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22 April 2015, Volume 10 Issue 4 Previous Issue    Next Issue

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Structural and functional reorganization of propriospinal connections promotes functional recovery after spinal cord injury Linard Filli, Martin E. Schwab 2015, 10 (4):  509-513.  doi: 10.4103/1673-5374.155425 Abstract ( 343 )   PDF (1608KB) ( 672 )   Save Axonal regeneration and fiber regrowth is limited in the adult central nervous system, but research over the last decades has revealed a high intrinsic capacity of brain and spinal cord circuits to adapt and reorganize after smaller injuries or denervation. Short-distance fiber growth and synaptic rewiring was found in cortex, brain stem and spinal cord and could be associated with restoration of sensorimotor functions that were impaired by the injury. Such processes of structural plasticity were initially observed in the corticospinal system following spinal cord injury or stroke, but recent studies showed an equally high potential for structural and functional reorganization in reticulospinal, rubrospinal or propriospinal projections. Here we review the lesion-induced plastic changes in the propriospinal pathways, and we argue that they represent a key mechanism triggering sensorimotor recovery upon incomplete spinal cord injury. The formation or strengthening of spinal detour pathways bypassing supraspinal commands around the lesion site to the denervated spinal cord were identified as prominent neural substrate inducing substantial motor recovery in different species from mice to primates. Indications for the existence of propriospinal bypasses were also found in humans after cortical stroke. It is mandatory for current research to dissect the biological mechanisms underlying spinal circuit remodeling and to investigate how these processes can be stimulated in an optimal way by therapeutic interventions (e.g., fiber-growth enhancing interventions, rehabilitation). This knowledge will clear the way for the development of novel strategies targeting the remarkable plastic potential of propriospinal circuits to maximize functional recovery after spinal cord injury. Related Articles | Metrics

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Matrix interactions modulate neurotrophin-mediated neurite outgrowth and pathfinding Christopher M. Madl, Sarah C. Heilshorn 2015, 10 (4):  514-517.  doi: 10.4103/1673-5374.155426 Abstract ( 228 )   PDF (773KB) ( 660 )   Save Both matrix biochemistry and neurotrophic factors are known to modulate neurite outgrowth and pathfinding; however, the interplay between these two factors is less studied. While previous work has shown that the biochemical identity of the matrix can alter the outgrowth of neurites in response to neurotrophins, the importance of the concentration of cell-adhesive ligands is unknown. Using engineered elastin-like protein matrices, we recently demonstrated a synergistic effect between matrix-bound cell-adhesive ligand density and soluble nerve growth factor treatment on neurite outgrowth from dorsal root ganglia. This synergism was mediated by Schwann cell-neurite contact through L1CAM. Cell-adhesive ligand density was also shown to alter the pathfinding behavior of dorsal root ganglion neurites in response to a gradient of nerve growth factor. While more cell-adhesive matrices promoted neurite outgrowth, less cell-adhesive matrices promoted more faithful neurite pathfinding. These studies emphasize the importance of considering both matrix biochemistry and neurotrophic factors when designing biomaterials for peripheral nerve regeneration. Related Articles | Metrics

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Novel applications of trophic factors, Wnt and WISP for neuronal repair and regeneration in metabolic disease 2015, 10 (4):  518-528.  doi: 10.4103/1673-5374.155427 Abstract ( 268 )   PDF (216KB) ( 953 )   Save Diabetes mellitus affects almost 350 million individuals throughout the globe resulting in significant morbidity and mortality. Of further concern is the growing population of individuals that remain undiagnosed but are susceptible to the detrimental outcomes of this disorder. Diabetes mellitus leads to multiple complications in the central and peripheral nervous systems that include cognitive impairment, retinal disease, neuropsychiatric disease, cerebral ischemia, and peripheral nerve degeneration. Although multiple strategies are being considered, novel targeting of trophic factors, Wnt signaling, Wnt1 inducible signaling pathway protein 1, and stem cell tissue regeneration are considered to be exciting prospects to overcome the cellular mechanisms that lead to neuronal injury in diabetes mellitus involving oxidative stress, apoptosis, and autophagy. Pathways that involve insulin-like growth factor-1, fibroblast growth factor, epidermal growth factor, and erythropoietin can govern glucose homeostasis and are intimately tied to Wnt signaling that involves Wnt1 and Wnt1 inducible signaling pathway protein 1 (CCN4) to foster control over stem cell proliferation, wound repair, cognitive decline, β-cell proliferation, vascular regeneration, and programmed cell death. Ultimately, cellular metabolism through Wnt signaling is driven by primary metabolic pathways of the mechanistic target of rapamycin and AMP activated protein kinase. These pathways offer precise biological control of cellular metabolism, but are exquisitely sensitive to the different components of Wnt signaling. As a result, unexpected clinical outcomes can ensue and therefore demand careful translation of the mechanisms that govern neural repair and regeneration in diabetes mellitus. Related Articles | Metrics

