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1. An optimized flow cytometry based assay for detection of aquaporin-4 M1 antibody in demyelinating disorders of the central nervous system | |||
Jin Weina,Li Yujing,Yang Chun-sheng,Qi Yuan,Fu Ying,Li Minshu,Yan Yaping | |||
Clinical Medicine 26 May 2016 | |||
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Abstract: BACKGROUND: Several techniques have been developed for NMO-IgG detection but the sensitivity needs to be improved. Furthermore, the relevance of serostatus with clinical features and diagnosis need further multi-center comparative studies. OBJECTIVE: To set up a flow cytometry based assay (FACS) for detecting AQP4-M1 antibody in demyelinating disorders of the central nervous system and further define its clinical use. METHODS: The NMO-IgG in 309 patients and healthy subjects from six clinical centers was detected by a modified FACS assay which using AQP4-M1-EGFP stably transfected 293T as antigen harboring cells. The assay's reliability was evaluated by compared with in-house cell-based assay (CBA), ELISA and commercial Euroimmun CBA assay. RESULTS: This FACS assay yielded a high sensitivity (77.5%) and specificity (100%) for AQP4-M1 detection of NMOSD patients. A good diagnostic potential was demonstrated by high ROC curves (0.964), 100% inter-laboratory reproducibility, and short detection time (2 hours). 7.5%-11.4% of patients originally detected as seronegative by in-house CBA or Euroimmun CBA was positive by FACS. 15.8% of NMO patients were seronegative even combining the results of CBA and FACS assays. CONCLUSIONS: The optimized FACS assay for AQP4 M1 might be a feasible tool for aiding NMOSD diagnosis. | |||
TO cite this article:Jin Weina,Li Yujing,Yang Chun-sheng, et al. An optimized flow cytometry based assay for detection of aquaporin-4 M1 antibody in demyelinating disorders of the central nervous system[OL].[26 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4692150 |
2. Glibenclamide Improves Survival and Neurological Outcome after Cardiac Arrest in Rats | |||
Huang Kaibin,Gu Yong,Hu Yafang,Ji Zhong,Wang Shengnan,Lin Zhenzhou,Li Xing,Xie Zuoshan,Pan Suyue | |||
Clinical Medicine 21 May 2016 | |||
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Abstract: Objectives: Glibenclamide (GBC) confers neuroprotection in animal models as well as retrospective clinical studies. This study determines whether GBC improves outcome after cardiac arrest in rats. Methods and Results: Male Sprague-Dawley rats successfully resuscitated from 8-min asphyxial cardiac arrest were randomized to GBC or Vehicle group. Rats in the GBC group were intraperitoneally administered GBC with a loading dose of 10 μg/kg at 10 mins and a maintenance dose of 1.2 μg at 6, 12, 18, and 24 hrs after return of spontaneous circulation (ROSC), while rats in the Vehicle group received equivalent volume of vehicle solution. Survival was recorded every day and neurologic deficit scores were assessed at 24, 48, 72 hrs and 7 days after ROSC (n = 22 in each group). Results showed that GBC treatment increased 7-day survival rate, reduced neurologic deficit scores and prevented neuronal loss in the hippocampal CA1 region. To investigate the neuroprotective effects of GBC in acute phase, we observed neuronal injury at 24 hrs after ROSC, and found that GBC significantly decreased the rate of neuronal necrosis and apoptosis. In addition, GBC reduced the mRNA expression of tumor necrosis factor α and monocyte chemoattractant protein-1 in the cortex after ROSC. Furthermore, the sulfonylurea receptor 1 and transient receptor potential M4 heteromers, the putative therapeutic targets of GBC, were up-regulated after cardiac arrest and cardiopulmonary resuscitation, indicating that they might be involved in neuroprotective effect of GBC. Conclusions: GBC treatment substantially improved survival and neurological outcome throughout a 7-day period after ROSC. The salutary effects of GBC was associated with suppression of neuronal necrosis and apoptosis, as well as inflammation in the brain. | |||
TO cite this article:Huang Kaibin,Gu Yong,Hu Yafang, et al. Glibenclamide Improves Survival and Neurological Outcome after Cardiac Arrest in Rats[OL].[21 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693594 |
3. Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury | |||
Gao Xiaoya,Huang Jianou,Hu Yafang,Gu Yong,Zhu Shuzhen,Huang Kaibin,Chen Jinyu,Pan Suyue | |||
Clinical Medicine 21 May 2016 | |||
