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15 April 2012, Volume 7 Issue 11 Previous Issue    Next Issue

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Biotinylated dextran amine anterograde tracing of the canine corticospinal tract Xiao Han, Guangming Lv, Huiqun Wu, Dafeng Ji, Zhou Sun, Yaofu Li, Lemin Tang 2012, 7 (11):  805-809.  Abstract ( 223 )   PDF (185KB) ( 1292 )   Save In this study, biotinylated dextran amine (BDA) was microinjected into the left cortical motor area of the canine brain. Fluorescence microscopy results showed that a large amount of BDA-labeled pyramidal cells were visible in the left cortical motor area after injection. In the left medulla oblongata, the BDA-labeled corticospinal tract was evenly distributed, with green fluorescence that had a clear boundary with the surrounding tissue. The BDA-positive corticospinal tract entered into the right lateral funiculus of the spinal cord and descended into the posterior part of the right lateral funiculus, close to the posterior horn, from cervical to sacral segments. There was a small amount of green fluorescence in the sacral segment. The distribution of BDA labeling in the canine central nervous system was consistent with the course of the corticospinal tract. Fluorescence labeling for BDA gradually diminished with time after injection. Our findings indicate that the BDA anterograde tracing technique can be used to visualize the localization and trajectory of the corticospinal tract in the canine central nervous system. Related Articles | Metrics

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Telomerase expression in the glial scar of rats with spinal cord injury Mingkun Yang, Weibin Sheng, Tao Xu, Kai Huang, Yanjiao Wang 2012, 7 (11):  810-814.  Abstract ( 204 )   PDF (155KB) ( 882 )   Save A rat model of spinal cord injury was established using the weight drop method. A cavity formed 14 days following spinal cord injury, and compact scar tissue formed by 56 days. Enzyme-linked immunosorbent assay and polymerase chain reaction enzyme-linked immunosorbent assay results demonstrated that glial fibrillary acidic protein and telomerase expression increased gradually after injury, peaked at 28 days, and then gradually decreased. Spearman rank correlation showed a positive correlation between glial fibrillary acidic protein expression and telomerase expression in the glial scar. These results suggest that telomerase promotes glial scar formation. Related Articles | Metrics

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A non-opioid pathway for dynorphin-caused spinal cord injury in rats Yu Chen, Liangbi Xiang, Jun Liu, Dapeng Zhou, Hailong Yu, Qi Wang, Wenfeng Han, Mingming Guo 2012, 7 (11):  815-820.  Abstract ( 211 )   PDF (435KB) ( 862 )   Save Intrathecal injection of dynorphin into rats via subarachnoid catheter induces damage to spinal cord tissue and motor function. Injection of the kappa opioid receptor antagonist nor-binaltorphine, or the excitatory amino acid N-methyl-D-aspartate receptor antagonist MK-801 into rats alleviated the pathological changes of dynorphin-caused spinal cord tissue injury and reduced the acid phosphatase activity in the spinal cord. The experimental findings indicate that there are opioid and non-opioid pathways for dynorphin-induced spinal cord injury, and that the non-opioid receptor pathway may be mediated by the excitatory amino acid N-methyl-D-aspartate receptor. References | Related Articles | Metrics

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Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion Hui Zhao, Zhiyong Li, Yali Wang, Qiuxia Zhang 2012, 7 (11):  821-826.  Abstract ( 206 )   PDF (235KB) ( 810 )   Save The present study established a rat model of vascular dementia induced by chronic cerebral hypoperfusion through permanent ligation of bilateral common carotid arteries. At 60 days after modeling, escape latency and swimming path length during hidden-platform acquisition training in Morris water maze significantly increased in the model group. In addition, the number of accurate crossings over the original platform significantly decreased, hippocampal CA1 synaptophysin and growth-associated protein 43 expression significantly decreased, cAMP response element-binding protein expression remained unchanged, and phosphorylated cAMP response element-binding protein expression significantly decreased. Results suggested that abnormal expression of hippocampal synaptic structural protein and cAMP response element-binding protein phosphorylation played a role in cognitive impairment following chronic cerebral hypoperfusion. Related Articles | Metrics

