: insights from fly neuromuscular junction Xiaolin Tian, Chunlai Wu 2015, 10 (5):  677-678.  doi: 10.4103/1673-5374.156942 Abstract ( 290 )   PDF (220KB) ( 897 )   Save The presynaptic active zone is a dynamic structure that orchestrates regulated release of neurotransmitters. Developmental and aging processes, and changes in neuronal network activity can all modulate the number, size and composition of active zone and thereby synaptic efficacy. However, very little is known about the mechanism that controls the structural stability of active zone. By studying a model synapse, the Drosophila neuromuscular junction, our recent work shed light on how two scaffolding proteins at the active zone regulate active zone stability by promoting a localized dephosphorylation event at the nerve terminal. Here we discuss the major insights from our findings and their implications for future research. Related Articles | Metrics

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Restoring nervous system structure and function using tissue engineered living scaffolds Laura A. Struzyna, James P. Harris, Kritika S. Katiyar, H. Isaac Chen, D. Kacy Cullen 2015, 10 (5):  679-685.  doi: 10.4103/1673-5374.156943 Abstract ( 206 )   PDF (1151KB) ( 949 )   Save Neural tissue engineering is premised on the integration of engineered living tissue with the host nervous system to directly restore lost function or to augment regenerative capacity following nervous system injury or neurodegenerative disease. Disconnection of axon pathways – the long-distance fibers connecting specialized regions of the central nervous system or relaying peripheral signals – is a common feature of many neurological disorders and injury. However, functional axonal regeneration rarely occurs due to extreme distances to targets, absence of directed guidance, and the presence of inhibitory factors in the central nervous system, resulting in devastating effects on cognitive and sensorimotor function. To address this need, we are pursuing multiple strategies using tissue engineered “living scaffolds”, which are preformed three-dimensional constructs consisting of living neural cells in a defined, often anisotropic architecture. Living scaffolds are designed to restore function by serving as a living labeled pathway for targeted axonal regeneration – mimicking key developmental mechanisms– or by restoring lost neural circuitry via direct replacement of neurons and axonal tracts. We are currently utilizing preformed living scaffolds consisting of neuronal clusters spanned by long axonal tracts as regenerative bridges to facilitate long-distance axonal regeneration and for targeted neurosurgical reconstruction of local circuits in the brain. Although there are formidable challenges in preclinical and clinical advancement, these living tissue engineered constructs represent a promising strategy to facilitate nervous system repair and functional recovery. Related Articles | Metrics

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Lesson from the neuromuscular junction: role of pattern and timing of nerve activity in synaptic development Morgana Favero, Alberto Cangiano, Giuseppe Busetto 2015, 10 (5):  686-688.  doi: 10.4103/1673-5374.156944 Abstract ( 207 )   PDF (844KB) ( 618 )   Save Related Articles | Metrics

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Synthetic and nature-derived lipid nanoparticles for neural regeneration Yuji S. Takeda, Qiaobing Xu 2015, 10 (5):  689-690.  doi: 10.4103/1673-5374.156946 Abstract ( 177 )   PDF (131KB) ( 752 )   Save Related Articles | Metrics

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Homeostatic regulation of brain functions by endocannabinoid signaling Chu Chen 2015, 10 (5):  691-692.  doi: 10.4103/1673-5374.156947 Abstract ( 223 )   PDF (351KB) ( 665 )   Save Related Articles | Metrics

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Staining neurons with Golgi techniques in degenerative diseases of the brain Stavros J. Baloyannis 2015, 10 (5):  693-695.  doi: 10.4103/1673-5374.156950 Abstract ( 373 )   PDF (634KB) ( 603 )   Save Related Articles | Metrics

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The brain compensatory mechanisms and Alzheimer’s disease progression: a new protective strategy Natalia Bobkova, Vasily Vorobyov 2015, 10 (5):  696-697.  doi: 10.4103/1673-5374.156954 Abstract ( 320 )   PDF (150KB) ( 697 )   Save Related Articles | Metrics