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Abstract:Co-treatment of neuroprotective reagents may improve the therapeutic efficacy of hypothermia in protecting neurons during ischemic stroke. This study aimed to find promising drugs that enhance the neuroprotective effect of mild hypothermia (MH). 26 candidate drugs were selected based on different targets. Primary cultured cortical neurons were exposed to oxygen-glucose deprivation and reoxygenation (OGD/R) to induce neuronal damage, followed by either single treatment (a drug or MH) or a combination of a drug and MH. Results showed that, compared with single treatment, combination of MH with brain derived neurotrophic factor, glibenclamide, dizocilpine, human urinary kallidinogenase or neuroglobin displayed higher proportion of neuronal cell viability. The latter three drugs also caused less apoptosis rate in combined treatment. Furthermore, co-treatment of those three drugs and MH decreased the level of reactive oxygen species (ROS) and intracellular calcium accumulation, as well as stabilized mitochondrial membrane potential (MMP), indicating the combined neuroprotective effects are probably via inhibiting mitochondrial apoptosis pathway. Taken together, the study suggests that combined treatment with hypothermia and certain neuroprotective reagents provide a better protection against OGD/R-induced neuronal injury. | |||
TO cite this article:Gao Xiaoya,Huang Jianou,Hu Yafang, et al. Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury[OL].[21 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4687456 |
4. Intermittent hypothermia is neuroprotective in an in vitro model of ischemic stroke | |||
Xu Suiyi,Hu Yafang,Li Weiping,Wu Yongming,Ji Zhong,Wang Shengnan,Li Ke,Pan Suyue | |||
Clinical Medicine 11 May 2016 | |||
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Abstract:OBJECTIVE:To investigate whether the intermittent hypothermia (IH) protects neurons against ischemic insult and the potential molecular targets using an in vitro ischemic model of oxygen glucose deprivation (OGD). METHODS: Fetal rat cortical neurons isolated from Day E18 rat embryos were subjected to 90-min OGD and hypothermia treatments during reoxygenation before examining the changes in microscopic morphology, cell viability, microtubule- associated protein 2 (MAP-2) release, intracellular pH value and calcium, reactive oxygen species (ROS) generation, mitochondrial membrane potential (△Ψm) and neuronal death using cell counting kit (CCK-8), enzyme-linked immunosorbent assay (ELISA), BCECF AM, Fluo-3 AM, DCFH-DA and dihydroethidium (DHE), JC-1 staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), respectively. RESULTS: 90-min OGD induced morphologic abnormalities, cell viability decline, MAP-2 release, intracellular acidosis, calcium overload, increased ROS generation, △Ψm decrease and cell death in primary neurons, which was partially inhibited by continuous hypothermia (CH) and intermittenthypothermia (IH). Interestingly, 6-h CH was insufficient to reduce intracellular calcium overload and stabilize mitochondrial membrane potential (△Ψm), while 12-h CH was effective in reversing the above changes. All IH treatments (6×1 h, 4×1.5 h or 3×2 h) effectively attenuated intracellular free calcium overload, inhibited ROS production, stabilized mitochondrial membrane potential (△Ψm) and reduced delayed cell death in OGD-treated cells. However, only IH intervals longer than 1.5 h appeared to be effective in preventing cell viability loss and intracellular pH decline. CONCLUSION: Both CH and IH were neuroprotective in an in vitro model of ischemic stroke, and in spite of shorter hypothermia duration, IH could provide a comparable neuroprotection to CH. | |||
TO cite this article:Xu Suiyi,Hu Yafang,Li Weiping, et al. Intermittent hypothermia is neuroprotective in an in vitro model of ischemic stroke[OL].[11 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4687396 |
5. Occludin Deficiency with BACE1 Elevation in Cerebral Amyloid Angiopathy | |||
CHENG Xin,HE Ping,YAO Hailan,DONG Qiang,LI Rena,SHEN Yong | |||
Clinical Medicine 17 February 2014 | |||
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Abstract:Objective: A significant cause of spontaneous hemorrhages in the elderly is cerebral amyloid angiopathy (CAA) which causes degeneration of cerebral vessels, however, the mechanisms are unclear. Methods: We isolated leptomeningeal vessels from rapidly autopsied brains (average postmortem intervals 3.28 hours) with 9 cases of CAA and 10 cases of age-matched controls and used molecular, cell biology and immunohistochemical approaches to examine β-site APP cleaving enzyme 1 (BACE1) protein expression and enzymatic activities as well as tight junction molecular components in small and medium-sized arteries of the cerebral cortex and leptomeninges. Results: We not only identified in the cerebral vessels, including leptomeningeal and cortical vessels, but also found a significant elevation of both BACE1 protein levels and enzymatic activities in leptomeningeal vessels from CAA patients. Moreover, overexpression of BACE1 in endothelial cells resulted in a significant reduction of Occludin, a tight junction protein in blood vessels. Conclusion: These findings suggest that in addition to neurons, cerebral vascular cells express functional BACE1. Moreover, elevated vascular BACE1 may contribute to deficiency of Occludin in cerebral vessels, which ultimately plays a critical role in pathogenesis of CAA and its related hemorrhage. | |||