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Peripheral nerve regeneration with conduits: use of vein tubes Rodrigo Guerra Sabongi, Marcela Fernandes, João Baptista Gomes dos Santos 2015, 10 (4):  529-533.  doi: 10.4103/1673-5374.155428 Abstract ( 204 )   PDF (586KB) ( 979 )   Save Treatment of peripheral nerve injuries remains a challenge to modern medicine due to the complexity of the neurobiological nerve regenerating process. There is a greater challenge when the transected nerve ends are not amenable to primary end-to-end tensionless neurorraphy. When facing a segmental nerve defect, great effort has been made to develop an alternative to the autologous nerve graft in order to circumvent morbidity at donor site, such as neuroma formation, scarring and permanent loss of function. Tubolization techniques have been developed to bridge nerve gaps and have been extensively studied in numerous experimental and clinical trials. The use of a conduit intends to act as a vehicle for moderation and modulation of the cellular and molecular ambience for nerve regeneration. Among several conduits, vein tubes were validated for clinical application with improving outcomes over the years. This article aims to address the investigation and treatment of segmental nerve injury and draw the current panorama on the use of vein tubes as an autogenous nerve conduit. Related Articles | Metrics

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Towards reperfusion-centric preclinical stroke research: outside the box of “reperfusion injury” Chia Yi Kuan, Yu Yo Sun 2015, 10 (4):  534-536.  doi: 10.4103/1673-5374.155412 Abstract ( 156 )   PDF (250KB) ( 696 )   Save Related Articles | Metrics

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Breaking out from the neuroprotective logjam: combined treatment with remote ischemic conditioning and minocycline in the prehospital setting Jung Mi Park, David C. Hess 2015, 10 (4):  537-539.  doi: 10.4103/1673-5374.155413 Abstract ( 201 )   PDF (794KB) ( 977 )   Save Related Articles | Metrics

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Oleanolic acid: a promising neuroprotective agent for cerebral ischemia Caltana Laura, Nieto María Luisa, Brusco Alicia 2015, 10 (4):  540-541.  doi: 10.4103/1673-5374.155414 Abstract ( 169 )   PDF (1205KB) ( 816 )   Save Related Articles | Metrics

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Neuroprotection induced by NMDA preconditioning as a strategy to understand brain tolerance mechanism Leandra C. Constantino, Samuel Vandresen-Filho, Carla I. Tasca 2015, 10 (4):  542-543.  doi: 10.4103/1673-5374.155415 Abstract ( 186 )   PDF (129KB) ( 632 )   Save Related Articles | Metrics

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Pleiotrophin fights Brd2 for neuronal differentiation Pablo Garcia-Gutierrez, Mario Garcia-Dominguez 2015, 10 (4):  544-546.  doi: 10.4103/1673-5374.155416 Abstract ( 160 )   PDF (357KB) ( 689 )   Save Related Articles | Metrics

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Progesterone: a universal stimulus for neuronal cells? Verena Theis, Carsten Theiss 2015, 10 (4):  547-549.  doi: 10.4103/1673-5374.155417 Abstract ( 210 )   PDF (413KB) ( 612 )   Save Related Articles | Metrics

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Tuning of neocortical astrogenesis rates by Emx2 in neural stem cells Carmen Falcone, Antonello Mallamaci 2015, 10 (4):  550-551.  doi: 10.4103/1673-5374.155418 Abstract ( 219 )   PDF (492KB) ( 755 )   Save Related Articles | Metrics

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Tetrahydrohyperforin: a neuroprotective modified natural compound against Alzheimer’s disease Carla Montecinos-Oliva, Andreas Schüller, Nibaldo C. Inestrosa 2015, 10 (4):  552-554.  doi: 10.4103/1673-5374.155420 Abstract ( 186 )   PDF (453KB) ( 778 )   Save Related Articles | Metrics

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Perspectives on disrupted-in-schizophrenia 1 signaling in neurogenesis Jayanth S. Chandran 2015, 10 (4):  555-556.  doi: 10.4103/1673-5374.155419 Abstract ( 171 )   PDF (217KB) ( 646 )   Save Related Articles | Metrics