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The therapeutic potential of mesenchymal stem cells in Alzheimer’s disease: converging mechanisms Gadi Turgeman 2015, 10 (5):  698-699.  doi: 10.4103/1673-5374.156953 Abstract ( 193 )   PDF (509KB) ( 536 )   Save Related Articles | Metrics

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Enhanced neuronal degradation of amyloid-β oligomers allows synapse regeneration Clive Bate 2015, 10 (5):  700-701.  doi: 10.4103/1673-5374.156955 Abstract ( 231 )   PDF (197KB) ( 592 )   Save Related Articles | Metrics

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Evaluating rehabilitation interventions in Parkinson’s disease with functional MRI: a promising neuroprotective strategy Carlo Augusto Mallio, Bruno Beomonte Zobel, Carlo Cosimo Quattrocchi 2015, 10 (5):  702-703.  doi: 10.4103/1673-5374.156957 Abstract ( 188 )   PDF (143KB) ( 661 )   Save Related Articles | Metrics

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The innate immune system in Parkinson’s disease: a novel target promoting endogenous neuroregeneration Johannes CM Schlachetzki, Jürgen Winkler 2015, 10 (5):  704-706.  doi: 10.4103/1673-5374.156958 Abstract ( 279 )   PDF (339KB) ( 610 )   Save Related Articles | Metrics

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New insights on the standardization of peripheral nerve regeneration quantitative analysis Giulia Ronchi, Stefania Raimondo, Stefano Geuna, Giovanna Gambarotta 2015, 10 (5):  707-709.  doi: 10.4103/1673-5374.156962 Abstract ( 225 )   PDF (565KB) ( 855 )   Save Related Articles | Metrics

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Auditory nerve preservation and regeneration in man: relevance for cochlear implantation Helge Rask-Andersen, Wei Liu 2015, 10 (5):  710-712.  doi: 10.4103/1673-5374.156963 Abstract ( 412 )   PDF (644KB) ( 731 )   Save Related Articles | Metrics

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Dynamic expression of ATF3 as a novel tool to study activation and migration of endogenous spinal stem cells and their role in neural repair Miranda Mladinic, Andrea Nistri 2015, 10 (5):  713-714.  doi: 10.4103/1673-5374.156961 Abstract ( 269 )   PDF (301KB) ( 591 )   Save Related Articles | Metrics

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Aromatic L-amino acid decarboxylase cells in the spinal cord: a potential origin of monoamines Mengliang Zhang 2015, 10 (5):  715-717.  doi: 10.4103/1673-5374.156960 Abstract ( 195 )   PDF (617KB) ( 663 )   Save Related Articles | Metrics

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Can training extend current guidelines for cochlear implant candidacy? Amal Isaiah, Douglas E.H. Hartley 2015, 10 (5):  718-720.  doi: 10.4103/1673-5374.156964 Abstract ( 182 )   PDF (376KB) ( 622 )   Save Related Articles | Metrics

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The p75 neurotrophin receptor: at the crossroad of neural repair and death Rick B. Meeker, Kimberly S. Williams 2015, 10 (5):  721-725.  doi: 10.4103/1673-5374.156967 Abstract ( 376 )   PDF (524KB) ( 676 )   Save The strong repair and pro-survival functions of neurotrophins at their primary receptors, TrkA, TrkB and TrkC, have made them attractive candidates for treatment of nervous system injury and disease. However, difficulties with the clinical implementation of neurotrophin therapies have prompted the search for treatments that are stable, easier to deliver and allow more precise regulation of neurotrophin actions. Recently, the p75 neurotrophin receptor (p75NTR) has emerged as a potential target for pharmacological control of neurotrophin activity, supported in part by studies demonstrating 1) regulation of neural plasticity in the mature nervous system, 2) promotion of adult neurogenesis and 3) increased expression in neurons, macrophages, microglia, astrocytes and/or Schwann cells in response to injury and neurodegenerative diseases. Although the receptor has no intrinsic catalytic activity it interacts with and modulates the function of TrkA, TrkB, and TrkC, as well as sortilin and the Nogo receptor. This provides substantial cellular and molecular diversity for regulation of neuron survival, neurogenesis, immune responses and processes that support neural function. Upregulation of the p75NTR under pathological conditions places the receptor in a key position to control numerous processes necessary for nervous system recovery. Support for this possibility has come from recent studies showing that small, non-peptide p75NTR ligands can selectively modify pro-survival and repair functions. While a great deal remains to be discovered about the wide ranging functions of the p75NTR, studies summarized in this review highlight the immense potential for development of novel neuroprotective and neurorestorative therapies.  Related Articles | Metrics

