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    20 March 2015, Volume 10 Issue 3 Previous Issue    Next Issue
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    RAFting the rapids of axon regeneration signaling
    Jian Zhong
    2015, 10 (3):  341-343.  doi: 10.4103/1673-5374.153670
    Abstract ( 219 )   PDF (819KB) ( 740 )   Save
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    TAM receptors: two pathways to regulate adult neurogenesis
    Kassandra Johnson, Rui Ji
    2015, 10 (3):  344-345.  doi: 10.4103/1673-5374.153671
    Abstract ( 214 )   PDF (188KB) ( 792 )   Save
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    Targeting the body to protect the brain: inducing neuroprotection with remotely-applied near infrared light
    Daniel M. Johnstone, John Mitrofanis, Jonathan Stone
    2015, 10 (3):  349-351.  doi: 10.4103/1673-5374.153673
    Abstract ( 234 )   PDF (246KB) ( 690 )   Save
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    Functional regeneration of the brain: white matter matters
    Teng Guan, Jiming Kong
    2015, 10 (3):  355-356.  doi: 10.4103/1673-5374.153675
    Abstract ( 363 )   PDF (333KB) ( 1351 )   Save
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    Empowering sonic hedgehog to rescue brain cells after ischemic stroke
    Olga V. Chechneva, Wenbin Deng
    2015, 10 (3):  360-362.  doi: 10.4103/1673-5374.153677
    Abstract ( 216 )   PDF (315KB) ( 685 )   Save
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    Current view of neurotransmitter changes underlying tinnitus
    Augustine C. Lee, Donald A. Godfrey
    2015, 10 (3):  368-370.  doi: 10.4103/1673-5374.153680
    Abstract ( 258 )   PDF (365KB) ( 708 )   Save
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    Radial glia interact with primary olfactory axons to regulate development of the olfactory bulb
    Daniel A. Amaya, Jenny A.K. Ekberg, James A. St John
    2015, 10 (3):  374-376.  doi: 10.4103/1673-5374.153706
    Abstract ( 200 )   PDF (454KB) ( 643 )   Save
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    Tamoxifen and Src kinase inhibitors as neuroprotective/neuroregenerative drugs after spinal cord injury
    Iris K. Salgado, Aranza I. Torrado, Jose M. Santiago, Jorge D. Miranda
    2015, 10 (3):  385-390.  doi: 10.4103/1673-5374.153685
    Abstract ( 240 )   PDF (461KB) ( 765 )   Save

    Spinal cord injury (SCI) is a devastating condition that produces significant changes in the lifestyle of patients. Many molecular and cellular events are triggered after the initial physical impact to the cord. Two major phases have been described in the field of SCI: an acute phase and late phase. Most of the therapeutic strategies are focused on the late phase because this provides an opportunity to target cellular events like apoptosis, demyelination, scar formation and axonal outgrowth. In this mini-review, we will focus on two agents (tamoxifen and a Src kinase family inhibitor known as PP2) that have been shown in our laboratory to produce neuroprotective (increase cell survival) and/or regenerative (axonal outgrowth) actions. The animal model used in our laboratory is adult female rat (~250 g) with a moderate contusion (12.5 mm) to the spinal cord at the T10 level, using the MASCIS impactor device. Tamoxifen or PP2 was administered by implantation of a 15 mg pellet (Innovative Research of America, Sarasota, FL, USA) or by intraperitoneal injections (1.5 mg/kg, every 3 days), respectively, to produce a long-term effect (28 days). Tamoxifen and the Src kinase inhibitor, PP2, are drugs that in rats with a moderate spinal cord injury promote functional locomotor recovery, increase spared white matter tissue, and stimulate axonal outgrowth. Moreover, tamoxifen reduces the formation of reactive oxygen species. Therefore, these drugs are possible therapeutic agents that have a neuroprotective/regenerative activity in vertebrates with SCI.