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Prazosin: a potential new management tool for iatrogenic autonomic dysreflexia in individuals with spinal cord injury? Mei M.Z. Zheng, Aaron A. Phillips, Stacy L. Elliott, Andrei V. Krassiouko 2015, 10 (4):  557-558.  doi: 10.4103/1673-5374.155422 Abstract ( 228 )   PDF (178KB) ( 647 )   Save Related Articles | Metrics

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Dendrite pathology and neurodegeneration: focus on mTOR Adriana Di Polo 2015, 10 (4):  559-561.  doi: 10.4103/1673-5374.155421 Abstract ( 223 )   PDF (495KB) ( 1062 )   Save Related Articles | Metrics

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Chemokines and their receptors: important mediators to be aware of in neuroregenerative approaches for spinal cord injury Friederike Knerlich-Lukoschus 2015, 10 (4):  562-564.  doi: 10.4103/1673-5374.155423 Abstract ( 260 )   PDF (768KB) ( 721 )   Save Related Articles | Metrics

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Tubular conduits, cell-based therapy and exercise to improve peripheral nerve regeneration Camila Oliveira Goulart, Ana Maria Blanco Martinez 2015, 10 (4):  565-567.  doi: 10.4103/1673-5374.155424 Abstract ( 196 )   PDF (655KB) ( 512 )   Save Related Articles | Metrics

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Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia: a molecular docking study exploring possible neuroprotection Anand Kumar Pandey, Pallab Bhattacharya, Swet Chand Shukla, Sudip Paul, Ranjana Patnaik 2015, 10 (4):  568-575.  doi: 10.4103/1673-5374.155429 Abstract ( 110 )   PDF (1381KB) ( 783 )   Save The main pathophysiology of cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Resveratrol has been reported to be one of the most potent chemopreventive agents that can inhibit cellular processes associated with ischemic stroke. Matrix metalloproteinases (MMPs) has been considered as a potential drug target for the treatment of cerebral ischemia. To explore this, we tried to investigate the interaction of resveratrol with MMPs through molecular docking studies. At 30 minutes before and 2 hours after cerebral ischemia/reperfusion induced by occlusion of the middle cerebral artery, 40 mg/kg resveratrol was intraperitoneally administered. After resveratrol administration, neurological function and brain edema were significantly alleviated, cerebral infarct volume was significantly reduced, and nitrite and malondialdehyde levels in the cortical and striatal regions were significantly decreased. The molecular docking study of resveratrol and MMPs revealed that resveratrol occupied the active site of MMP-2 and MMP-9. The binding energy of the complexes was –37.848672 kJ/mol and –36.6345 kJ/mol for MMP-2 and MMP-9, respectively. In case of MMP-2, Leu 164, Ala 165 and Thr 227 were engaged in H-Bonding with resveratrol and in case of MMP-9, H-bonding was found with Glu 402, Ala 417 and Arg 424 residues. These findings collectively reveal that resveratrol exhibits neuroprotective effects on cerebral ischemia through inhibiting MMP-2 and MMP-9 activity. Related Articles | Metrics

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Electrical stimulation of the vagus nerve protects against cerebral ischemic injury through an anti-inflammatory mechanism Yao-xian Xiang, Wen-xin Wang, Zhe Xue, Lei Zhu, Sheng-bao Wang, Zheng-hui Sun 2015, 10 (4):  576-582.  doi: 10.4103/1673-5374.155430 Abstract ( 143 )   PDF (1225KB) ( 877 )   Save Vagus nerve stimulation exerts protective effects against ischemic brain injury; however, the underlying mechanisms remain unclear. In this study, a rat model of focal cerebral ischemia was established using the occlusion method, and the right vagus nerve was given electrical stimulation (constant current of 0.5 mA; pulse width, 0.5 ms; frequency, 20 Hz; duration, 30 seconds; every 5 minutes for a total of 60 minutes) 30 minutes, 12 hours, and 1, 2, 3, 7 and 14 days after surgery. Electrical stimulation of the vagus nerve substantially reduced infarct volume, improved neurological function, and decreased the expression levels of tumor necrosis factor-α and interleukin-6 in rats with focal cerebral ischemia. The experimental findings indicate that the neuroprotective effect of vagus nerve stimulation following cerebral ischemia may be associated with the inhibition of tumor necrosis factor-α and interleukin-6 expression. Related Articles | Metrics