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Advances in regenerative therapies for spinal cord injury: a biomaterials approach Magdalini Tsintou, Kyriakos Dalamagkas, Alexander Marcus Seifalian 2015, 10 (5):  726-742.  doi: 10.4103/1673-5374.156966 Abstract ( 256 )   PDF (1315KB) ( 1140 )   Save Spinal cord injury results in the permanent loss of function, causing enormous personal, social and economic problems. Even though neural regeneration has been proven to be a natural mechanism, central nervous system repair mechanisms are ineffective due to the imbalance of the inhibitory and excitatory factors implicated in neuroregeneration. Therefore, there is growing research interest on discovering a novel therapeutic strategy for effective spinal cord injury repair. To this direction, cell-based delivery strategies, biomolecule delivery strategies as well as scaffold-based therapeutic strategies have been developed with a tendency to seek for the answer to a combinatorial approach of all the above. Here we review the recent advances on regenerative/neural engineering therapies for spinal cord injury, aiming at providing an insight to the most promising repair strategies, in order to facilitate future research conduction. Related Articles | Metrics

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The role of exosomes in peripheral nerve regeneration Rosanna C. Ching, Paul J. Kingham 2015, 10 (5):  743-747.  doi: 10.4103/1673-5374.156968 Abstract ( 235 )   PDF (301KB) ( 999 )   Save Peripheral nerve injuries remain problematic to treat, with poor functional recovery commonly observed. Injuries resulting in a nerve gap create specific difficulties for axonal regeneration. Approaches to address these difficulties include autologous nerve grafts (which are currently the gold standard treatment) and synthetic conduits, with the latter option being able to be impregnated with Schwann cells or stem cells which provide an appropriate micro-environment for neuronal regeneration to occur. Transplanting stem cells, however, infers additional risk of malignant transformation as well as manufacturing difficulties and ethical concerns, and the use of autologous nerve grafts and Schwann cells requires the sacrifice of a functioning nerve. A new approach utilizing exosomes, secreted extracellular vesicles, could avoid these complications. In this review, we summarize the current literature on exosomes, and suggest how they could help to improve axonal regeneration following peripheral nerve injury. Related Articles | Metrics

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Encephalic hemodynamic phases in subarachnoid hemorrhage: how to improve the protective effect in patient prognoses Marcelo de Lima Oliveira, Daniel Silva de Azevedo, Milena Krajnyk de Azevedo, Ricardo de Carvalho Nogueira, Manoel Jacobsen Teixeira, Edson Bor-Seng-Shu 2015, 10 (5):  748-752.  doi: 10.4103/1673-5374.156969 Abstract ( 266 )   PDF (412KB) ( 852 )   Save Subarachnoid hemorrhage is frequently associated with poor prognoses. Three different hemodynamic phases were identified during subarachnoid hemorrhage: oligemia, hyperemia, and vasospasm. Each phase is associated with brain metabolic changes. In this review, we correlated the hemodynamic phases with brain metabolism and potential treatment options in the hopes of improving patient prognoses. Related Articles | Metrics