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    A new look at auranofin, dextromethorphan and rosiglitazone for reduction of glia-mediated inflammation in neurodegenerative diseases
    Jocelyn M. Madeira, Stephanie M. Schindler, Andis Klegeris
    2015, 10 (3):  391-393.  doi: 10.4103/1673-5374.153686
    Abstract ( 230 )   PDF (129KB) ( 813 )   Save

    Neurodegenerative disorders including Alzheimer’s disease are characterized by chronic inflammation in the central nervous system. The two main glial types involved in inflammatory reactions are microglia and astrocytes. While these cells normally protect neurons by providing nutrients and growth factors, disease specific stimuli can induce glial secretion of neurotoxins. It has been hypothesized that reducing glia-mediated inflammation could diminish neuronal loss. This hypothesis is supported by observations that chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) is linked with lower incidences of neurodegenerative disease. It is possible that the NSAIDs are not potent enough to appreciably reduce chronic neuroinflammation after disease processes are fully established. Gold thiol compounds, including auranofin, comprise another class of medications effective at reducing peripheral inflammation. We have demonstrated that auranofin inhibits human microglia- and astrocyte-mediated neurotoxicity. Other drugs which are currently used to treat peripheral inflammatory conditions could be helpful in neurodegenerative disease. Three different classes of anti-inflammatory compounds, which have a potential to inhibit neuroinflammation are highlighted below.

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    Electroacupuncture in the repair of spinal cord injury: inhibiting the Notch signaling pathway and promoting neural stem cell proliferation
    Xin Geng, Tao Sun, Jing-hui Li, Ning Zhao, Yong Wang, Hua-lin Yu
    2015, 10 (3):  394-403.  doi: 10.4103/1673-5374.153687
    Abstract ( 228 )   PDF (3408KB) ( 916 )   Save

    Electroacupuncture for the treatment of spinal cord injury has a good clinical curative effect, but the underlying mechanism is unclear. In our experiments, the spinal cord of adult Sprague-Dawley rats was clamped for 60 seconds. Dazhui (GV14) and Mingmen (GV4) acupoints of rats were subjected to electroacupuncture. Enzyme-linked immunosorbent assay revealed that the expression of serum inflammatory factors was apparently downregulated in rat models of spinal cord injury after electroacupuncture. Hematoxylin-eosin staining and immunohistochemistry results demonstrated that electroacupuncture contributed to the proliferation of neural stem cells in rat injured spinal cord, and suppressed their differentiation into astrocytes. Real-time quantitative PCR and western blot assays showed that electroacupuncture inhibited activation of the Notch signaling pathway induced by spinal cord injury. These findings indicate that electroacupuncture repaired the injured spinal cord by suppressing the Notch signaling pathway and promoting the proliferation of endogenous neural stem cells.

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    Visual bone marrow mesenchymal stem cell transplantation in the repair of spinal cord injury
    Rui-ping Zhang, Cheng Xu, Yin Liu, Jian-ding Li, Jun Xie
    2015, 10 (3):  404-411.  doi: 10.4103/1673-5374.153688
    Abstract ( 222 )   PDF (2990KB) ( 897 )   Save

    An important factor in improving functional recovery from spinal cord injury using stem cells is maximizing the number of transplanted cells at the lesion site. Here, we established a contusion model of spinal cord injury by dropping a weight onto the spinal cord at T7–8. Superparamagnetic iron oxide-labeled bone marrow mesenchymal stem cells were transplanted into the injured spinal cord via the subarachnoid space. An outer magnetic field was used to successfully guide the labeled cells to the lesion site. Prussian blue staining showed that more bone marrow mesenchymal stem cells reached the lesion site in these rats than in those without magnetic guidance or superparamagnetic iron oxide labeling, and immunofluorescence revealed a greater number of complete axons at the lesion site. Moreover, the Basso, Beattie and Bresnahan (BBB) locomotor rating scale scores were the highest in rats with superparamagnetic labeling and magnetic guidance. Our data confirm that superparamagnetic iron oxide nanoparticles effectively label bone marrow mesenchymal stem cells and impart sufficient magnetism to respond to the external magnetic field guides. More importantly, superparamagnetic iron oxide-labeled bone marrow mesenchymal stem cells can be dynamically and non-invasively tracked in vivo using magnetic resonance imaging. Superparamagnetic iron oxide labeling of bone marrow mesenchymal stem cells coupled with magnetic guidance offers a promising avenue for the clinical treatment of spinal cord injury.