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Systematic review of long-term Xingnao Kaiqiao needling efficacy in ischemic stroke treatment Zhi-xin Yang, Jia-hong Xie Yong-ping Liu, Guang-xin Miao, Ying-han Wang, Sheng-mei Wu, Yuan Li 2015, 10 (4):  583-588.  doi: 10.4103/1673-5374.155431 Abstract ( 178 )   PDF (1403KB) ( 939 )   Save OBJECTIVE: To systematically evaluate the long-term effect and safety of Xingnao Kaiqiao needling method in ischemic stroke treatment. DATA RETRIEVAL: We retrieved relevant random and semi-random controlled trials that used the Xingnao Kaiqiao needling method to treat ischemic stroke compared with various control treatments such as conventional drugs or other acupuncture therapies. Searched databases included China National Knowledge Infrastructure, Weipu Information Resources System, Wanfang Medical Data System, Chinese Biomedical Literature Database, Cochrane Library, and PubMed, from May 2006 to July 2014. SELECTION CRITERIA: Two authors independently conducted literature screening, quality evaluation, and data extraction. The quality of articles was evaluated according to the Cochrane Reviewers’ Handbook 5.1, and the study was carried out using Cochrane system assessment methods. RevMan 5.2 was used for meta-analysis of the included studies. MAIN OUTCOME MEASURES: Mortality rate, recurrence rate, and disability rate were observed. RESULTS: Nine randomized and semi-randomized controlled trials treating 931 cases of ischemic stroke were included in this review. Meta-analysis results showed that there were no significant differences in mortality reduction (risk ratio (RR) = 0.58, 95% confidence interval (CI): 0.17–1.93, Z = 0.89, P = 0.37) or recurrence rate (RR = 0.55, 95%CI: 0.18–1.70, Z = 1.04, P = 0.30) of ischemic stroke patients between the Xingnao Kaiqiao needling and control treatment groups. However, the Xingnao Kaiqiao needling method had a tendency towards higher efficacy in mortality reduction and recurrence rates. The Xingnao Kaiqiao needling method was significantly better than that of the control treatment in reducing disability rate (RR = 0.51, 95%CI: 0.27–0.98, Z = 2.03, P < 0.05). CONCLUSION: The Xingnao Kaiqiao needling method has a better effect than control treatment in reducing disability rate. The long-term effect of Xingnao Kaiqiao needling against ischemic stroke is better than that of control treatment. However, the limitations of this study limit the strength of the conclusions. Randomized controlled trials with a strict, reasonable design, and multi-center, large-scale samples and follow-up are necessary to draw conclusions about Xingnao Kaiqiao needling. Related Articles | Metrics

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Enhancing hippocampal blood flow after cerebral ischemia and vasodilating basilar arteries: in vivo and in vitro neuroprotective effect of antihypertensive DDPH Li Sun, Qin Li, Wei-ting Wang, Yu-hua Chen, Lian-jun Guo 2015, 10 (4):  589-593.  doi: 10.4103/1673-5374.155432 Abstract ( 199 )   PDF (463KB) ( 673 )   Save 1-(2,6-Dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino)-propane hydrochloride (DDPH) is a novel antihypertensive agent based on structural characteristics of mexiletine and verapamine. We investigated the effect of DDPH on vasodilatation and neuroprotection in a rat model of cerebral ischemia in vivo, and a rabbit model of isolated basilar arteries in vitro. Our results show that DDPH (10 mg/kg) significantly increased hippocampal blood flow in vivo in cerebral ischemic rats, and exerted dose-dependent relaxation of isolated basilar arteries contracted by histamine or KCl in the in vitro rabbit model. DDPH (3 × 10–5 M) also inhibited histamine-stimulated extracellular calcium influx and intracellular calcium release. Our findings suggest that DDPH has a vasodilative effect both in vivo and in vitro, which mediates a neuroprotective effect on ischemic nerve tissue. Related Articles | Metrics

