31 results on '"Jiang, Jiyao"'
Search Results
2. Self‐Disassembling and Oxygen‐Generating Porphyrin‐Lipoprotein Nanoparticle for Targeted Glioblastoma Resection and Enhanced Photodynamic Therapy.
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Chen, Yaoxing, Ma, Yuxiao, Shi, Kexin, Chen, Huan, Han, Xiao, Wei, Chenxuan, Lyu, Yingqi, Huang, Yukun, Yu, Renhe, Song, Yun, Song, Qingxiang, Jiang, Jiyao, Feng, Junfeng, Lin, Yingying, Chen, Jun, Chen, Hongzhuan, Zheng, Gang, Gao, Xiaoling, and Jiang, Gan
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- 2024
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3. Mortality Prediction in Severe Traumatic Brain Injury Using Traditional and Machine Learning Algorithms.
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Wu, Xiang, Sun, Yuyao, Xu, Xiao, Steyerberg, Ewout W., Helmrich, Isabel R.A. Retel, Lecky, Fiona, Guo, Jianying, Li, Xiang, Feng, Junfeng, Mao, Qing, Xie, Guotong, Maas, Andrew I.R., Gao, Guoyi, and Jiang, Jiyao
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- 2023
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4. Intracranial Pressure Monitoring in the Intensive Care Unit for Patients with Severe Traumatic Brain Injury: Analysis of the CENTER-TBI China Registry.
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Yang, Chun, Ma, Yuxiao, Xie, Li, Wu, Xiang, Hui, Jiyuan, Jiang, Jiyao, Gao, Guoyi, and Feng, Junfeng
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HOSPITAL mortality ,INTENSIVE care patients ,BRAIN injuries ,INTRACRANIAL pressure ,MEDICAL care ,MEDICAL care costs ,PRESSURE ulcers - Abstract
Background: Although the current guidelines recommend the use of intracranial pressure (ICP) monitoring in patients with severe traumatic brain injury (sTBI), the evidence indicating benefit is limited. The present study aims to evaluate the impact of ICP monitoring on patients with sTBI in the intensive care unit (ICU). Methods: The patient data were obtained from the Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury China Registry, a prospective, multicenter, longitudinal, observational, cohort study. Patients with sTBI who were admitted to 52 ICUs across China, managed with ICP monitoring or without, were analyzed in this study. Patients with missing information on discharge survival status, Glasgow Coma Scale score on admission to hospital, and record of ICP monitoring application were excluded from the analysis. Data on demographic characteristics, injury, clinical features, treatments, survival at discharge, discharge destination, and length of stay were collected and assessed. The primary end point was survival state at discharge, and death from any cause was considered the event of interest. Results: A total of 2029 patients with sTBI were admitted to the ICU; 737 patients (36.32%) underwent ICP monitoring, and 1292 (63.68%) were managed without ICP monitoring. There was a difference between management with and without ICP monitoring on in-hospital mortality in the unmatched cohort (18.86% vs. 26.63%, p < 0.001) and the propensity-score-matched cohort (19.82% vs. 26.83%, p = 0.003). Multivariate logistic regressions also indicated that increasing age, higher injury severity score, lower Glasgow Coma Scale score, unilateral and bilateral pupillary abnormalities, systemic hypotension (SBP ≤ 90 mm Hg), hypoxia (SpO2 < 95%) on arrival at the hospital, and management without ICP monitoring were associated with higher in-hospital mortality. However, the patients without ICP monitoring had a lower length of stay in the ICU (11.79 vs. 7.95 days, p < 0.001) and hospital (25.96 vs. 21.71 days, p < 0.001), and a higher proportion of survivors were discharged to the home with better recovery in self-care. Conclusions: Although ICP monitoring was not widely used by all of the centers participating in this study, patients with sTBI managed with ICP monitoring show a better outcome in overall survival. Nevertheless, the use of ICP monitoring makes the management of sTBI more complex and increases the costs of medical care by prolonging the patient's stay in the ICU or hospital. [ABSTRACT FROM AUTHOR]
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- 2022
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5. Direct Current Electric Field Coordinates the Migration of BV2 Microglia via ERK/GSK3β/Cofilin Signaling Pathway.