TO cite this article:CHENG Xin,HE Ping,YAO Hailan, et al. Occludin Deficiency with BACE1 Elevation in Cerebral Amyloid Angiopathy[OL].[17 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4585653 |
6. Optimization of Emergency Procedures to Improve the Efficiency of Thrombolytic Therapy of Acute Stroke | |||
CHENG Xin,LING Yifeng,FANG Kun,LIU Huaye,HU Zupeng,DONG Qiang | |||
Clinical Medicine 17 February 2014 | |||
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Abstract:Background and Purpose: Efficacy of thrombolytic therapy for ischemic stroke decreases with time elapsed from symptom onset. We hope that through our optimized emergency thrombolytic procedures could reduce in-hospital delays. Methods: A series of interventions to reduce treatment delays were implemented since July 2011. In-hospital delays were analyzed as annual median door-to-needle(DNT) in minutes and the rate of DNT≤60 minutes.Results: A total of 2,903 patients with cerebral infarction were admitted between January 2008 and June 2013, 150 patients received intravenous thrombolytic therapy. The median age was 67 year-old (interquartile range [IQR]: 59-74). Male percentage was 64.7%. The baseline median National Institutes of Health Stroke Scale (NIHSS) score was 10(IQR 5-15). Percentage of thrombolytic use was increased from 1.9% to 9.2% (P<0.001). Median DNT was reduced from 100 minutes (IQR 85-114) to 69 minutes (IQR 53-94) (P<0.001). Rate of DNT ≤ 60 minutes was increased from 6.5% to 41.2% (P<0.001).Conclusions: Achieving DNT≤60 minutes for the majority of thrombolytic therapy candidates is still our goal. Further simplifying the thrombolytic procedures to treat the patients faster will help us to achieve this goal in the future. | |||
TO cite this article:CHENG Xin,LING Yifeng,FANG Kun, et al. Optimization of Emergency Procedures to Improve the Efficiency of Thrombolytic Therapy of Acute Stroke[OL].[17 February 2014] http://en.paper.edu.cn/en_releasepaper/content/4585734 |
7. The mitochondrial dynamics and cell cycle were changed by autophagy inhibition | |||
Mengcui Gui,Bo Chen,Shanshan Yu,Bitao Bu | |||
Clinical Medicine 22 September 2013 | |||
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Abstract:Objective: To testify the association among autophagy, mitochondrial dynamics and cell cycle in dividing neuroblastoma cells. Method and material: The N2a cells were cultured in vitro and treated with different concentrations of 3-Methyladenine (3-MA). The cell ability was detected by MTT assay. And then cells were randomly divided into control (cells cultured in formal culture medium) and 3-MA groups (cells treated with 10mmol/L 3-MA). At different time points (3h, 6h, 12h, and 24h), the cell cycle was analyzed by flow cytometry. Western-blot was used to detect the expressions of mitofission 1 (Fis1), mitofusin 2 (Mfn2), microtubule-associated protein 1 light chain 3 (LC3), cell cycle-dependent kinase 4 (CDK4) and cdc2. Result: Flow cytometry showed that 3-MA group had significantly high percentage of G2/M, and low percentage of G0/G1, relative to those in the control group (p<0.05). The expressions of Fis1, LC3, CDK4 were significantly up-regulated in the 3-MA group at the four time point (p<0.01 or p<0.05) than those in the control group. Mfn2 was initially decreased in 3-MA group, then significantly increased when treated for 6h or 12h (p<0.01). The cdc2 was significantly increased after cells were treated with 3-MA at the 3h and 6h time points, and than dropped significantly at the 12h and 24h time point due to cell death (p<0.01). Expression of Mfn2 was significantly increased at 6h and 12h (p<0.01) in the 3-MA group. Conclusion: The autophagy inhibition induced by specific inhibitor 3-MA, causes changes of cell cycle progression and mitochondrial dynamics, accompanying by cell death. There are interactions among cell cycle, mitochondrial dynamics and autophagy. ????? | |||
TO cite this article:Mengcui Gui,Bo Chen,Shanshan Yu, et al. The mitochondrial dynamics and cell cycle were changed by autophagy inhibition[OL].[22 September 2013] http://en.paper.edu.cn/en_releasepaper/content/4560709 |
8. An enriched environment elevates corticosteroid receptor levels in the hippocampus and restores cognitive function in a rat model of chronic cerebral hypoperfusion | |||
ZHANG Lei,ZHANG Junjian,SUN Huimin,ZHU Hong,LIU Hui,YANG Ying | |||
Clinical Medicine 19 December 2011 | |||