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Resuscitation therapy for traumatic brain injury-induced coma in rats: mechanisms of median nerve electrical stimulation Zhen Feng, Ying-jun Zhong, Liang Wang, Tian-qi Wei 2015, 10 (4):  594-598.  doi: 10.4103/1673-5374.155433 Abstract ( 225 )   PDF (365KB) ( 947 )   Save In this study, rats were put into traumatic brain injury-induced coma and treated with median nerve electrical stimulation. We explored the wake-promoting effect, and possible mechanisms, of median nerve electrical stimulation. Electrical stimulation upregulated the expression levels of orexin-A and its receptor OX1R in the rat prefrontal cortex. Orexin-A expression gradually increased with increasing stimulation, while OX1R expression reached a peak at 12 hours and then decreased. In addition, after the OX1R antagonist, SB334867, was injected into the brain of rats after traumatic brain injury, fewer rats were restored to consciousness, and orexin-A and OXIR expression in the prefrontal cortex was downregulated. Our findings indicate that median nerve electrical stimulation induced an up-regulation of orexin-A and OX1R expression in the prefrontal cortex of traumatic brain injury-induced coma rats, which may be a potential mechanism involved in the wake-promoting effects of median nerve electrical stimulation. Related Articles | Metrics

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Short-term use of antiepileptic drugs is neurotoxic to the immature brain Yu Liu, Xue-ying Wang, Dan Li, Lin Yang, Shao-ping Huang 2015, 10 (4):  599-604.  doi: 10.4103/1673-5374.155434 Abstract ( 239 )   PDF (5078KB) ( 789 )   Save Previous studies have shown that the long-term use of antiepileptic drugs can cause nervous system damage. However, short-term antiepileptic drug treatment is frequently given to infants, especially neonates, to control seizure. Whether the short-term use of antiepileptic drugs is neurotoxic remains unclear. In the present study, immature rats, 3–21 days of age, were intraperitoneally injected with phenobarbital and/or topiramate for 3 consecutive days. Hematoxylin-eosin and immunohistochemical staining revealed that phenobarbital and topiramate, individually or in combination, were cytotoxic to hippocampal CA1 neurons and inhibited the expression of GluR1 and NR2B, excitatory glutamate receptor subunits. Furthermore, the combination of the two drugs caused greater damage than either drug alone. The results demonstrate that the short-term use of antiepileptic drugs damages neurons in the immature brain and that the combined use of antiepileptic drugs exacerbates damage. Our findings suggest that clinicians should consider the potential neurotoxic risk associated with the combined use of antiepileptic drugs in the treatment of seizure. Related Articles | Metrics

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Puerarin exhibits greater distribution and longer retention time in neurons than astrocytes in a co-cultured system Shu-Yong Wei, Jie Tong, Qiang Xue, Fang-hong Shang, Yan-jun Li, Yang Liu, Bin-bin Feng, Xiao-yu Xu 2015, 10 (4):  605-609.  doi: 10.4103/1673-5374.155435 Abstract ( 164 )   PDF (1080KB) ( 725 )   Save The phytoestrogen puerarin has been shown to protect neurons and astrocytes in the brain, and is therefore an attractive drug in the treatment of Alzheimer’s disease, Parkinson’s disease and cerebral ischemia. Whether puerarin exhibits the same biological processes in neurons and astrocytes in vitro has rarely been reported. In this study, cortical neurons and astrocytes of newborn Sprague-Dawley rats were separated, identified and co-cultured in a system based on Transwell membranes. The retention time and distribution of puerarin in each cell type was detected by fluorescence spectrophotometry and fluorescence microscope. The concentration of puerarin in both co-cultured and separately cultured neurons was greater than that of astrocytes. Puerarin concentration reached a maximum 20 minutes after it was added. At 60 minutes after its addition, a scant amount of drug was detected in astrocytes; however in both separately cultured and co-cultured neurons, the concentration of puerarin achieved a stable level of about 12.8 ng/mL. The results indicate that puerarin had a higher concentration and longer retention time in neurons than that observed in astrocytes. Related Articles | Metrics

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Neuroprotective effect of interleukin-6 regulation of voltage-gated Na+ channels of cortical neurons is time- and dose-dependent Wei Xia, Guo-yi Peng, Jiang-tao Sheng, Fang-fang Zhu, Jing-fang Guo, Wei-qiang Chen 2015, 10 (4):  610-617.  doi: 10.4103/1673-5374.155436 Abstract ( 196 )   PDF (1005KB) ( 701 )   Save Interleukin-6 has been shown to be involved in nerve injury and nerve regeneration, but the effects of long-term administration of high concentrations of interleukin-6 on neurons in the central nervous system is poorly understood. This study investigated the effects of 24 hour exposure of interleukin-6 on cortical neurons at various concentrations (0.1, 1, 5 and 10 ng/mL) and the effects of 10 ng/mL interleukin-6 exposure to cortical neurons for various durations (2, 4, 8, 24 and 48 hours) by studying voltage-gated Na+ channels using a patch-clamp technique. Voltage-clamp recording results demonstrated that interleukin-6 suppressed Na+ currents through its receptor in a time- and dose-dependent manner, but did not alter voltage-dependent activation and inactivation. Current-clamp recording results were consistent with voltage-clamp recording results. Interleukin-6 reduced the action potential amplitude of cortical neurons, but did not change the action potential threshold. The regulation of voltage-gated Na+ channels in rat cortical neurons by interleukin-6 is time- and dose-dependent. Related Articles | Metrics