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Neuroprotective effects of ginsenoside Rg1-induced neural stem cell transplantation on hypoxic-ischemic encephalopathy Ying-bo Li, Yan Wang, Ji-ping Tang, Di Chen, Sha-li Wang 2015, 10 (5):  753-759.  doi: 10.4103/1673-5374.156971 Abstract ( 293 )   PDF (1484KB) ( 972 )   Save Ginsenoside Rg1 is the major pharmacologically active component of ginseng, and is reported to have various therapeutic actions. To determine whether it induces the differentiation of neural stem cells, and whether neural stem cell transplantation after induction has therapeutic effects on hypoxic-ischemic encephalopathy, we cultured neural stem cells in 10–80 μM ginsenoside Rg1. Immunohistochemistry revealed that of the concentrations tested, 20 mM ginsenoside Rg1 had the greatest differentiation-inducing effect and was the concentration used for subsequent experiments. Whole-cell patch clamp showed that neural stem cells induced by 20 μM ginsenoside Rg1 were more mature than non-induced cells. We then established neonatal rat models of hypoxic-ischemic encephalopathy using the suture method, and ginsenoside Rg1-induced neural stem cells were transplanted via intracerebroventricular injection. These tests confirmed that neural stem cells induced by ginsenoside had fewer pathological lesions and had a significantly better behavioral capacity than model rats that received saline. Transplanted neural stem cells expressed neuron-specific enolase, and were mainly distributed in the hippocampus and cerebral cortex. The present data suggest that ginsenoside Rg1-induced neural stem cells can promote the partial recovery of complicated brain functions in models of hypoxic-ischemic encephalopathy. Related Articles | Metrics

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Changes of resting cerebral activities in subacute ischemic stroke patients Ping Wu, Fang Zeng, Yong-xin Li, Bai-li Yu, Li-hua Qiu, Wei Qin, Ji Li, Yu-mei Zhou, Fan-rong Liang 2015, 10 (5):  760-765.  doi: 10.4103/1673-5374.156977 Abstract ( 203 )   PDF (483KB) ( 1049 )   Save This study aimed to detect the difference in resting cerebral activities between ischemic stroke patients and healthy participants, define the abnormal site, and provide new evidence for pathological mechanisms, clinical diagnosis, prognosis prediction and efficacy evaluation of ischemic stroke. At present, the majority of functional magnetic resonance imaging studies focus on the motor dysfunction and the acute stage of ischemic stroke. This study recruited 15 right-handed ischemic stroke patients at subacute stage (15 days to 11.5 weeks) and 15 age-matched healthy participants. A resting-state functional magnetic resonance imaging scan was performed on each subject to detect cerebral activity. Regional homogeneity analysis was used to investigate the difference in cerebral activities between ischemic stroke patients and healthy participants. The results showed that the ischemic stroke patients had lower regional homogeneity in anterior cingulate and left cerebrum and higher regional homogeneity in cerebellum, left precuneus and left frontal lobe, compared with healthy participants. The experimental findings demonstrate that the areas in which regional homogeneity was different between ischemic stroke patients and healthy participants are in the cerebellum, left precuneus, left triangle inferior frontal gyrus, left inferior temporal gyrus and anterior cingulate. These locations, related to the motor, sensory and emotion areas, are likely potential targets for the neural regeneration of subacute ischemic stroke patients. Related Articles | Metrics

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Lateral intracerebroventricular injection of Apelin-13 inhibits apoptosis after cerebral ischemia/reperfusion injury Xiao-ge Yan, Bao-hua Cheng, Xin Wang, Liang-cai Ding, Hai-qing Liu, Jing Chen, Bo Bai 2015, 10 (5):  766-771.  doi: 10.4103/1673-5374.157243 Abstract ( 167 )   PDF (1009KB) ( 676 )   Save Apelin-13 inhibits neuronal apoptosis caused by hydrogen peroxide, yet apoptosis following cerebral ischemia-reperfusion injury has rarely been studied. In this study, Apelin-13 (0.1 μg/g) was injected into the lateral ventricle of middle cerebral artery occlusion model rats. TTC, TUNEL, and immunohistochemical staining showed that compared with the cerebral ischemia/reperfusion group, infarct volume and apoptotic cell number at the ischemic penumbra region were decreased in the Apelin-13 treatment group. Additionally, Apelin-13 treatment increased Bcl-2 immunoreactivity and decreased caspase-3 immunoreactivity. Our findings suggest that Apelin-13 is neuroprotective against cerebral ischemia/reperfusion injury through inhibition of neuronal apoptosis. Related Articles | Metrics

