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| 1 | Hypoxic preconditioning stimulates angiogenesis in ischemic penumbra after acute cerebral infarction显示文摘Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute cerebral infarction,but the mechanisms underlying this protection remain unclear.To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis,we induced a photochemical model of cerebral infarction in an inbred line of mice(BALB/c).Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment.Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction,mainly in neurons and vascular endothelial cells.Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31.Moreover,hypoxic preconditioning reduced the infarct volume and improved neurological function in mice.These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra,which promoted angiogenesis. | Sijie Li Yanbo Zhang Guo Shao Mingfeng Yang Jingzhong Niu Guowei Lv Xunming Ji | 2013 | Neural Regeneration Research2013，8，31： | 31 |
| 2 | Status of hyperhomocysteinemia in China: results from the China Stroke High-risk Population Screening Program, 2018显示文摘A nationwide survey was conducted from October 2018 to September 2019 to assess the prevalence of hyperhomocysteinemia(Hhcy)and its influencing factors in China.A standardized questionnaire was used to collect information.Hhcy was defined as the level of serum homocysteine(HCY)≥15.0µmol/L.The H-type hypertension(HHYP)was defined as hypertension with an elevated serum HCY(≥15.0µmol/L).Finally,110551 residents≥40 years of age from 31 provinces in the mainland of China were included.Overall,the median serum HCY level was 10.9µmol/L(interquartile range 7.9–15.1).A total of 28633 participants(25.9%)were defined as Hhcy.The Hhcy prevalence ranged from 7.9%in Shanghai to 56.8%in Tianjin.The data showed that serum HCY levels were associated with age,male gender,cigarette smoking,hypertension,diabetes,ethnicity,endurance in exercise(inverse),and fruit and vegetable intake(inverse).In addition,15486 participants were defined as HHYP,and the rate was 14.0%.HHYP was an independent predictor of stroke with an adjusted odds ratio of 1.752(95%CI 1.338–2.105).The geographical distribution pattern of the Hhcy epidemic reflects dynamic differences,and national strategies should be carried out to further improve the care of patients with Hhcy across China. | Wenjun Tu Feng Yan Baohua Chao Xunming Ji Longde Wang | 2021 | Frontiers of Medicine2021，15，6： | 12 |
| 3 | Gabapentin inhibits central sensitization during migraine显示文摘Peripheral and central sensitizations are phenomena that occur during migraine.The role of gabapentin,a migraine preventive drug,on central sensitization remains unclear.In this study,a rat model of migraine was established by electrical stimulation of the trigeminal ganglion,and the animals were given intragastric gabapentin.Changes in amino acid content in the cerebrospinal fluid and protein kinase C membrane translocation in the spinal trigeminal nucleus were examined to clarify the mechanisms underlying the efficacy of gabapentin in the treatment of central sensitization during migraine.Electrophysiology,liquid chromatography-mass spectrometry and western blot analysis results revealed that gabapentin reduces neuronal excitability in the spinal nucleus in the trigeminal nerve,decreases excitatory amino acid content and inhibits the activation of protein kinase C.This provides evidence that excitatory amino acids and protein kinase C are involved in the formation and maintenance of central sensitization during migraine.Gabapentin inhibits migraine by reducing excitatory amino acid content in the cerebrospinal fluid and inhibiting protein kinase C activation. | Yanbo Zhang Guo Shao Wei Zhang Sijie Li Jingzhong Niu Dongmei Hu Mingfeng Yang Xunming Ji | 2013 | Neural Regeneration Research2013，8，32： | 12 |