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Propofol effectively inhibits lithium-pilocarpine- induced status epilepticus in rats via downregulation of N-methyl-D-aspartate receptor 2B subunit expression Henglin Wang, Zhuoqiang Wang, Weidong Mi, Cong Zhao, Yanqin Liu, Yongan Wang, Haipeng Sun 2012, 7 (11):  827-832.  Abstract ( 182 )   PDF (222KB) ( 1100 )   Save null References | Related Articles | Metrics

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Ketamine inhibits c-Jun protein expression in mouse hippocampus following cerebral ischemia/reperfusion injury Feng Xiao, Liangzhi Xiong, Qingxiu Wang, Long Zhou, Qingshan Zhou 2012, 7 (11):  833-836.  Abstract ( 189 )   PDF (198KB) ( 764 )   Save A model of cerebral ischemia and reperfusion was established in mice. Mice were treated with ketamine via intraperitoneal injection immediately following ischemia or ischemia/reperfusion. Ketamine did not remarkably change infarct volume in mice immediately following ischemia, but injection immediately following ischemia/reperfusion significantly decreased infarct volume. Ketamine injection immediately after ischemia or ischemia/reperfusion inhibited c-Jun protein expression in mouse hippocampus, but nuclear factor kappa B expression was unaltered. In addition, the Longa scale score for neural impairment was not reduced in mice following cerebral ischemia/reperfusion. These results indicate that ketamine can protect mice against cerebral ischemia and reperfusion injury by modulating c-Jun protein expression in mouse hippocampus. Related Articles | Metrics

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Propofol inhibits inflammation and lipid peroxidation following cerebral ischemia/ reperfusion in rabbits Xiaodong Wei, Xing Wan, Bo Zhao, Jiabao Hou, Min Liu, Bangchang Cheng 2012, 7 (11):  837-841.  Abstract ( 188 )   PDF (153KB) ( 944 )   Save The present study established a rabbit model of global cerebral ischemia using the ‘six-vessel’ method, which was reperfused after 30 minutes of ischemia. Rabbits received intravenous injection of propofol at 5 mg/kg prior to ischemia and 20 mg/kg per hour after ischemia until samples were prepared. Results revealed that propofol inhibited serum interleukin-8, endothelin-1 and malondialdehyde increases and promoted plasma superoxide dismutase activity after cerebral ischemia/reperfusion. In addition, cerebral cortex edema was attenuated with little neuronal nuclear degeneration and pyknosis with propofol treatment. The cross-sectional area of neuronal nuclei was, however, increased following propofol treatment. These findings suggested that propofol could improve anti-oxidant activity and inhibit synthesis of inflammatory factors to exert a protective effect on cerebral ischemia/reperfusion injury. Related Articles | Metrics

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The role of microtubule-associated protein 1B in axonal growth and neuronal migration in the central nervous system* Maoguang Yang, Minfei Wu, Peng Xia, Chunxin Wang, Peng Yan, Qi Gao, Jian Liu, Haitao Wang, Xingwei Duan, Xiaoyu Yang 2012, 7 (11):  842-848.  Abstract ( 200 )   PDF (154KB) ( 908 )   Save In this review, we discuss the role of microtubule-associated protein 1B (MAP1B) and its phosphorylation in axonal development and regeneration in the central nervous system. MAP1B exhibits similar functions during axonal development and regeneration. MAP1B and phosphorylated MAP1B in neurons and axons maintain a dynamic balance between cytoskeletal components, and regulate the stability and interaction of microtubules and actin to promote axonal growth, neural connectivity and regeneration in the central nervous system. Related Articles | Metrics