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CX3 chemokine receptor 1 deficiency leads to reduced dendritic complexity and delayed maturation of newborn neurons in the adult mouse hippocampus Feng Xiao, Jun-mei Xu, Xing-hua Jiang 2015, 10 (5):  772-777.  doi: 10.4103/1673-5374.156979 Abstract ( 259 )   PDF (957KB) ( 818 )   Save Previous studies have shown that microglia impact the proliferation and differentiation of neurons during hippocampal neurogenesis via the fractalkine/CX3 chemokine receptor 1 (CX3CR1) signaling pathway. However, whether microglia can influence the maturation and dendritic growth of newborn neurons during hippocampal neurogenesis remains unclear. In the present study, we found that the number of doublecortin-positive cells in the hippocampus was decreased, and the dendritic length and number of intersections in newborn neurons in the hippocampus were reduced in transgenic adult mice with CX3CR1 deficiency (CX3CR1GFP/GFP). Furthermore, after experimental seizures were induced with kainic acid in these CX3CR1-deficient mice, the expression of c-fos, a marker of neuronal activity, was reduced compared with wild-type mice. Collectively, the experimental findings indicate that the functional maturation of newborn neurons during hippocampal neurogenesis in adult mice is delayed by CX3CR1 deficiency. Related Articles | Metrics

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Effective components of Chinese herbs reduce central nervous system function decline induced by iron overload Xian-hui Dong, Jiang-tao Bai, Wei-na Kong, Xiao-ping He, Peng Yan, Tie-mei Shao, Wen-guo Yu, Xi-qing Chai, Yan-hua Wu, Cong Liu 2015, 10 (5):  778-785.  doi: 10.4103/1673-5374.156981 Abstract ( 142 )   PDF (2517KB) ( 601 )   Save Abnormally increased levels of iron in the brain trigger cascade amplification in Alzheimer’s disease patients, resulting in neuronal death. This study investigated whether components extracted from the Chinese herbs epimedium herb, milkvetch root and kudzuvine root could relieve the abnormal expression of iron metabolism-related protein in Alzheimer’s disease patients. An APPswe/PS1ΔE9 double transgenic mouse model of Alzheimer’s disease was used. The intragastric administration of compounds from epimedium herb, milkvetch root and kudzuvine root improved pathological alterations such as neuronal edema, increased the number of neurons, downregulated divalent metal transporter 1 expression, upregulated ferroportin 1 expression, and inhibited iron overload in the cerebral cortex of mice with Alzheimer’s disease. These compounds reduced iron overload-induced impairment of the central nervous system, indicating a new strategy for developing novel drugs for the treatment of Alzheimer’s disease. Related Articles | Metrics

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MicroRNA-124 slows down the progression of Huntington’s disease by promoting neurogenesis in the striatum Tian Liu, Wooseok Im, Inhee Mook-Jung, Manho Kim 2015, 10 (5):  786-791.  doi: 10.4103/1673-5374.156978 Abstract ( 250 )   PDF (643KB) ( 909 )   Save MicroRNA-124 contributes to neurogenesis through regulating its targets, but its expression both in the brain of Huntington’s disease mouse models and patients is decreased. However, the effects of microRNA-124 on the progression of Huntington’s disease have not been reported. Results from this study showed that microRNA-124 increased the latency to fall for each R6/2 Huntington’s disease transgenic mouse in the rotarod test. 5-Bromo-2’-deoxyuridine (BrdU) staining of the striatum shows an increase in neurogenesis. In addition, brain-derived neurotrophic factor and peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein levels in the striatum were increased and SRY-related HMG box transcription factor 9 protein level was decreased. These findings suggest that microRNA-124 slows down the progression of Huntington’s disease possibly through its important role in neuronal differentiation and survival.  Related Articles | Metrics

