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16 September 2014, Volume 9 Issue 17 Previous Issue    Next Issue

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Extracellular matrices, artificial neural scaffolds and the promise of neural regeneration Christian B. Ricks, Samuel S. Shin, Christopher Becker, Ramesh Grandhi 2014, 9 (17):  1573-1577.  doi: 10.4103/1673-5374.141778 Abstract ( 221 )   PDF (684KB) ( 663 )   Save Over last 20 years, extracellular matrices have been shown to be useful in promoting tissue regeneration. Recently, they have been used and have had success in achieving neurogenesis. Recent  developments in extracellular matrix design have allowed their successful in vivo incorporation to engender an environment favorable for neural regeneration in animal models. Promising treatments under investigation include manipulation of the intrinsic extracellular matrix and incorporation of engineered naometer-sized scaffolds through which inhibition of molecules serving as barriers to neuroregeneration and delivery of neurotrophic factors and/or cells for successful tissue regeneration can be achieved. Further understanding of the changes incurred within the extracellular matrix following central nervous system injury will undoubtedly help design a clinically efficacious extracellular matrix scaffold that can mitigate or reverse neural degeneration in the clinical setting. Related Articles | Metrics

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Selective CDK inhibitors: promising candidates for future clinical traumatic brain injury trials Shruti V. Kabadi, Alan I. Faden 2014, 9 (17):  1578-1580.  doi: 10.4103/1673-5374.141779 Abstract ( 305 )   PDF (155KB) ( 638 )   Save Traumatic brain injury induces secondary injury that contributes to neuroinflammation, neuronal loss, and neurological dysfunction. One important injury mechanism is cell cycle activation which causes neuronal apoptosis and glial activation. The neuroprotective effects of both non-selective (Flavopiridol) and selective (Roscovitine and CR-8) cyclin-dependent kinase inhibitors have been shown across multiple experimental traumatic brain injury models and species. Cyclin-dependent kinaseinhibitors, administered as a single systemic dose up to 24 hours after traumatic brain injury, provide strong neuroprotection-reducing neuronal cell death, neuroinflammation and neurological dysfunction. Given their effectiveness and long therapeutic window, cyclin-dependent kinase inhibitors appear to be promising candidates for clinical traumatic brain injury trials. Related Articles | Metrics

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Induction of ischemic tolerance as a promising treatment against diabetic retinopathy Ruth E. Rosenstein, Diego C. Fernandez 2014, 9 (17):  1581-1584.  doi: 10.4103/1673-5374.141782 Abstract ( 207 )   PDF (160KB) ( 678 )   Save Diabetic retinopathy is a leading cause of acquired blindness, and it is the most common ischemic disorder of the retina. Available treatments are not very effective. Efforts to inhibit diabetic retinopathy have focused either on highly specific therapeutic approaches for pharmacologic targets or using genetic approaches to change expression of certain enzymes. However, it might be wise to choose innovative treatment modalities that act by multiple potential mechanisms. The resistance to ischemic injury, or ischemic tolerance, can be transiently induced by prior exposure to a non-injurious preconditioning stimulus. A complete functional and histologic protection against retinal ischemic damage can be achieved by previous preconditioning with non-damaging ischemia. In this review, we will discuss evidence that supports that ischemic conditioning could help avert the dreaded consequences that results from retinal diabetic damage. Related Articles | Metrics

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Neuroprotective effects of vagus nerve stimulation on traumatic brain injury Long Zhou, Jinhuang Lin, Junming Lin, Guoju Kui, Jianhua Zhang, Yigang Yu 2014, 9 (17):  1585-1591.  doi: 10.4103/1673-5374.141783 Abstract ( 178 )   PDF (1209KB) ( 777 )   Save Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue. Related Articles | Metrics