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Does repair of spinal cord injury follow the evolutionary theory? Zhicheng Zhang, Fang Li, Tiansheng Sun 2012, 7 (11):  849-852.  Abstract ( 180 )   PDF (109KB) ( 784 )   Save Lower vertebrates, such as fish and amphibians, and higher vertebrates in embryonic development can acquire complete regeneration of complex body structures, including the spinal cord, an important part of the central nervous system. However, with species evolution and development, this regenerative capacity gradually weakens and even disappears, but the cellular and molecular mechanisms remain poorly understood. We explored the differences in mechanisms of spinal cord regeneration capability between lower and higher vertebrates, investigated differences in their cellular and molecular mechanisms and between the spinal cord structures of lower vertebrates and mammals, such as rat and monkey, to search for theoretical evidence and therapeutic targets for nerve regeneration in human spinal cord. Related Articles | Metrics

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Effect of age on click-evoked otoacoustic emission A systematic review Jinfeng Liu, Ningyu Wang 2012, 7 (11):  853-861.  Abstract ( 162 )   PDF (234KB) ( 897 )   Save OBJECTIVE: The aims of this study were to investigate the changes of the total intensity of transient evoked otoacoustic emission (TEOAE) and signal-to-noise ratio in various frequency bands as a function of aging, and to explore the role of age-related decline of cochlear outer hair cells. DATA SOURCES: The literature was searched using the PubMed database using ‘transient-evoked otoacoustic emissions’ as a keyword. Articles were limited as follows: Species was ‘Humans’; languages were ‘English and Chinese’; publication date between 1990-01-01 and 2010-12-31. The references of the found were also searched to obtain additional articles. DATA SELECTION: Inclusion criteria: (1) Articles should involve the total TEOAE level or signal-to-noise ratio. (2) The measurement and analysis system used was Otodynamics ILO analysis system (ILO88, ILO92, ILO96 or ILO292). (3) Studies involved groups of greater than 10 subjects and TEOAE results were from normally hearing ears. (4) If more papers from the same author or laboratory analyzed the same subjects, only one was used. MAIN OUTCOME MEASURES: The correlations of the age scale with the total level and signal-to-noise ratio of TEOAE was determined, respectively. RESULTS: (1) TEOAE total level gradually increased until 2 months of age, and then decreased with increasing age. Significant negative correlations between total TEOAE level and age were found (r = -0.885, P = 0.000). (2) The most rapid decrease of TEOAE amplitude occurred at 1 year old. The total TEOAE level decreased about 4.25 dB SPL between 2 months to 1 year old, then about 0.26-0.52 dB SPL from 1 year to 10 years old, about 0.23 dB SPL from 11 years to 25 years old, and about 0.14 dB SPL from 26 years to 60 years old. (3) The signal-to-noise ratio in the frequency bands centered at 1.5, 2, 3 and 4 kHz decreased with increasing age after 2 months of age. Significant negative correlations between the signal-to-noise ratio and age were found for frequency bands ranging from 1.5 kHz to 4 kHz, with the highest correlations at 4 kHz (r = -0.890, P < 0.01), then at 3 kHz (r = -0.889, P < 0.01), at 2 kHz (r = -0.850, P < 0.01) and at 1.5 kHz (r = -0.705, P < 0.05). Conversely, a positive correlation between the signal-to-noise ratio centered at 1 kHz and age was found, but was not statistically significant (r = 0.298, P = 0.374). CONCLUSION: The total TEOAE response level decreased with increasing age after the first 2 months of age. The signal-to-noise ratio also decreased with increasing age in frequency bands above 1.5 kHz. The signal-to-noise ratio in higher frequencies decreased faster than in lower frequencies, leading to the maximum signal-to-noise ratio shift form 3.2-4.0 kHz in neonates to 1.5 kHz in adults, and further decreasing the total TEOAE response level. The age-related TEOAE spectrum peak shift is most likely because the outer hair cells functioning in higher frequencies are more prone to damage than those for lower frequencies. Related Articles | Metrics