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Ma, Yuxiao, Yang, Chun, Liang, Qian, He, Zhenghui, Weng, Weiji, Lei, Jin, Skudder-Hill, Loren, Jiang, Jiyao, and Feng, Junfeng
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Direct current electric field (DCEF) steers the migration of various neural cells. Microglia, as macrophage of the central nervous system (CNS), however, have not been reported to engage in electrotaxis. Here, we applied electric fields to an in vitro environment and found directional migration of BV2 microglia toward the cathode, in a DCEF strength-dependent manner. Transcriptome analysis then revealed significant changes in the mitogen-activated protein kinase cascades. In terms of mechanism, DCEF coordinated microglia movement by regulating the ERK/GSK3β/cofilin signaling pathway, and PMA (protein kinase C activator) reversed cell migration through intervention of the ERK/GSK3β/cofilin axis. Meanwhile, LiCl (GSK3β inhibitor) showed similar functions to PMA in the electrotaxis of microglia. Furthermore, pharmacological and genetic suppression of GSK3β or cofilin also modulated microglia directional migration under DCEF. Collectively, we discovered the electrotaxis of BV2 microglia and the essential role of the ERK/GSK3β/cofilin axis in regulating cell migration via modulation of F-actin redistribution. This research highlights new insight toward mediating BV2 directional migration and provides potential direction for novel therapeutic strategies of CNS diseases. [ABSTRACT FROM AUTHOR]
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- 2022
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6. Epidemiological Characteristics of Older Patients with Traumatic Brain Injury in China.
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Yang, Chun, Lang, Lijian, He, Zhenghui, Hui, Jiyuan, Jiang, Jiyao, Gao, Guoyi, and Feng, Junfeng
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- 2022
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7. Brain Extract of Subacute Traumatic Brain Injury Promotes the Neuronal Differentiation of Human Neural Stem Cells via Autophagy.
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He, Zhenghui, Lang, Lijian, Hui, Jiyuan, Ma, Yuxiao, Yang, Chun, Weng, Weiji, Huang, Jialin, Zhao, Xiongfei, Zhang, Xiaoqi, Liang, Qian, Jiang, Jiyao, and Feng, Junfeng
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Background: After a traumatic brain injury (TBI), the cell environment is dramatically changed, which has various influences on grafted neural stem cells (NSCs). At present, these influences on NSCs have not been fully elucidated, which hinders the finding of an optimal timepoint for NSC transplantation. Methods: Brain extracts of TBI mice were used in vitro to simulate the different phase TBI influences on the differentiation of human NSCs. Protein profiles of brain extracts were analyzed. Neuronal differentiation and the activation of autophagy and the WNT/CTNNB pathway were detected after brain extract treatment. Results: Under subacute TBI brain extract conditions, the neuronal differentiation of hNSCs was significantly higher than that under acute brain extract conditions. The autophagy flux and WNT/CTNNB pathway were activated more highly within the subacute brain extract than in the acute brain extract. Autophagy activation by rapamycin could rescue the neuronal differentiation of hNSCs within acute TBI brain extract. Conclusions: The subacute phase around 7 days after TBI in mice could be a candidate timepoint to encourage more neuronal differentiation after transplantation. The autophagy flux played a critical role in regulating neuronal differentiation of hNSCs and could serve as a potential target to improve the efficacy of transplantation in the early phase. [ABSTRACT FROM AUTHOR]
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- 2022
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8. Prospective Randomized Evaluation of Decompressive Ipsilateral Craniectomy for Traumatic Acute Epidural Hematoma (PREDICT-AEDH): study protocol for a randomized controlled trial.
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Yang, Chun, Huang, Xianjian, Feng, Junfeng, Xie, Li, Hui, Jiyuan, Li, Weiping, and Jiang, Jiyao
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EPIDURAL hematoma ,DECOMPRESSIVE craniectomy ,RANDOMIZED controlled trials ,RESEARCH protocols ,CEREBRAL infarction ,SURGICAL indications - Abstract
Background: The expeditious surgical evacuation of acute epidural hematoma (AEDH) is an attainable gold standard and is often expected to have a good clinical outcome for patients with surgical indications. However, controversy exists on the optimal surgical options for AEDH, especially for patients with brain herniation. Neurosurgeons are confronted with the decision to evacuate the hematoma with decompressive craniectomy (DC) or craniotomy.Methods/design: Patients of both sexes, age between 18 and 65 years, who presented to the emergency room with a clinical and radiological diagnosis of AEDH with herniation, were assessed against the inclusion and exclusion criteria to be enrolled in the study. Clinical and radiological information, including diagnosis of AEDH, treatment procedures, and follow-up data at 1, 3, and 6 months after injury, was collected from 120 eligible patients in 51 centers. The patients were randomized into groups of DC versus craniotomy in a 1:1 ratio. The primary outcome was the Glasgow Outcome Score-Extended (GOSE) at 6 months post-injury. Secondary outcomes included incidence of postoperative cerebral infarction, incidence of additional craniocerebral surgery, and other evaluation indicators within 6 months post-injury.Discussion: This study is expected to support neurosurgeons in their decision to evacuate the epidural hematoma with or without a DC, especially in patients with brain herniation, and provide additional evidence to improve the knowledge in clinical practice.Trial Registration: ClinicalTrials.gov NCT04261673 . Registered on 04 February 2020. [ABSTRACT FROM AUTHOR]- Published
- 2021
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9. Role of Asparagine Endopeptidase in Mediating Wild-Type p53 Inactivation of Glioblastoma.