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Mechanisms underlying attenuation of apoptosis of cortical neurons in the hypoxic brain by flavonoids from the stems and leaves of Scutellaria baicalensis Georgi Guangxin Miao, Hongxiang Zhao, Ke Guo, Jianjun Cheng, Shufeng Zhang, Xiaofeng Zhang, Zhenling Cai, Hong Miao, Yazhen Shang 2014, 9 (17):  1592-1598.  doi: 10.4103/1673-5374.141784 Abstract ( 249 )   PDF (1045KB) ( 662 )   Save Flavonoids from the stems and leaves of Scutellaria baicalensis Georgi, an antioxidant, markedly improve memory impairments and neuronal injuries. In the present study, primary cortical neurons of rats were exposed to potassium cyanide to establish a model of in vitro neural cell apoptosis. Inhibition of apoptosis by flavonoids from the stems and leaves of Scutellaria baicalensis Georgi at concentrations of 18.98, 37.36, and 75.92 μg/mL was detected using this model. These flavonoids dramatically increased cell survival, inhibited cell apoptosis and excessive production of malondialdehyde, and increased the activities of superoxide dismutase, glutathione peroxidase, and Na+-K+-ATPase in primary cortical neurons exposed to potassium cyanide. The flavonoids from the stems and leaves of Scutellaria baicalensis Georgi were originally found to have a polyhydric structure and to protect against cerebral hypoxia in in vitro and in vivo models, including hypoxia induced by potassium cyanide or cerebral ischemia. The present study suggests that flavonoids from the stems and leaves of Scutellaria baicalensis Georgi exert neuroprotective effects via modulation of oxidative stress, such as malondialdehyde, superoxide dismutase, glutathione peroxidase and Na+-K+-ATPase disorders induced by potassium cyanide. References | Related Articles | Metrics

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Autophagy occurs within an hour of adenosine triphosphate treatment after nerve cell damage: the neuroprotective effects of adenosine triphosphate against apoptosis Na Lu, Yong Wang, Baoying Wang, Honggang Zhao, Dongliang Li 2014, 9 (17):  1599-1605.  doi: 10.4103/1673-5374.141811 Abstract ( 218 )   PDF (2133KB) ( 948 )   Save After hypoxia, ischemia, or inflammatory injuries to the central nervous system, the damaged cells release a large amount of adenosine triphosphate, which may cause secondary neuronal death. Autophagy is a form of cell death that also has neuroprotective effects. Cell Counting Kit assay, monodansylcadaverine staining, flow cytometry, western blotting, and real-time PCR were used to determine the effects of exogenous adenosine triphosphate treatment at different concentrations (2, 4, 6, 8, 10 mmol/L) over time (1, 2, 3, and 6 hours) on the apoptosis and autophagy of SH-SY5Y cells. High concentrations of extracellular adenosine triphosphate induced autophagy and apoptosis of SH-SY5Y cells. The enhanced autophagy first appeared, and peaked at 1 hour after treatment with adenosine triphosphate. Cell apoptosis peaked at 3 hours, and persisted through 6 hours. With prolonged exposure to the adenosine triphosphate treatment, the fraction of apoptotic cells increased. These data suggest that the SH-SY5Y neural cells initiated autophagy against apoptosis within an hour of adenosine triphosphate treatment to protect themselves against injury. References | Related Articles | Metrics

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Tooth loss inhibits neurogenesis in the dentate gyrus of adult mice Shaochen Su, Tao Qi, Baoli Su, Huibin Gu, Jianlin Wang, Lan Yang 2014, 9 (17):  1606-1609.  doi: 10.4103/1673-5374.141786 Abstract ( 311 )   PDF (756KB) ( 1368 )   Save Tooth loss has been shown to affect learning and memory in mice and increases the risk of Alzheimer’s disease. The dentate gyrus is strongly associated with cognitive function. This study hypothesized that tooth loss affects neurons in the dentate gyrus. Adult male mice were randomly assigned to either the tooth loss group or normal control group. In the tooth loss group, the left maxillary and mandibular molars were extracted. Normal control mice did not receive any intervention. Immunofluorescence staining revealed that the density and absorbance of doublecortin- and neuronal nuclear antigen-positive cells were lower in the tooth loss group than in the normal control group. These data suggest that tooth loss may inhibit neurogenesis in the dentate gyrus of adult mice. References | Related Articles | Metrics