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Mismatch negativity, social cognition, and functional outcomes in patients after traumatic brain injury Hui-yan Sun, Qiang Li, Xi-ping Chen, Lu-yang Tao 2015, 10 (4):  618-623.  doi: 10.4103/1673-5374.155437 Abstract ( 224 )   PDF (509KB) ( 758 )   Save Mismatch negativity is generated automatically, and is an early monitoring indicator of neuronal integrity impairment and functional abnormality in patients with brain injury, leading to decline of cognitive function. Antipsychotic medication cannot affect mismatch negativity. The present study aimed to explore the relationships of mismatch negativity with neurocognition, daily life and social functional outcomes in patients after brain injury. Twelve patients with traumatic brain injury and 12 healthy controls were recruited in this study. We examined neurocognition with the Wechsler Adult Intelligence Scale-Revised China, and daily and social functional outcomes with the Activity of Daily Living Scale and Social Disability Screening Schedule, respectively. Mismatch negativity was analyzed from electroencephalogram recording. The results showed that mismatch negativity amplitudes decreased in patients with traumatic brain injury compared with healthy controls. Mismatch negativity amplitude was negatively correlated with measurements of neurocognition and positively correlated with functional outcomes in patients after traumatic brain injury. Further, the most significant positive correlations were found between mismatch negativity in the fronto-central region and measures of functional outcomes. The most significant positive correlations were also found between mismatch negativity at the FCz electrode and daily living function. Mismatch negativity amplitudes were extremely positively associated with Social Disability Screening Schedule scores at the Fz electrode in brain injury patients. These experimental findings suggest that mismatch negativity might efficiently reflect functional outcomes in patients after traumatic brain injury. Related Articles | Metrics

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Motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment: a diffusion tensor imaging study Jin Hyun Kim, Yong Min Kwon, Su Min Son 2015, 10 (4):  624-630.  doi: 10.4103/1673-5374.155438 Abstract ( 149 )   PDF (514KB) ( 881 )   Save Previous diffusion tensor imaging (DTI) studies regarding pediatric patients with motor dysfunction have confirmed the correlation between DTI parameters of the injured corticospinal tract and the severity of motor dysfunction. There is also evidence that DTI parameters can help predict the prognosis of motor function of patients with cerebral palsy. But few studies are reported on the DTI parameters that can reflect the motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment. In the present study, 36 pediatric patients with hemiplegic cerebral palsy were included. Before and after rehabilitation treatment, DTI was used to measure the fiber number (FN), fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of bilateral corticospinal tracts. Functional Level of Hemiplegia scale (FxL) was used to assess the therapeutic effect of rehabilitative therapy on clinical hemiplegia. Correlation analysis was performed to assess the statistical interrelationship between the change amount of DTI parameters and FxL. DTI findings obtained at the initial and follow-up evaluations demonstrated that more affected corticospinal tract yielded significantly decreased FN and FA values and significantly increased ADC value compared to the less affected corticospinal tract. Correlation analysis results showed that the change amount of FxL was positively correlated to FN and FA values, and the correlation to FN was stronger than the correlation to FA. The results suggest that FN and FA values can be used to evaluate the motor function outcomes of pediatric patients with hemiplegic cerebral palsy after rehabilitation treatment and FN is of more significance for evaluation.  Related Articles | Metrics