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Upregulated Ras/Raf/ERK1/2 signaling pathway: a new hope in the repair of spinal cord injury Tao Liu, Fu-jiang Cao, Dong-dong Xu, Yun-qiang Xu, Shi-qing Feng 2015, 10 (5):  792-796.  doi: 10.4103/1673-5374.156984 Abstract ( 145 )   PDF (649KB) ( 645 )   Save An increasing number of studies report that the Ras/Raf/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway has a death-promoting apoptotic function in neural cells. We hypothesized that the Ras/Raf/ERK1/2 signaling pathway may be abnormally regulated in rat injured spinal cord models. The weight drop method was used to establish rat spinal cord injury at T9. Western blot analysis and immunohistochemical staining revealed Ras expression was dramatically elevated, and the phosphorylations of A-Raf, B-Raf and C-Raf were all upregulated in the injured spinal cord. Both mitogen-activated protein kinase kinase 1/2 and ERK1/2, which belong to the Ras/Raf signaling kinases, were upregulated. These results indicate that Ras/Raf/ERK1/2 signaling may be upregulated in injured spinal cord and are involved in recovery after spinal cord injury. Related Articles | Metrics

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Bibliometric profile of neurogenic bladder in the literature: a 20-year bibliometric analysis Yuan Gao, Bo Qu, Yan Shen, Xiao-jing Su, Xiao-yan Dong, Xue-mei Chen, Yu-hong Zhou, Hong-ying Pi 2015, 10 (5):  797-803.  doi: 10.4103/1673-5374.156985 Abstract ( 189 )   PDF (951KB) ( 965 )   Save Neurogenic bladder is a dysfunction of the lower urinary tract caused by nervous system disorder. We investigated the trends in publication of articles under the topic “neurogenic bladder” using bibliometric analysis. Articles on neurogenic bladder, published between 1995 and 2014, were retrieved from the ISI Web of Science citation database. We analyzed the search results for authors, countries, institutions, journals, and top-cited papers. A total of 1,904 articles were retrieved. There was a small increase in the number of articles on neurogenic bladder from 1995 (n = 43) to 2014 (n = 117). The USA was the leading country in the total number of articles (n = 598). However, the number of publications from China has rapidly increased, and China was ranked second in 2014. Emmanuel Chartier-Kastler (n = 65) was the most productive author, and University of Paris VI (Paris 6) (n = 61) was the most productive institution. The Journal of Urology published the greatest number of articles on this topic (n = 285). Articles on neurogenic bladder were often published in a professional journal under the category Urology & Nephrology, Neurosciences & Neurology, or Rehabilitation. Visualization analysis based on co-citation networks was conducted using CiteSpace III. Visualization analysis revealed that the hot spots in neurogenic bladder were botulinum toxin-A, prazosin, bethanechol, and afferent pathways. These findings provide new insight into the publication trends and hot spots in neurogenic bladder. Related Articles | Metrics

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Autologous nerve graft repair of different degrees of sciatic nerve defect: stress and displacement at the anastomosis in a three-dimensional finite element simulation model Cheng-dong Piao, Kun Yang, Peng Li, Min Luo 2015, 10 (5):  804-807.  doi: 10.4103/1673-5374.156986 Abstract ( 305 )   PDF (532KB) ( 659 )   Save In the repair of peripheral nerve injury using autologous or synthetic nerve grafting, the magnitude of tensile forces at the anastomosis affects its response to physiological stress and the ultimate success of the treatment. One-dimensional stretching is commonly used to measure changes in tensile stress and strain; however, the accuracy of this simple method is limited. Therefore, in the present study, we established three-dimensional finite element models of sciatic nerve defects repaired by autologous nerve grafts. Using PRO E 5.0 finite element simulation software, we calculated the maximum stress and displacement of an anastomosis under a 5 N load in 10-, 20-, 30-, 40-mm long autologous nerve grafts. We found that maximum displacement increased with graft length, consistent with specimen force. These findings indicate that three-dimensional finite element simulation is a feasible method for analyzing stress and displacement at the anastomosis after autologous nerve grafting. Related Articles | Metrics