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Lin, Yingying, Liao, Keman, Miao, Yifeng, Qian, Zhongrun, Fang, Zhaoyuan, Yang, Xi, Nie, Quanmin, Jiang, Gan, Liu, Jianhua, Yu, Yiyi, Wan, Jieqing, Zhang, Xiaohua, Hu, Yaomin, Jiang, Jiyao, and Qiu, Yongming
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GLIOBLASTOMA multiforme ,ASPARAGINE ,VESICLES (Cytology) ,ISOCITRATE dehydrogenase ,ENZYME-linked immunosorbent assay ,KI-67 antigen ,PROTEIN metabolism ,DISEASE progression ,RESEARCH ,XENOGRAFTS ,PROTEASE inhibitors ,ANIMAL experimentation ,RESEARCH methodology ,PROTEOLYTIC enzymes ,GLIOMAS ,EVALUATION research ,MEDICAL cooperation ,COMPARATIVE studies ,CONNECTIVE tissue cells ,CELL lines ,EPITHELIAL cells ,MICE ,PHARMACODYNAMICS - Abstract
Background: Isocitrate dehydrogenase wild-type (WT) glioblastoma (GBM) accounts for 90% of all GBMs, yet only 27% of isocitrate dehydrogenase WT-GBMs have p53 mutations. However, the tumor surveillance function of WT-p53 in GBM is subverted by mechanisms that are not fully understood.Methods: We investigated the proteolytic inactivation of WT-p53 by asparaginyl endopeptidase (AEP) and its effects on GBM progression in cancer cells, murine models, and patients' specimens using biochemical and functional assays. The sera of healthy donors (n = 48) and GBM patients (n = 20) were examined by enzyme-linked immunosorbent assay. Furthermore, effects of AEP inhibitors on GBM progression were evaluated in murine models (n = 6-8 per group). The statistical significance between groups was determined using two-tailed Student t tests.Results: We demonstrate that AEP binds to and directly cleaves WT-p53, resulting in the inhibition of WT-p53-mediated tumor suppressor function in both tumor cells and stromal cells via extracellular vesicle communication. High expression of uncleavable p53-N311A-mutant rescue AEP-induced tumorigenesis, proliferation, and anti-apoptotic abilities. Knock down or pharmacological inhibition of AEP reduced tumorigenesis and prolonged survival in murine models. However, overexpression of AEP promoted tumorigenesis and shortened the survival time. Moreover, high AEP levels in GBM tissues were associated with a poor prognosis of GBM patients (n = 83; hazard ratio = 3.94, 95% confidence interval = 1.87 to 8.28; P < .001). A correlation was found between high plasma AEP levels and a larger tumor size in GBM patients (r = 0.6, P = .03), which decreased dramatically after surgery.Conclusions: Our results indicate that AEP promotes GBM progression via inactivation of WT-p53 and may serve as a prognostic and therapeutic target for GBM. [ABSTRACT FROM AUTHOR]- Published
- 2020
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10. Tailored Lipoprotein‐Like miRNA Delivery Nanostructure Suppresses Glioma Stemness and Drug Resistance through Receptor‐Stimulated Macropinocytosis.
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Jiang, Gan, Chen, Huan, Huang, Jialin, Song, Qingxiang, Chen, Yaoxing, Gu, Xiao, Jiang, Zhenhuan, Huang, Yukun, Lin, Yingying, Feng, Junfeng, Jiang, Jiyao, Bao, Yinghui, Zheng, Gang, Chen, Jun, Chen, Hongzhuan, and Gao, Xiaoling
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DRUG resistance ,MICRORNA ,RNA interference ,NANOSTRUCTURES ,TREATMENT effectiveness ,DRUG resistance in cancer cells ,SOX2 protein - Abstract
Glioma initiating cells (GICs) function as the seed for the propagation and relapse of glioma. Designing a smart and efficient strategy to target the GICs and to suppress the multiple signaling pathways associated with stemness and chemoresistance is essential to achieving a cancer cure. Inspired by the metabolic difference in endocytosis between GICs, differentiated glioma cells, and normal cells, a tailored lipoprotein‐like nanostructure is developed to amplify their internalization into GICs through receptor‐stimulated macropinocytosis. As CXCR4 is highly expressed on GICs and glioma tumor sites, meanwhile, the activation of CXCR4 induces the receptor‐stimulated macropinocytosis pathway in GICs, this CXCR4 receptor‐stimulated lipoprotein‐like nanoparticle (SLNP) achieves efficient accumulation in GICs in vitro and in vivo. By carrying microRNA‐34a in the core, this tailored SLNP reduces sex‐determining region Y‐box 2 and Notch1 expression, powerfully inhibits GICs stemness and chemoresistance, and significantly prolongs the survival of GICs‐bearing mice. Taken together, a tailored lipoprotein‐based nanostructure realizes efficient GICs accumulation and therapeutic effect through receptor‐stimulated macropinocytosis, providing a powerful nanoplatform for RNA interference drugs to combat glioma. [ABSTRACT FROM AUTHOR]
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- 2020
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11. Comprehensive Proteomic Profiling of Patients’ Tears Identifies Potential Biomarkers for the Traumatic Vegetative State.