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Matrix metalloproteinase 9 level as an indicator for restenosis following cervical and intracranial angioplasty and stenting Jun-peng Liu, Yin-zhou Wang, Yong-kun Li, Qiong Cheng, Zheng Zheng 2015, 10 (4):  631-635.  doi: 10.4103/1673-5374.155439 Abstract ( 165 )   PDF (486KB) ( 683 )   Save Cervical and intracranial angioplasty and stenting is an effective and safe method of reducing the risk of ischemic stroke, but it may be affected by in-stent restenosis. The present study investigated serum level of matrix metalloproteinase 9 as a predictor of restenosis after 40 patients underwent cervical and/or intracranial angioplasty and stenting. Results showed that restenosis occurred in 30% (3/10) of patients when the serum level of matrix metalloproteinase 9 at 3 days after surgery was 2.5 times higher than preoperative level. No restenosis occurred when the serum level of matrix metalloproteinase 9 at 3 days after surgery was not 2.5 times higher than preoperative level. Restenosis occurred in 12% (2/17) of patients when the serum level of matrix metalloproteinase 9 was higher than preoperative level for more than 30 days after surgery, but only occurred in 4% (1/23) of patients when the serum level of matrix metalloproteinase 9 was higher than preoperative level for less than 30 days after surgery. However, the differences observed were not statistically significant (P > 0.05). Experimental findings indicate that when the serum level of matrix metalloproteinase 9 is 2.5 times higher than preoperative level at 3 days after cervical and intracranial angioplasty and stenting, it may serve as a predictor of in-stent restenosis Related Articles | Metrics

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Propofol injection combined with bone marrow mesenchymal stem cell transplantation better improves electrophysiological function in the hindlimb of rats with spinal cord injury  than monotherapy Yue-xin Wang, Jing-jing Sun, Mei Zhang, Xiao-hua Hou, Jun Hong, Ya-jing Zhou, Zhi-yong Zhang 2015, 10 (4):  636-643.  doi: 10.4103/1673-5374.155440 Abstract ( 170 )   PDF (1367KB) ( 936 )   Save The repair effects of bone marrow mesenchymal stem cell transplantation on nervous system damage are not satisfactory. Propofol has been shown to protect against spinal cord injury. Therefore, this study sought to explore the therapeutic effects of their combination on spinal cord injury. Rat models of spinal cord injury were established using the weight drop method. Rats were subjected to bone marrow mesenchymal stem cell transplantation via tail vein injection and/or propofol injection via tail vein using an infusion pump. Four weeks after cell transplantation and/or propofol treatment, the cavity within the spinal cord was reduced. The numbers of PKH-26-positive cells and horseradish peroxidase-positive nerve fibers apparently increased in the spinal cord. Latencies of somatosensory evoked potentials and motor evoked potentials in the hindlimb were noticeably shortened, amplitude was increased and hindlimb motor function was obviously improved. Moreover, the combined effects were better than cell transplantation or propofol injection alone. The above data suggest that the combination of propofol injection and bone marrow mesenchymal stem cell transplantation can effectively improve hindlimb electrophysiological function, promote the recovery of motor funtion, and play a neuroprotective role in spinal cord injury in rats. Related Articles | Metrics

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Exercise promotes motor functional recovery in rats with corticospinal tract injury: anti-apoptosis mechanism Ting-ting Hou, Xiao-yu Yang, Peng Xia, Su Pan, Jian Liu, Zhi-ping Qi 2015, 10 (4):  644-650.  doi: 10.4103/1673-5374.155441 Abstract ( 203 )   PDF (1547KB) ( 587 )   Save Studies have shown that exercise interventions can improve functional recovery after spinal cord injury, but the mechanism of action remains unclear. To investigate the mechanism, we established a unilateral corticospinal tract injury model in rats by pyramidotomy, and used a single pellet reaching task and horizontal ladder walking task as exercise interventions postoperatively. Functional recovery of forelimbs and forepaws in the rat models was noticeably enhanced after the exercises. Furthermore, TUNEL staining revealed significantly fewer apoptotic cells in the spinal cord of exercised rats, and western blot analysis showed that spinal cord expression of the apoptosis-related protein caspase-3 was significantly lower, and the expression of Bcl-2 was significantly higher, while the expression of Bax was not signifiantly changed after exercise, compared with the non-exercised group. Expression of these proteins decreased with time after injury, towards the levels observed in sham-operated rats, however at 4 weeks postoperatively, caspase-3 expression remained significantly greater than in sham-operated rats. The present findings indicate that a reduction in apoptosis is one of the mechanisms underlying the improvement of functional recovery by exercise interventions after corticospinal tract injury. Related Articles | Metrics