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Acupuncture and vitamin B12 injection for Bell’s palsy: no high-quality evidence exists Li-li Wang, Ling Guan, Peng-liang Hao, Jin-long Du, Meng-xue Zhang 2015, 10 (5):  808-813.  doi: 10.4103/1673-5374.156987 Abstract ( 440 )   PDF (363KB) ( 721 )   Save OBJECTIVE: To assess the efficacy of acupuncture combined with vitamin B12 acupoint injection versus acupuncture alone to reduce incomplete recovery in patients with Bell’s palsy. DATA RETRIEVAL: A computer-based online retrieval of Medline, Web of Science, CNKI, CBM databases until April 2014 was performed for relevant trials, using the key words “Bell’s palsy or idiopathic facial palsy or facial palsy” and “acupuncture or vitamin B12 or methylcobalamin”. STUDY SELECTION: All randomized controlled trials that compared acupuncture with acupuncture combined with vitamin B12 in patients with Bell’s palsy were included in the meta-analysis. The initial treatment lasted for at least 4 weeks. The outcomes of incomplete facial recovery were monitored. The scoring index varied and the definition of healing was consistent. The combined effect size was calculated by using relative risk (RR) with 95% confidence interval (CI) using the fixed effect model of Review Manager. MAIN OUTCOME MEASURES: Incomplete recovery rates were chosen as the primary outcome. RESULTS: Five studies involving 344 patients were included in the final analysis. Results showed  that the incomplete recovery rate of Bell’s palsy patients was 44.50% in the acupuncture combined with vitamin B12 group but 62.57% in the acupuncture alone group. The major acupoints were Taiyang (EX-HN5), Jiache (ST6), Dicang (ST4) and Sibai (ST2). The combined effect size showed that acupuncture combined with vitamin B12 was better than acupuncture alone for the treatment of Bell’s palsy (RR = 0.71, 95%CI: 0.58–0.87; P = 0.001), this result held true when 8 patients lost to follow up in one study were included into the analyses (RR = 0.70, 95%CI: 0.58–0.86; P = 0.0005). In the subgroup analyses, the therapeutic effect in patients of the electroacupuncture subgroup was better than in the non-electroacupuncture subgroup (P = 0.024). There was no significant difference in the incomplete recovery rate by subgroup analysis on drug types and treatment period. Most of the included studies were moderate or low quality, and bias existed. CONCLUSION: In patients with Bell’s palsy, acupuncture combined with vitamin B12 can reduce the risk of incomplete recovery compared with acupuncture alone in our meta-analysis. Because of study bias and methodological limitations, this conclusion is uncertain and the clinical application of acupuncture combined with vitamin B12 requires further exploration. Related Articles | Metrics

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High-dose thalidomide increases the risk of peripheral neuropathy in the treatment of ankylosing spondylitis Hong-xia Xue, Wen-yi Fu, Hua-dong Cui, Li-li Yang, Ning Zhang, Li-juan Zhao 2015, 10 (5):  814-818.  doi: 10.4103/1673-5374.156988 Abstract ( 312 )   PDF (205KB) ( 1593 )   Save Thalidomide is an effective drug for the treatment of ankylosing spondylitis but might induce peripheral neuropathy. This major adverse reaction has attracted much concern. The current study aimed to observe the incidence of thalidomide-induced peripheral neuropathy among ankylosing spondylitis patients for 1 year after treatment. In this study, 207 ankylosing spondylitis cases received thalidomide treatment, while 116 ankylosing spondylitis cases received other treatments. Results showed that the incidence of thalidomide-induced peripheral neuropathy in the thalidomide group was higher than that in the non-thalidomide group. There was no significant difference in the incidence of neuropathy between the < 6 months medication and ≥ 6 months medication groups. There were no differences in the mean age, gender, or daily dose between the two groups. The incidence of peripheral neuropathy among patients receiving 25, 50, 75, or 100 mg thalidomide per day was 4.6%, 8.5%, 17.1%, 21.7%, respectively. The incidence was significantly different between the groups receiving 25 mg and 100 mg thalidomide. In conclusion, thalidomide can induce peripheral neuropathy within 1 year after treatment of ankylosing spondylitis; however, age and gender have no obvious impact on the incidence of peripheral neuropathy. The incidence of peripheral neuropathy is associated with increasing daily doses of thalidomide. Related Articles | Metrics