| 4 | An overview of graphene-based hydroxyapatite composites for orthopedic applications显示文摘Hydroxyapatite(HA)is an attractive bioceramic for hard tissue repair and regeneration due to its physicochemical similarities to natural apatite.However,its low fracture toughness,poor tensile strength and weak wear resistance become major obstacles for potential clinical applications.One promising method to tackle with these problems is exploiting graphene and its derivatives(graphene oxide and reduced graphene oxide)as nanoscale reinforcement fillers to fabricate graphene-based hydroxyapatite composites in the form of powders,coatings and scaffolds.The last few years witnessed increasing numbers of studies on the preparation,mechanical and biological evaluations of these novel materials.Herein,various preparation techniques,mechanical behaviors and toughen mechanism,the in vitro/in vivo biocompatible analysis,antibacterial properties of the graphene-based HA composites are presented in this review. | Ming Li Pan Xiong Feng Yan Sijie Li Changhong Ren Zhichen Yin Ang Li Huafang Li Xunming Ji Yufeng Zheng Yan Cheng | 2018 | Bioactive Materials2018，3，1： | 9 |
| 5 | A more consistent intraluminal rhesus monkey model of ischemic stroke显示文摘Endovascular surgery is advantageous in experimentally induced ischemic stroke because it causes fewer cranial traumatic lesions than invasive surgery and can closely mimic the pathophysiology in stroke patients. However, the outcomes are highly variable, which limits the accuracy of evaluations of ischemic stroke studies. In this study, eight healthy adult rhesus monkeys were randomized into two groups with four monkeys in each group: middle cerebral artery occlusion at origin segment(M1) and middle cerebral artery occlusion at M2 segment. The blood flow in the middle cerebral artery was blocked completely for 2 hours using the endovascular microcoil placement technique(1 mm × 10 cm)(undetachable), to establish a model of cerebral ischemia. The microcoil was withdrawn and the middle cerebral artery blood flow was restored. A reversible middle cerebral artery occlusion model was identified by hematoxylin-eosin staining, digital subtraction angiography, magnetic resonance angiography, magnetic resonance imaging, and neurological evaluation. The results showed that the middle cerebral artery occlusion model was successfully established in eight adult healthy rhesus monkeys, and ischemic lesions were apparent in the brain tissue of rhesus monkeys at 24 hours after occlusion. The rhesus monkeys had symptoms of neurological deficits. Compared with the M1 occlusion group, the M2 occlusion group had lower infarction volume and higher neurological scores. These experimental findings indicate that reversible middle cerebral artery occlusion can be produced with the endovascular microcoil technique in rhesus monkeys. The M2 occluded model had less infarction and less neurological impairment, which offers the potential for application in the field of brain injury research. | Bo Zhao Guowei Shang Jian Chen Xiaokun Geng Xin Ye Guoxun Xu Ju Wang Jiasheng Zheng Hongjun Li Fauzia Akbary Shengli Li Jing Lu Feng Ling Xunming Ji | 2014 | Neural Regeneration Research2014，9，23： | 6 |
| 6 | Protective effects of remote ischemic preconditioning in rat hindlimb on ischemia- reperfusion injury显示文摘Three cycles of remote ischemic pre-conditioning induced by temporarily occluding the bilateral femoral arteries (10 minutes) prior to 10 minutes of reperfusion were given once a day for 3 days before the animal received middle artery occlusion and reperfusion surgery. The results showed that brain infarct volume was significantly reduced after remote ischemic pre-conditioning. Scores in the forelimb placing test and the postural reflex test were significantly lower in rats having undergone remote ischemic pre-conditioning compared with those who did not receive remote ischemic pre-conditioning. Thus, neurological function was better in rats having undergone remote ischemic pre-conditioning compared with those who did not receive remote ischemic pre-conditioning. These results indicate that remote ischemic pre-conditioning in rat hindlimb exerts protective effects in ischemia-reperfusion injury. | Ying Zhang Xiangrong Liu Feng Yan Lianqiu Min Xunming Ji Yumin Luo | 2012 | Neural Regeneration Research2012，7，8： | 5 |