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    Feasibility of 3.0 T diffusion-weighted nuclear magnetic resonance imaging in the evaluation of functional recovery of rats with complete spinal cord injury
    Duo Zhang, Xiao-hui Li, Xu Zhai, Xi-jing He
    2015, 10 (3):  412-418.  doi: 10.4103/1673-5374.153689
    Abstract ( 212 )   PDF (1865KB) ( 1040 )   Save

    Diffusion tensor imaging is a sensitive way to reflect axonal necrosis and degeneration, glial cell regeneration and demyelination following spinal cord injury, and to display microstructure changes in the spinal cord in vivo. Diffusion tensor imaging technology is a sensitive method to diagnose spinal cord injury; fiber tractography visualizes the white matter fibers, and directly displays the structural integrity and resultant damage of the fiber bundle. At present, diffusion tensor imaging is restricted to brain examinations, and is rarely applied in the evaluation of spinal cord injury. This study aimed to explore the fractional anisotropy and apparent diffusion coefficient of diffusion tensor magnetic resonance imaging and the feasibility of diffusion tensor tractography in the evaluation of complete spinal cord injury in rats. The results showed that the average combined scores were obviously decreased after spinal cord transection in rats, and then began to increase over time. The fractional anisotropy scores after spinal cord transection in rats were significantly lower than those in normal rats (P < 0.05); the apparent diffusion coefficient was significantly increased compared with the normal group (P < 0.05). Following spinal cord transection, fractional anisotropy scores were negatively correlated with apparent diffusion coefficient values (r = –0.856, P < 0.01), and positively correlated with the average combined scores (r = 0.943, P < 0.01), while apparent diffusion coefficient values had a negative correlation with the average combined scores (r = –0.949, P < 0.01). Experimental findings suggest that, as a non-invasive examination, diffusion tensor magnetic resonance imaging can provide qualitative and quantitative information about spinal cord injury. The fractional anisotropy score and apparent diffusion coefficient have a good correlation with the average combined scores, which reflect functional recovery after spinal cord injury.

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    Changes in the blood-nerve barrier after sciatic nerve cold injury: indications supporting early treatment
    Hao Li, Jian-ping Jia, Min Xu, Lei Zhang
    2015, 10 (3):  419-424.  doi: 10.4103/1673-5374.153690
    Abstract ( 155 )   PDF (2904KB) ( 897 )   Save

    Severe edema in the endoneurium can occur after non-freezing cold injury to the peripheral nerve, which suggests damage to the blood-nerve barrier. To determine the effects of cold injury on the blood-nerve barrier, the sciatic nerve on one side of Wistar rats was treated with low temperatures (3–5°C) for 2 hours. The contralateral sciatic nerve was used as a control. We assessed changes in the nerves using Evans blue as a fluid tracer and morphological methods. Excess fluid was found in the endoneurium 1 day after cold injury, though the tight junctions between cells remained closed. From 3 to 5 days after the cold injury, the fluid was still present, but the tight junctions were open. Less tracer leakage was found from 3 to 5 days after the cold injury compared with 1 day after injury. The cold injury resulted in a breakdown of the blood-nerve barrier function, which caused endoneurial edema. However, during the early period, the breakdown of the blood-nerve barrier did not include the opening of tight junctions, but was due to other factors. Excessive fluid volume produced a large increase in the endoneurial fluid pressure, prevented liquid penetration into the endoneurium from the microvasculature. These results suggest that drug treatment to patients with cold injuries should be administered during the early period after injury because it may be more difficult for the drug to reach the injury site through the microcirculation after the tissue fluid pressure becomes elevated.