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Efficacy and safety of nerve growth factor for the treatment of neurological diseases: a meta-analysis of 64 randomized controlled trials involving 6,297 patients Meng Zhao, Xiao-yan Li, Chun-ying Xu, Li-ping Zou 2015, 10 (5):  819-828.  doi: 10.4103/1673-5374.156989 Abstract ( 214 )   PDF (872KB) ( 1222 )   Save OBJECTIVE: China is the only country where nerve growth factor is approved for large-scale use as a clinical medicine. More than 10 years ago, in 2003, nerve growth factor injection was listed as a national drug. The goal of this article is to evaluate comprehensively the efficacy and safety of nerve growth factor for the treatment of neurological diseases. DATA RETRIEVAL: A computer-based retrieval was performed from six databases, including the Cochrane Library, PubMed, EMBASE, Sino Med, CNKI, and the VIP database, searching from the clinical establishment of nerve growth factor for treatment until December 31, 2013. The key words for the searches were “nerve growth factor, randomized controlled trials” in Chinese and in English. DATA SELECTION: Inclusion criteria: any study published in English or Chinese referring to randomized controlled trials of nerve growth factor; patients with neurological diseases such as peripheral nerve injury, central nerve injury, cranial neuropathy, and nervous system infections; patients older than 7 years; similar research methods and outcomes assessing symptoms; and measurement of nerve conduction velocities. The meta-analysis was conducted using Review Manager 5.2.3 software. MAIN OUTCOME MEASURES: The total effective rate, the incidence of adverse effects, and the nerve conduction velocity were recorded for each study. RESULTS: Sixty-four studies involving 6,297 patients with neurological diseases were included. The total effective rate in the group treated with nerve growth factor was significantly higher than that in the control group (P < 0.0001, RR: 1.35, 95%CI: 1.30–1.40). The average nerve conduction velocity in the nerve growth factor group was significantly higher than that in the control group (P < 0.00001, MD: 4.59 m/s, 95%CI: 4.12–5.06). The incidence of pain or scleroma at the injection site in the nerve growth factor group was also higher than that in the control group (P < 0.00001, RR: 6.30, 95%CI: 3.53–11.27), but such adverse effects were mild. CONCLUSION: Nerve growth factor can significantly improve nerve function in patients with nervous system disease and is safe and effective. Related Articles | Metrics

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Recovery of a degenerated corticospinal tract after injury in a patient with intracerebral hemorrhage: confirmed by diffusion tensor tractography imaging You Sung Seo, Sung Ho Jang 2015, 10 (5):  829-831.  doi: 10.4103/1673-5374.156990 Abstract ( 247 )   PDF (552KB) ( 646 )   Save Related Articles | Metrics

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Ligustrazine monomer against cerebral ischemia/reperfusion injury Hai-jun Gao, Peng-fei Liu, Pei-wen Li, Zhuo-yan Huang, Feng-bo Yu, Ting Lei, Yong Chen, Ye Cheng, Qing-chun Mu,Hai-yan Huang 2015, 10 (5):  832-840.  doi: 10.4103/1673-5374.156991 Abstract ( 176 )   PDF (553KB) ( 1091 )   Save Ligustrazine (2,3,5,6-tetramethylpyrazine) is a major active ingredient of the Szechwan lovage rhizome and is extensively used in treatment of ischemic cerebrovascular disease. The mechanism of action of ligustrazine use against ischemic cerebrovascular diseases remains unclear at present. This study summarizes its protective effect, the optimum time window of administration, and the most effective mode of administration for clinical treatment of cerebral ischemia/reperfusion injury. We examine the effects of ligustrazine on suppressing excitatory amino acid release, promoting migration, differentiation and proliferation of endogenous neural stem cells. We also looked at its effects on angiogenesis and how it inhibits thrombosis, the inflammatory response, and apoptosis after cerebral ischemia. We consider that ligustrazine gives noticeable protection from cerebral ischemia/reperfusion injury. The time window of ligustrazine administration is limited. The protective effect and time window of a series of derivative monomers of ligustrazine such as 2-[(1,1-dimethylethyl)oxidoimino]methyl]-3,5,6-trimethylpyrazine, CXC137 and CXC195 after cerebral ischemia were better than ligustrazine. Related Articles | Metrics