| 7 | Loss of Wip1 aggravates brain injury after ischaemia/reperfusion by overactivating microglia显示文摘Background and purpose The inflammatory response mediated by microglia/macrophages is closely related to cerebral ischaemia/reperfusion injury.Wild-type p53-induced protein phosphatase 1(Wip1),a serine/threonine phosphatase,is expressed in various tissues.A growing number of reports have suggested that Wip1 is a negative regulator of inflammation in peripheral tissue;however,its role in the central nervous system(CNS)remains unclear.This study aimed to clarify whether Wip1 can inhibit CNS inflammation by regulating microglia/macrophage functions after ischaemic injury.Methods A model of middle cerebral artery occlusion and reperfusion was established in mice.CNS inflammation was simulated by lipopolysaccharide treatment of primary microglia.Laser speckle imaging was used to monitor regional cerebral blood flow.Behavioural outcomes were assessed with a TreadScan gait analysis system.TTC staining was used to evaluate the infarct volume,and western blotting and immunofluorescence staining were applied to detect the phenotypical transformation of microglia.ELISA was performed to detect the levels of inflammatory factors.Results Wip1 expression was increased after ischaemia/reperfusion.Wip1-knockout(KO)mice displayed more severe brain injury than wild-type mice,as indicated by aggravated motor dysfunction,greater brain infarct volumes and higher expression of inflammatory cytokines(interleukin-6 and tumour necrosis factor alpha)in the brain.We also found that Wip1 depletion increased microglial/macrophage activation in both in vitro and in vivo models,which all showed activation of microglia/macrophages.Lentivirus-Ppm1d reversed the injury induced by Wip1-KO.Conclusions Our results suggest that Wip1 may inhibit neuroinflammation by inhibiting microglial/macrophage activation after brain ischaemia/reperfusion injury. | Feng Yan Xiang Cheng Ming Zhao Shenghui Gong Ying Han Liping Ding Di Wu Yumin Luo Wei Zuo Lingling Zhu Ming Fan Xunming Ji | 2021 | Stroke & Vascular Neurology2021，6，3： | 4 |
| 8 | Interactions between remote ischemic conditioning and post-stroke sleep regulation显示文摘Sleep disturbances are common in patients with stroke,and sleep quality has a critical role in the onset and outcome of stroke.Poor sleep exacerbates neurological injury,impedes nerve regeneration,and elicits serious complications.Thus,exploring a therapy suitable for patients with stroke and sleep disturbances is imperative.As a multi-targeted nonpharmacological intervention,remote ischemic conditioning can reduce the ischemic size of the brain,improve the functional outcome of stroke,and increase sleep duration.Preclinical/clinical evidence showed that this method can inhibit the inflammatory response,mediate the signal transductions of adenosine,activate the efferents of the vagal nerve,and reset the circadian clocks,all of which are involved in sleep regulation.In particular,cytokines tumor necrosis factorα(TNFα)and adenosine are sleep factors,and electrical vagal nerve stimulation can improve insomnia.On the basis of the common mechanisms of remote ischemic conditioning and sleep regulation,a causal relationship was proposed between remote ischemic conditioning and post-stroke sleep quality. | Xian Wang Xunming Ji | 2021 | Frontiers of Medicine2021，15，6： | 4 |
| 9 | Antithrombin Ⅲ associated with fibrinogen predicts the risk of cerebral ischemic stroke 显示文摘 | Ran Meng Zhi-Yong Li Xunming Ji | 2011 | Clinical Neurology and Neurosurgery2011，113，5： | 1 |
| 10 | MicroRNA-124–Mediated Regulation of Inhibitory Member of Apoptosis-Stimulating Protein of p53 Family in Experimental Stroke显示文摘 | Xiangrong Liu Fang Li Shangfeng Zhao Yumin Luo Jun Kang Haiping Zhao Feng Yan Sijie Li Xunming Ji | 2013 | Stroke2013，，7： | 1 |
| 11 | Neuroprotective effect of morroniside on focal cerebral ischemia in rats显示文摘 | Wen Wang Jingdong Xu Lei Li Peichang Wang Xunming Ji Houxi Ai Li Zhang Lin Li | 2010 | Brain Research Bulletin2010，，5： | 1 |
| 12 | Validation of fast diffusion kurtosis MRI for imaging acute ischemia in a rodent model of stroke显示文摘 | Phillip Zhe Sun Yu Wang Emiri Mandeville Suk‐Tak Chan Eng H. Lo Xunming Ji | 2014 | NMR Biomed2014，，11： | 1 |
| 13 | Neuroinflammation: The role and consequences显示文摘 | Monty Lyman Dafydd G. Lloyd Xunming Ji Marcela P. Vizcaychipi Daqing Ma | 2014 | Neuroscience Research2014，，： | 1 |