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Damage of hippocampal neurons in rats with chronic alcoholism Ailin Du, Hongbo Jiang, Lei Xu, Na An, Hui Liu, Yinsheng Li, Ruiling Zhang 2014, 9 (17):  1610-1615.  doi: 10.4103/1673-5374.141787 Abstract ( 278 )   PDF (763KB) ( 1300 )   Save Chronic alcoholism can damage the cytoskeleton and aggravate neurological deficits. However, the effect of chronic alcoholism on hippocampal neurons remains unclear. In this study, a model of chronic alcoholism was established in rats that were fed with 6% alcohol for 42 days. Endogenous hydrogen sulfide content and cystathionine-beta-synthase activity in the hippocampus of rats with chronic alcoholism were significantly increased, while F-actin expression was decreased. Hippocampal neurons in rats with chronic alcoholism appeared to have a fuzzy nuclear membrane, mitochondrial edema, and ruptured mitochondrial crista. These findings suggest that chronic alcoholism can cause learning and memory decline in rats, which may be associated with the hydrogen sulfide/cystathionine-beta-synthase system, mitochondrial damage and reduced expression of F-actin. Related Articles | Metrics

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Methylmercury chloride damage to the adult rat hippocampus cannot be detected by proton magnetic resonance spectroscopy Zhiyan Lu, Jinwei Wu, Guangyuan Cheng, Jianying Tian, Zeqing Lu, Yongyi Bi 2014, 9 (17):  1616-1620.  doi: 10.4103/1673-5374.141789 Abstract ( 171 )   PDF (1724KB) ( 605 )   Save Previous studies have found that methylmercury can damage hippocampal neurons and accordingly cause cognitive dysfunction. However, a non-invasive, safe and accurate detection method for detecting hippocampal injury has yet to be developed. This study aimed to detect methylmercury-induced damage on hippocampal tissue using proton magnetic resonance spectroscopy. Rats were given a subcutaneous injection of 4 and 2 mg/kg methylmercury into the neck for 50 consecutive days. Water maze and pathology tests confirmed that cognitive function had been impaired and that the ultrastructure of hippocampal tissue was altered after injection. The results of proton magnetic resonance spectroscopy revealed that the nitrogen-acetyl aspartate/creatine, choline complex/creatine and myoinositol/creatine ratio in rat hippocampal tissue were unchanged. Therefore, proton magnetic resonance spectroscopy can not be used to determine structural damage in the adult rat hippocampus caused by methylmercury chloride. Related Articles | Metrics

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Neuroprotective effects of Buyang Huanwu decoction on cerebral ischemia-induced neuronal damage Qingchun Mu, Pengfei Liu, Xitong Hu, Haijun Gao, Xu Zheng, Haiyan Huang 2014, 9 (17):  1621-1627.  doi: 10.4103/1673-5374.141791 Abstract ( 262 )   PDF (366KB) ( 741 )   Save Among the various treatment methods for stroke, increasing attention has been paid to traditional Chinese medicines. Buyang Huanwu decoction is a commonly used traditional Chinese medicine for the treatment of stroke. This paper summarizes the active components of the Chinese herb, which is composed of Huangqi (Radix Astragali seu Hedysari), Danggui (Radix Angelica sinensis), Chishao (Radix Paeoniae Rubra), Chuanxiong (Rhizoma Ligustici Chuanxiong), Honghua (Flos Carthami), Taoren (Semen Persicae) and Dilong (Pheretima), and identifies the therapeutic targets and underlying mechanisms that contribute to the neuroprotective properties of Buyang Huanwu decoction. Related Articles | Metrics