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    Gene transfection mediated by polyethyleneimine-polyethylene glycol nanocarrier prevents cisplatin-induced spiral ganglion cell damage
    Guan-gui Chen, Min Mao, Li-zi Qiu, Qi-ming Liu
    2015, 10 (3):  425-431.  doi: 0.4103/1673-5374.153691
    Abstract ( 231 )   PDF (1679KB) ( 637 )   Save

    Polyethyleneimine-polyethylene glycol (PEI-PEG), a novel nanocarrier, has been used for transfection and gene therapy in a variety of cells. In our previous study, we successfully carried out PEI-PEG-mediated gene transfer in spiral ganglion cells. It remains unclear whether PEI-PEG could be used for gene therapy with X-linked inhibitor of apoptosis protein (XIAP) in the inner ear. In the present study, we performed PEI-PEG-mediated XIAP gene transfection in the cochlea of Sprague-Dawley rats, via scala tympani fenestration, before daily cisplatin injections. Auditory brainstem reflex tests demonstrated the protective effects of XIAP gene therapy on auditory function. Immunohistochemical staining revealed XIAP protein expression in the cytoplasm of cells in the spiral ganglion, the organ of Corti and the stria vascularis. Reverse transcription-PCR detected high levels of XIAP mRNA expression in the cochlea. The present findings suggest that PEI-PEG nanocarrier-mediated XIAP gene transfection results in XIAP expression in the cochlea, prevents damage to cochlear spiral ganglion cells, and protects hearing.

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    c-Jun N-terminal kinase 3 expression in the retina of ocular hypertension mice: a possible target to reduce ganglion cell apoptosis
    Yue He, Jie Chen, Shu-guang Zhang, Yuan-sheng Yuan, Yan Li, Hong-bin Lv, Jin-hua Gan
    2015, 10 (3):  432-437.  doi: 10.4103/1673-5374.153692
    Abstract ( 158 )   PDF (1707KB) ( 796 )   Save

    Glaucoma, a type of optic neuropathy, is characterized by the loss of retinal ganglion cells. It remains controversial whether c-Jun N-terminal kinase (JNK) participates in the apoptosis of retinal ganglion cells in glaucoma. This study sought to explore a possible mechanism of action of JNK signaling pathway in glaucoma-induced retinal optic nerve damage. We established a mouse model of chronic ocular hypertension by reducing the aqueous humor followed by photocoagulation using the laser ignition method. Results showed significant pathological changes in the ocular tissues after the injury. Apoptosis of retinal ganglion cells increased with increased intraocular pressure, as did JNK3 mRNA expression in the retina. These data indicated that the increased expression of JNK3 mRNA was strongly associated with the increase in intraocular pressure in the retina, and correlated positively with the apoptosis of retinal ganglion cells.

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    Neuroprotective effects of SMADs in a rat model of cerebral ischemia/reperfusion
    Fang-fang Liu, Chao-ying Liu, Xiao-ping Li, Sheng-zhe Zheng, Qing-quan Li, Qun Liu, Lei Song
    2015, 10 (3):  438-444.  doi: 10.4103/1673-5374.153693
    Abstract ( 204 )   PDF (666KB) ( 755 )   Save

    Previous studies have shown that up-regulation of transforming growth factor β1 results in neuroprotective effects. However, the role of the transforming growth factor β1 downstream molecule, SMAD2/3, following ischemia/reperfusion remains unclear. Here, we investigated the neuroprotective effects of SMAD2/3 by analyzing the relationships between SMAD2/3 expression and cell apoptosis and inflammation in the brain of a rat model of cerebral ischemia/reperfusion. Levels of SMAD2/3 mRNA were up-regulated in the ischemic penumbra 6 hours after cerebral ischemia/reperfusion, reached a peak after 72 hours and were then decreased at 7 days. Phosphorylated SMAD2/3 protein levels at the aforementioned time points were consistent with the mRNA levels. Over-expression of SMAD3 in the brains of the ischemia/reperfusion model rats via delivery of an adeno-associated virus containing the SMAD3 gene could reduce tumor necrosis factor-α and interleukin-1β mRNA levels, down-regulate expression of the pro-apoptotic gene, capase-3, and up-regulate expression of the anti-apoptotic protein, Bcl-2. The SMAD3 protein level was negatively correlated with cell apoptosis. These findings indicate that SMAD3 exhibits neuroprotective effects on the brain after ischemia/reperfusion through anti-inflammatory and anti-apoptotic pathways.