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Abstract:An enriched environment (EE) is beneficial for modifying certain behaviors, particularly in tasks involving complex cognitive functions. In models of chronic cerebral hypoperfusion (CCH), the ability of an EE to stimulate cognitive recovery depends on hippocampal synaptic plasticity and brain-derived neurotrophic factor. The mechanisms that underlie this observation, however, have not been adequately studied. Corticosteroid receptors play an important role in cognitive function. Here we investigated the effects of CCH and an EE on serum corticosteroid concentrations and on levels of the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR) in the rat hippocampus. Rats were randomly divided into four treatment groups that received either permanent bilateral ligation of the common carotid arteries or sham surgery. These procedures were followed by 4 weeks of either an EE or standard housing. After the environmental treatment, the spatial learning and memory abilities of these animals were examined using the Morris water maze. In addition, the levels of MR and GR proteins in the hippocampus were determined. We found that CCH impaired the spatial cognitive function of rats and that exposure to an EE reversed these spatial cognitive deficits. CCH also reduced the amount of MR and GR proteins in the hippocampus, but an EE often restored these levels. Our results demonstrate that EE exposure restores cognitive impairments induced by CCH and up-regulates MR and GR expression. As such, MR and GR may contribute to the beneficial effects of an EE in rats with CCH. | |||
TO cite this article:ZHANG Lei,ZHANG Junjian,SUN Huimin, et al. An enriched environment elevates corticosteroid receptor levels in the hippocampus and restores cognitive function in a rat model of chronic cerebral hypoperfusion[J]. |
9. Research Advances on the Genetics of Parkinson\ | |||
He Xianghua,Xi Jing,He Li,Xu Yanming | |||
Clinical Medicine 27 February 2009 | |||
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Abstract:Pakinson’s disease(PD) is a neurodegenerative disease with about 1% of the population affected. Recently, multiple genes were found to be related with Parkinson’s disease. This review aimed to analyze some causative genes about Parkinson’s disease, to summarize the function of pathogenic genes about this condition, and to review related genes that China have studied. In clusion, Parkinson’s disease is a movement disorder that until now has no effective ways to cure the disease.And more and more new genes are found to increase the risk of developing the condition. To date, there are 13 type of genes found to be associated with PD. And the mechanisms for genes underlie how to make the whole things changed still remains unknown. | |||
TO cite this article:He Xianghua,Xi Jing,He Li, et al. Research Advances on the Genetics of Parkinson\[OL].[27 February 2009] http://en.paper.edu.cn/en_releasepaper/content/29763 |
10. The Association of the Neuronal Protective Effect of Cerebral Ischemic Preconditioning with Concentrations of Extracellular Amino Acids in Rats | |||
Min Zhang,Wenbin Li,Heshan Mei ,Yong-Li Wang,Li Li | |||
Clinical Medicine 30 October 2008 | |||
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Abstract:The present study was undertaken to observe changes in concentrations of glutamate, aspartate and γ-aminobutyric acid (GABA) in the CA1 hippocampus during the acquirement of brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP) using cerebral microdialysis and high performance liquid chromatography techniques in rats. An initial, moderate and synchronous increase in glutamate, aspartate and GABA was first evoked by the lethal ischemic insult for 8 min which was verified to induce delayed neuronal death (DND) in the CA1 hippocampus. GABA quickly recovered to and kept at control level after reperfusion, but both glutamate and aspartate levels increased secondly in more magnitudes within the early stage of reperfusion. When the animals were pretreated 2 days before the lethal ischemic insult with a CIP for 3 min which protected the pyramidal neurons against DND normally induced by the lethal brain ischemia, the second peaks of glutamate and aspartate was prevented completely. The results suggested first in vivo that the protective effect of the CIP against DND of pyramidal neurons in the CA1 hippocampus normally induced by lethal brain ischemia might be associated with suppressing the increase in extracellular concentrations of both glutamate and aspartate. | |||
TO cite this article:Min Zhang,Wenbin Li,Heshan Mei , et al. The Association of the Neuronal Protective Effect of Cerebral Ischemic Preconditioning with Concentrations of Extracellular Amino Acids in Rats[OL].[30 October 2008] http://en.paper.edu.cn/en_releasepaper/content/25259 |
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