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Human umbilical cord mesenchymal stem cells promote peripheral nerve repair via paracrine mechanisms Zhi-yuan Guo, Xun Sun, Xiao-long Xu, Qing Zhao, Jiang Peng, Yu Wang 2015, 10 (4):  651-658.  doi: 10.4103/1673-5374.155442 Abstract ( 236 )   PDF (3404KB) ( 826 )   Save Human umbilical cord-derived mesenchymal stem cells (hUCMSCs) represent a promising young-state stem cell source for cell-based therapy. hUCMSC transplantation into the transected sciatic nerve promotes axonal regeneration and functional recovery. To further clarify the paracrine effects of hUCMSCs on nerve regeneration, we performed human cytokine antibody array analysis, which revealed that hUCMSCs express 14 important neurotrophic factors. Enzyme-linked immunosorbent assay and immunohistochemistry showed that brain-derived neurotrophic factor, glial-derived neurotrophic factor, hepatocyte growth factor, neurotrophin-3, basic fibroblast growth factor, type I collagen, fibronectin and laminin were highly expressed. Treatment with hUCMSC-conditioned medium enhanced Schwann cell viability and proliferation, increased nerve growth factor and brain-derived neurotrophic factor expression in Schwann cells, and enhanced neurite growth from dorsal root ganglion explants. These findings suggest that paracrine action may be a key mechanism underlying the effects of hUCMSCs in peripheral nerve repair. Related Articles | Metrics

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Connexin: a potential novel target for protecting the central nervous system? Hong-yan Xie,Yu Cui,Fang Deng,Jia-chun Feng 2015, 10 (4):  659-666.  doi: 10.4103/1673-5374.155444 Abstract ( 237 )   PDF (409KB) ( 999 )   Save Connexin subunits are proteins that form gap junction channels, and play an important role in communication between adjacent cells. This review article discusses the function of connexins/hemichannels/gap junctions under physiological conditions, and summarizes the findings regarding the role of connexins/hemichannels/gap junctions in the physiological and pathological mechanisms underlying central nervous system diseases such as brain ischemia, traumatic brain and spinal cord injury, epilepsy, brain and spinal cord tumor, migraine, neuroautoimmune disease, Alzheimer’s disease, Parkinson’s disease, X-linked Charcot-Marie-Tooth disease, Pelizaeus-Merzbacher-like disease, spastic paraplegia and maxillofacial dysplasia. Connexins are considered to be a potential novel target for protecting the central nervous system. Related Articles | Metrics

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Effects of cilostazol on the progression and regression of symptomatic intracranial artery stenosis: it reduces the risk of ischemic stroke Wen-hui Zhang, Fang-fang Cai, Zhong-min Wen 2015, 10 (4):  667-672.  doi: 10.4103/1673-5374.155443 Abstract ( 195 )   PDF (839KB) ( 803 )   Save OBJECTIVE: To assess the efficacy and safety of cilostazol on the progression and regression of symptomatic intracranial artery stenosis. DATA RETRIVAL: We searched the main databases for eligible trials including Medline (from 1966 to June 2014), Embase (from 1980 to June 2014), Cochrane Library (Issue 6, 2014), Chinese National Knowledge Infrastructure (from 1995 to June 2014), Current Controlled Trials (http://controlled-trials.com), Clinical Trials.gov (http://clinicaltrials.gov), and Chinese Clinical Trial Registry (http://www.chictr.org). All studies regarding prevention and treatment of symptomatic intracranial arterial stenosis by cilostazol were collected. The Mesh or text keywords were the English words: “cilostazol, phosphodiesterase 3 inhibitor, atherosclerosis, and ischemic stroke.” No restrictions were put on publications or publication language. SELECTION CRITERIA: Grade A or B randomized controlled trials were selected according to the quality of evaluation criteria from the Cochrane Collaboration, in which cilostazol and aspirin were used to evaluate the effects of cilostazol in the treatment of patients with symptomatic intracranial artery stenosis. The quality of study methodology was evaluated based on criteria described in Cochrane Reviewer’s Handbook 5.0.1. RevMan 5.2 software was used for data analysis. MAIN OUTCOME MEASURES: Clinical efficacy and safety of cilostazol in stopping progression and promoting regression of symptomatic intracranial artery stenosis were measured by magnetic resonance angiography and transcranial Doppler. RESULTS: Two randomized controlled trials with a total of 203 patients were included in this study. The results showed that while cilostazol was associated with a significantly reduced progression of intracranial artery stenosis (OR = 0.21, 95%CI: 0.09–0.47, P < 0.01), it had no beneficial effect on symptom regression (OR = 1.42, 95%CI: 0.80–2.51, P = 0.24). During the follow-up period, although some adverse effects developed, including headache, gastrointestinal disturbance, and dizziness, incidences of bleeding were lower than in aspirin-treated patients. CONCLUSION: Cilostazol may prevent the progression of symptomatic intracranial artery stenosis, which could reduce the incidence of ischemic stroke. Related Articles | Metrics