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    Chinese herbal formula Tongluo Jiunao injection protects against cerebral ischemia by activating neurotrophin 3/tropomyosin-related kinase C pathway
    Peiman Alesheikh, Arezou Mashoufi, Hui-ling Tang, Wei Zhang, Bo Di, Yang-yang Yan, Peng-tao Li, Yan-shu Pan
    2015, 10 (3):  445-450.  doi: 10.4103/1673-5374.153694
    Abstract ( 240 )   PDF (1474KB) ( 676 )   Save

    The Chinese herbal formula Tongluo Jiunao, containing the active components Panax notoginseng and Gardenia jasminoides, has recently been patented and is in use clinically. It is known to be neuroprotective in cerebral ischemia, but the underlying pathway remains poorly understood. In the present study, we established a rat model of cerebral ischemia by occlusion of the middle cerebral artery, and administered Tongluo Jiunao, a positive control (Xuesai Tong, containing Panax notoginseng) or saline intraperitoneally to investigate the pathway involved in the action of Tongluo Jiunao injection. 2,3,5-Triphenyltetrazolium chloride (TTC) staining showed that the cerebral infarct area was significantly smaller in model rats that received Tongluo Jiunao than in those that received saline. Enzyme-linked immunosorbent assay revealed significantly greater expression of neurotrophin 3 and growth-associated protein 43 in ischemic cerebral tissue, and serum levels of neurotrophin 3, in the Tongluo Jiunao group than in the saline group. The reverse transcription polymerase chain reaction and immunohistochemical staining showed that after treatment with Tongluo Jiunao or Xuesai Tong, tropomyosin-related kinase C gene expression and immunoreactivity were significantly elevated compared with saline, with the greatest expression observed after Tongluo Jiunao treatment. These findings suggest that Tongluo Jiunao injection exerts a neuroprotective effect in rats with cerebral ischemia by activating the neurotrophin 3/tropomyosin-related kinase C pathway.

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    Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes
    Sang Gun Lee, Dae Young Yoo, Hyo Young Jung, Sung Min Nam, Jong Whi Kim, Jung Hoon Choi, Sun Shin Yi, Moo-Ho Won,Yeo Sung Yoon, In Koo Hwang, Seung Myung Moon
    2015, 10 (3):  451-456.  doi: 10.4103/1673-5374.153695
    Abstract ( 198 )   PDF (1816KB) ( 720 )   Save

    In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7–21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

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    Acupuncture inhibits Notch1 and Hes1 protein expression in the basal ganglia of rats with cerebral hemorrhage
    Wei Zou Qiu-xin Chen, Xiao-wei Sun, Qing-bin Chi, Hong-yu Kuang, Xue-ping Yu, Xiao-hong Dai
    2015, 10 (3):  457-462.  doi: 10.4103/1673-5374.153696
    Abstract ( 232 )   PDF (2203KB) ( 851 )   Save

    Notch pathway activation maintains neural stem cells in a proliferating state and increases nerve repair capacity. To date, studies have rarely focused on changes or damage to signal transduction pathways during cerebral hemorrhage. Here, we examined the effect of acupuncture in a rat model of cerebral hemorrhage. We examined four groups: in the control group, rats received no treatment. In the model group, cerebral hemorrhage models were established by infusing non-heparinized blood into the brain. In the acupuncture group, modeled rats had Baihui (DU20) and Qubin (GB7) acupoints treated once a day for 30 minutes. In the DAPT group, modeled rats had 0.15 µg/mL DAPT solution (10 mL) infused into the brain. Immunohistochemistry and western blot results showed that acupuncture effectively inhibits Notch1 and Hes1 protein expression in rat basal ganglia. These inhibitory effects were identical to DAPT, a Notch signaling pathway inhibitor. Our results suggest that acupuncture has a neuroprotective effect on cerebral hemorrhage by inhibiting Notch-Hes signaling pathway transduction in rat basal ganglia after cerebral hemorrhage