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Virtual reality training improves balance function Yurong Mao, Peiming Chen, Le Li, Dongfeng Huang 2014, 9 (17):  1628-1634.  doi: 10.4103/1673-5374.141795 Abstract ( 197 )   PDF (589KB) ( 917 )   Save Virtual reality is a new technology that simulates a three-dimensional virtual world on a computer and enables the generation of visual, audio, and haptic feedback for the full immersion of users. Users can interact with and observe objects in three-dimensional visual space without limitation. At present, virtual reality training has been widely used in rehabilitation therapy for balance dysfunction. This paper summarizes related articles and other articles suggesting that virtual reality training can improve balance dysfunction in patients after neurological diseases. When patients perform virtual reality training, the prefrontal, parietal cortical areas and other motor cortical networks are activated. These activations may be involved in the reconstruction of neurons in the cerebral cortex. Growing evidence from clinical studies reveals that virtual reality training improves the neurological function of patients with spinal cord injury, cerebral palsy and other neurological impairments. These findings suggest that virtual reality training can activate the cerebral cortex and improve the spatial orientation capacity of patients, thus facilitating the cortex to control balance and increase motion function. Related Articles | Metrics

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Publication trends in studies examining radix notoginseng as a treatment for ischemic brain injury Haiping Li, Luo Qiang, Chunyang Zhang, Chaohui Wang, Zhenxing Mu, Ligang Jiang 2014, 9 (17):  1635-1642.  doi: 10.4103/1673-5374.141792 Abstract ( 211 )   PDF (394KB) ( 631 )   Save Acute ischemic stroke has become a major disease burden with high mortality and morbidity rates. There is a lack of evidence-based medicine confirming the efficacy of common treatments. Panax notoginseng saponins, the main active ingredient of radix notoginseng, have a neuroprotective role in ischemic brain injury, and have been popularized as a maintenance treatment for acute cerebral infarction and its sequelae. We conducted literature searches on the Web of Science, ClinicalTrials.gov, Cochrane Collaboration, CNKI, Wanfang and the China Scientific & Technological Achievements Database and analyzed the experimental and clinical outcomes of studies investigating the use of radix notoginseng in the treatment of ischemic brain injury to improve the understanding of relevant research trends and existing problems. We found that over the past 10 years, China has maintained its interest in Panax notoginseng research, while such studies are scarce on the Web of Science. However, Chinese researchers often focus on the neuroprotective role of radix notoginseng in ischemic brain injury, but there are no large-scale clinical data to confirm its efficacy and safety. There remains a need for more rigorous large-sample randomized controlled clinical trials with long-term follow-up, to determine whether radix notoginseng lowers stroke recurrence and improves patient’s quality of life. Related Articles | Metrics

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Stem cell transplantation for treating stroke: status, trends and development Wenxin Huo, Xiaoyang Liu, Cheng Tan, Yingying Han, Chunyang Kang, Wei Quan, Jiajun Chen 2014, 9 (17):  1643-1648.  doi: 10.4103/1673-5374.141793 Abstract ( 214 )   PDF (253KB) ( 757 )   Save The developing approaches of thrombolytic therapy, endovascular treatment, neuroprotective therapy, and stem cell therapy have enabled breakthroughs in stroke treatment. In this study, we summarize and analyze trends and progress in stem cell transplantation for stroke treatment by retrieval of literature from Thomson Reuters Web of Science database, the NIH Clinical Trial Planning Grant Program, and Clinical Trials Registration Center in North America. In the last 10 years, there has been an increasing number of published articles on stem cell transplantation for stroke treatment. In particular, research from the USA and China has focused on stem cell transplantation. A total of 2,167 articles addressing stem cell transplantation for stroke treatment from 2004 to 2013 were retrieved from the Thomson Reuters Web of Science database. The majority of these articles were from the USA (854, 39.4%), with the journal Stroke publishing the most articles (145, 6.7%). Of the published articles, 143 were funded by the National Institutes of Health (accounting for 6.6% of total publications), and 91 by the National Natural Science Foundation of China. Between 2013 and 2014, the National Institutes of Health provided financial support ($130 million subsidy) for 329 research projects on stroke therapy using stem cell transplantation. In 2014, 215 new projects were approved, receiving grants of up to $70,440,000. Ninety clinical trials focusing on stem cell transplantation for stroke were registered in the Clinical Trial Registration Center in North America, with 40 trials registered in the USA (ranked first place). China had the maximum number of registered research or clinical trials (10 projects). Related Articles | Metrics