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Department of Rheumatism, Shengjing Hospital, China Medical University, Shenyang 110004, Liaoning Province, China Naizhi Wang, Yingying Guo, Lili Yang, Wenyi Fu, Yanbing Xu, Linxin Hou, Shuai Zhao, Ning Zhang 2012, 7 (11):  862-866.  Abstract ( 274 )   PDF (121KB) ( 992 )   Save In this historical cohort study, 236 patients with primary rheumatoid arthritis were treated with the tumor necrosis factor inhibitors, etanercept or infliximab (n = 80), or by conventional methods (n = 156). Results revealed that 11 patients developed varying types of peripheral neuropathy at 1-2 years post-treatment (mean 16 months). The incidence of peripheral neuropathy in the tumor necrosis factor inhibitors treatment group was 8.8% (7/80), which was significantly higher than the conventional treatment group (2.6%; 4/156). The relative risk of developing peripheral neuropathy in the tumor necrosis factor inhibitors treatment group was 3.41 (95% confidence interval: 1.03-11.31). Comparison of the tumor necrosis factor inhibitors revealed that etanercept and infliximab had no significant difference in terms of inducing peripheral neuropathy. Experimental findings indicate that tumor necrosis factor inhibitors may increase the risk of peripheral neuropathy. Related Articles | Metrics

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Remodeling of motor cortex function in acute cerebral infarction patients following human urinary kallidinogenase A functional magnetic resonance imaging evaluation after 6 months Xuezhu Song, Lixin Han, Yan Liu 2012, 7 (11):  867-873.  Abstract ( 203 )   PDF (270KB) ( 852 )   Save A total of 29 patients were treated within 48 hours after acute subcortical cerebral infarction with Xuesaitong or Xuesaitong plus human urinary kallidinogenase for 14 days. Neurological deficits, activity of daily living, and evaluations of distal upper limb motor functions at the 6-month follow-up showed that patients treated with Xuesaitong plus human urinary kallidinogenase recovered better than with Xuesaitong alone. In addition, functional MRI revealed that activation sites were primarily at the ipsilesional side of injury in all patients. Human urinary kallidinogenase induced hyperactivation of the ipsilesional primary sensorimotor cortex, premotor cortex, supplementary motor area, and contralesional posterior parietal cortex. Results showed that human urinary kallidinogenase improved symptoms of neurological deficiency by enhancing remodeling of long-term cortical motor function in patients with acute cerebral infarction. Related Articles | Metrics

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Levels of soluble delta-like ligand 1 in the serum and cerebrospinal fluid of tuberculous meningitis patients Jinghong Li, Jinyi Li, Yanjie Jia 2012, 7 (11):  874-878.  Abstract ( 166 )   PDF (215KB) ( 824 )   Save In this study, the levels of soluble delta-like ligand 1 in cerebrospinal fluid and serum of 50 patients with tuberculous meningitis, 30 patients with viral meningitis, 20 patients with purulent meningitis and 40 subjects without central nervous system disease were determined using an enzyme-linked immunosorbent assay. The mean levels of soluble delta-like ligand 1 in both cerebrospinal fluid and serum from patients with tuberculous meningitis were significantly higher compared with those from patients with viral meningitis or purulent meningitis or from subjects without central nervous system disease. Meanwhile, the level of soluble delta-like ligand 1 gradually decreased as tuberculous meningitis patients recovered. If patients deteriorated after treatment, the level of soluble delta-like ligand 1 in cerebrospinal fluid gradually increased. There was no correlation between the level of soluble delta-like ligand 1 and the protein level/cell number in cerebrospinal fluid. Our findings indicate that the levels of soluble delta-like ligand 1 in cerebrospinal fluid and serum are reliable markers for the diagnosis of tuberculous meningitis and for monitoring treatment progress. At the same time, this index is not influenced by protein levels or cell numbers in cerebrospinal fluid. Related Articles | Metrics