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    Is effect of transcranial direct current stimulation on visuomotor coordination dependent on task difficulty?
    Yong Hyun Kwon, Kyung Woo Kang, Sung Min Son, Na Kyung Lee
    2015, 10 (3):  463-466.  doi: 10.4103/1673-5374.153697
    Abstract ( 244 )   PDF (148KB) ( 626 )   Save

    Transcranial direct current stimulation (tDCS), an emerging technique for non-invasive brain stimulation, is increasingly used to induce changes in cortical excitability and modulate motor behavior, especially for upper limbs. The purpose of this study was to investigate the effects of tDCS of the primary motor cortex on visuomotor coordination based on three levels of task difficulty in healthy subjects. Thirty-eight healthy participants underwent real tDCS or sham tDCS. Using a single-blind, sham-controlled crossover design, tDCS was applied to the primary motor cortex. For real tDCS conditions, tDCS intensity was 1 mA while stimulation was applied for 15 minutes. For the sham tDCS, electrodes were placed in the same position, but the stimulator was turned off after 5 seconds. Visuomotor tracking task, consisting of three levels (levels 1, 2, 3) of difficulty with higher level indicating greater difficulty, was performed before and after tDCS application. At level 2, real tDCS of the primary motor cortex improved the accurate index compared to the sham tDCS. However, at levels 1 and 3, the accurate index was not significantly increased after real tDCS compared to the sham tDCS. These findings suggest that tasks of moderate difficulty may improve visuomotor coordination in healthy subjects when tDCS is applied compared with easier or more difficult tasks.

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    Ulinastatin suppresses endoplasmic reticulum stress and apoptosis in the hippocampus of rats with acute paraquat poisoning
    Hai-feng Li, Shi-xing Zhao, Bao-peng Xing, Ming-li Sun
    2015, 10 (3):  467-472.  doi: 10.4103/1673-5374.153698
    Abstract ( 168 )   PDF (1248KB) ( 1029 )   Save

    Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline. Hematoxylin-eosin staining showed that most hippocampal cells were contracted and nucleoli had disappeared in the paraquat group. Fewer cells in the hippocampus were concentrated and nucleoli had disappeared in the ulinastatin group. Western blot assay showed that expressions of GRP78 and cleaved-caspase-3 were significantly lower in the ulinastatin group than in the paraquat group. Immunohistochemical findings showed that CHOP immunoreactivity was significantly lower in the ulinastatin group than in the paraquat group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining showed that the number of apoptotic cells was reduced in the paraquat and ulinastatin groups. These data confirmed that endoplasmic reticular stress can be induced by acute paraquat poisoning. Ulinastatin can effectively inhibit this stress as well as cell apoptosis, thereby exerting a neuroprotective effect.

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    Connecting the P300 to the diagnosis and prognosis of unconscious patients
    Ran Li, Wei-qun Song, Ju-bao Du, Su Huo, Gui-xiang Shan
    2015, 10 (3):  473-480.  doi: 10.4103/1673-5374.153699
    Abstract ( 182 )   PDF (496KB) ( 668 )   Save

    The residual consciousness of unconscious patients can be detected by studying the P300, a wave among event-related potentials. Previous studies have applied tones, the subject’s name and other names as stimuli. However, the results were not satisfactory. In this study, we changed the constituent order of subjects’ two-character names to create derived names. The subject’s derived names, together with tones and their own names, were used as auditory stimuli in event-related potential experiments. Healthy controls and unconscious patients were included in this study and made to listen to these auditory stimuli. In the two paradigms, a sine tone followed by the subject’s own name and the subject’s derived name followed by the subject’s own name were used as standard and deviant stimuli, respectively. The results showed that all healthy controls had the P300 using both paradigms, and that the P300 in the second paradigm had a longer latency and two peaks. All minimally conscious state patients had the P300 in the first paradigm and the majority of them had the P300 in the second paradigm. Most vegetative state patients had no P300. Patients who showed the P300 in the two paradigms had more residual consciousness, and patients with the two-peak P300 had a higher probability of awakening within a short time. Our experimental findings suggest that the P300 event-related potential could reflect the conscious state of unconscious patients.