| 14 | Non-pharmaceutical therapies for stroke: Mechanisms and clinical implications显示文摘 | Fan Chen Zhifeng Qi Yuming Luo Taylor Hinchliffe Guanghong Ding Ying Xia Xunming Ji | 2013 | Progress in Neurobiology2013，，： | 1 |
| 15 | The role of different cues in the brain mechanism on visual spatial attention显示文摘在大脑的视觉空间注意机制被事件相关的潜力(ERP ) 通过 precue 目标的视觉搜索范例在 16 个年轻题目学习技术,与由汉字和区域暗示的不同规模的专心的范围 cued。结果证明汉字暗示的反应时间为小区域暗示特别为区域暗示比那长得多。与外面的干扰,在区域暗示下面的目标刺激识别在汉字暗示下面是比那快得多的。与相比在区域暗示下面,在汉字暗示下面的目标能导致以后的 P1 的增加, N1 减少并且 P2 增加。区域暗示和汉字暗示之间的差别被干扰类型影响,这应该也被注意。在外面的干扰下面,没有重要差别在区域暗示和汉字暗示之间被发现;然而,它不是在干扰下面的原因。就外面的干扰和内部干扰之间的差别而言,我们能断定随在目标识别的困难的增加,在由在二种暗示下面的目标刺激的前面的正面的资源的消费有明显的差别。 | SONG Weiqun LUO Yuejia CHI Song JI Xunming LING Feng ZHAO Lun WANG Maobin SHI Jiannong | 2006 | Progress in Natural Science:Materials International2006，16，10： | 1 |
| 16 | A new method of noninvasive brain-edema monitoring in stroke:cerebral electrical impedance measurement显示文摘 | LiXu Liu WeiWei Dong XunMing Ji | 2006 | Neurological Research2006，，： | 1 |
| 17 | Upper limb ischemic preconditioning prevents recurrent stroke in intracranial arterial stenosis显示文摘 | Ran M Karam A Xunming Ji | 2012 | Neurology2012，79，10： | 1 |
| 18 | MicroRNA-424 Protects Against Focal Cerebral Ischemia and Reperfusion Injury in Mice by Suppressing Oxidative Stress显示文摘 | Ping Liu Haiping Zhao Rongliang Wang Peng Wang Zhen Tao Li Gao Feng Yan Xiangrong Liu Shun Yu Xunming Ji Yumin Luo | 2015 | Stroke2015，，： | 1 |
| 19 | Exploring novel experimental treatments for major neurodegenerative disorders显示文摘Acute and chronic neurodegenerative disorders such as ischemic stroke or Alzheimer's disease(AD)impose a major burden on patients,their relatives,caregivers,and health care systems in general.The socioeconomic impact of neurodegenerative disorders is anticipated to escalate due to a globally ageing population and the increasing prevalence of sedentary lifestyle and inappropriate dietary habits.On the contrary. | Xunming Ji Piotr Walczak Johannes Boltze | 2023 | Neuroprotection2023，1，2： | 0 |
| 20 | Preserving cognitive function in patients with Alzheimer's disease:The Alzheimer's disease neuroprotection research initiative(ADNRI)显示文摘The global trend toward aging populations has resulted in an increase in the occurrence of Alzheimer's disease(AD)and associated socioeconomic burdens.Abnormal metabolism of amyloid-β(Aβ)has been proposed as a significant pathomechanism in AD,supported by results of recent clinical trials using anti-Aβantibodies.Nonetheless,the cognitive benefits of the current treatments are limited.The etiology of AD is multifactorial,encompassing Aβand tau accumulation,neuroinflammation,demyelination,vascular dysfunction,and comorbidities,which collectively lead to widespread neurodegeneration in the brain and cognitive impairment.Hence,solely removing Aβfrom the brain may be insufficient to combat neurodegeneration and preserve cognition.To attain effective treatment for AD,it is necessary to(1)conduct extensive research on various mechanisms that cause neurodegeneration,including advances in neuroimaging techniques for earlier detection and a more precise characterization of molecular events at scales ranging from cellular to the full system level;(2)identify neuroprotective intervention targets against different neurodegeneration mechanisms;and(3)discover novel and optimal combinations of neuroprotective intervention strategies to maintain cognitive function in AD patients.The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated,multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD.The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD,with the goal of halting or even reversing cognitive decline. | Jie Liu Heleen van Beusekom Xian-Le Bu Gong Chen Paulo Henrique Rosado de Castro Xiaochun Chen Xiaowei Chen Andrew N.Clarkson Tracy D.Farr Yuhong Fu Jianping Jia Jukka Jolkkonen Woojin Scott Kim Paula Korhonen Shen Li Yajie Liang Guang-Hui Liu Guiyou Liu Yu-Hui Liu Tarja Malm Xiaobo Mao Joaquim Miguel Oliveira Mike M.Modo Pedro Ramos-Cabrer Karsten Ruscher Weihong Song Jun Wang Xuanyue Wang Yun Wang Haitao Wu Lize Xiong Yi Yang Keqiang Ye Jin-Tai Yu Xin-Fu Zhou Marietta Zille Colin L.Masters Piotr Walczak Boltze Johannes Xunming Ji Yan-Jiang Wang | 2023 | Neuroprotection2023，1，2： | 0 |
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