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    Curcumin pretreatment and post-treatment both improve the antioxidative ability of neurons with oxygen-glucose deprivation
    Jing-xian Wu, Lu-yu Zhang, Yan-lin Chen, Shan-shan Yu, Yong Zhao, Jing Zhao
    2015, 10 (3):  481-489.  doi: 10.4103/1673-5374.153700
    Abstract ( 283 )   PDF (1236KB) ( 834 )   Save

    Recent studies have shown that induced expression of endogenous antioxidative enzymes thr-ough activation of the antioxidant response element/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway may be a neuroprotective strategy. In this study, rat cerebral cortical neurons cultured in vitro were pretreated with 10 μM curcumin or post-treated with 5 μM curcumin, respectively before or after being subjected to oxygen-glucose deprivation and reoxygenation for 24 hours. Both pretreatment and post-treatment resulted in a significant decrease of cell injury as indicated by propidium iodide/Hoechst 33258 staining, a prominent increase of Nrf2 protein expression as indicated by western blot analysis, and a remarkable increase of protein expression and enzyme activity in whole cell lysates of thioredoxin before ischemia, after ischemia, and after reoxygenation. In addition, post-treatment with curcumin inhibited early DNA/RNA oxidation as indicated by immunocytochemistry and increased nuclear Nrf2 protein by inducing nuclear accumulation of Nrf2. These findings suggest that curcumin activates the expression of thioredoxin, an antioxidant protein in the Nrf2 pathway, and protects neurons from death caused by oxygen-glucose deprivation in an in vitro model of ischemia/reperfusion. We speculate that pharmacologic stimulation of antioxidant gene expression may be a promising approach to neuroprotection after cerebral ischemia.

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    Compensatory recombination phenomena of neurological functions in central dysphagia patients
    Xiao-dong Yuan, Li-fu Zhou, Shu-juan Wang, Yan-sheng Zhao, Xiao-jie Wang, Li-li Zhang, Shou-hong Wang, Ya-jie Zhang, Li Chen
    2015, 10 (3):  490-497.  doi: 10.4103/1673-5374.153701
    Abstract ( 153 )   PDF (958KB) ( 656 )   Save

    We speculate that cortical reactions evoked by swallowing activity may be abnormal in patients with central infarction with dysphagia. The present study aimed to detect functional imaging features of cerebral cortex in central dysphagia patients by using blood oxygen level-dependent functional magnetic resonance imaging techniques. The results showed that when normal controls swallowed, primary motor cortex (BA4), insula (BA13), premotor cortex (BA6/8), supramarginal gyrus (BA40), and anterior cingulate cortex (BA24/32) were activated, and that the size of the activated areas were larger in the left hemisphere compared with the right. In recurrent cerebral infarction patients with central dysphagia, BA4, BA13, BA40 and BA6/8 areas were activated, while the degree of activation in BA24/32 was decreased. Additionally, more areas were activated, including posterior cingulate cortex (BA23/31), visual association cortex (BA18/19), primary auditory cortex (BA41) and parahippocampal cortex (BA36). Somatosensory association cortex (BA7) and left cerebellum in patients with recurrent cerebral infarction with central dysphagia were also activated. Experimental findings suggest that the cerebral cortex has obvious hemisphere lateralization in response to swallowing, and patients with recurrent cerebral infarction with central dysphagia show compensatory recombination phenomena of neurological functions. In rehabilitative treatment, using the favorite food of patients can stimulate swallowing through visual, auditory, and other nerve conduction pathways, thus promoting compensatory recombination of the central cortex functions.

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    What drives progressive motor deficits in patients with acute pontine infarction?
    Jue-bao Li, Rui-dong Cheng, Liang Zhou, Wan-shun Wen, Gen-ying Zhu, Liang Tian, Xiang-ming Ye
    2015, 10 (3):  501-504.  doi: 10.4103/1673-5374.153703
    Abstract ( 187 )   PDF (220KB) ( 1420 )   Save

    Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be responsible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.

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