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Tang, Qilin, Zhang, Chao, Wu, Xiang, Duan, Wenbin, Weng, Weiji, Feng, Junfeng, Mao, Qing, Chen, Shubin, Jiang, Jiyao, and Gao, Guoyi
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The vegetative state is a complex condition with unclear mechanisms and limited diagnostic, prognostic, and therapeutic methods. In this study, we aimed to explore the proteomic profile of tears from patients in a traumatic vegetative state and identify potential diagnostic markers using tears—a body fluid that can be collected non-invasively. Using iTRAQ quantitative proteomic technology, in the discovery phase, tear samples collected from 16 patients in a traumatic vegetative state and 16 normal individuals were analyzed. Among 1080 identified tear proteins, 57 were upregulated and 15 were downregulated in the patients compared to the controls. Bioinformatics analysis revealed that the differentially-expressed proteins were mainly involved in the wound response and immune response signaling pathways. Furthermore, we verified the levels of 7 differentially-expressed proteins in tears from 50 traumatic vegetative state patients and 50 normal controls (including the samples used in the discovery phase) using ELISA. The results showed that this 7-protein panel had a high discrimination ability for traumatic vegetative state (area under the curve = 0.999). In summary, the altered tear proteomic profile identified in this study provides a basis for potential tear protein markers for diagnosis and prognosis of the traumatic vegetative state and also provides novel insights into the mechanisms of traumatic vegetative state. [ABSTRACT FROM AUTHOR]
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- 2018
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12. Amplitude-Integrated Electroencephalography Predicts Outcome in Patients with Coma After Acute Brain Injury.
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You, Wendong, Tang, Qilin, Wu, Xiang, Feng, Junfeng, Mao, Qing, Gao, Guoyi, and Jiang, Jiyao
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Prognostication of coma patients after brain injury is important, yet challenging. In this study, we evaluated the predictive value of amplitude-integrated electroencephalography (aEEG) for neurological outcomes in coma patients. From January 2013 to January 2016, 128 coma patients after acute brain injury were prospectively enrolled and monitored with aEEG. The 6-month neurological outcome was evaluated using the Cerebral Performance Category Scale. aEEG monitoring commenced at a median of 7.5 days after coma onset. Continuous normal voltage predicted a good 6-month neurological outcome with a sensitivity of 93.6% and specificity of 85.2%. In contrast, continuous extremely low voltage, burst-suppression, or a flat tracing was correlated with poor 6-month neurological outcome with a sensitivity of 76.5% and specificity of 100%. In conclusion, aEEG is a promising predictor of 6-month neurological outcome for coma patients after acute brain injury. [ABSTRACT FROM AUTHOR]
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- 2018
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13. Right median nerve electrical stimulation for acute traumatic coma (the Asia Coma Electrical Stimulation trial): study protocol for a randomised controlled trial.
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Xiang Wu, Chao Zhang, Junfeng Feng, Qing Mao, Guoyi Gao, Jiyao Jiang, Wu, Xiang, Zhang, Chao, Feng, Junfeng, Mao, Qing, Gao, Guoyi, and Jiang, Jiyao
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BRAIN injury treatment ,NEURAL stimulation ,MEDIAN nerve ,COMA ,RANDOMIZED controlled trials ,BRAIN injuries ,ELECTRIC stimulation ,ARTIFICIAL respiration ,COMPARATIVE studies ,CONVALESCENCE ,CRITICAL care medicine ,FUNCTIONAL assessment ,ELECTROTHERAPEUTICS ,EXPERIMENTAL design ,LENGTH of stay in hospitals ,LONGITUDINAL method ,RESEARCH methodology ,MEDICAL cooperation ,RESEARCH protocols ,RESEARCH ,TIME ,EVALUATION research ,TREATMENT effectiveness ,GLASGOW Coma Scale ,DIAGNOSIS ,THERAPEUTICS - Abstract
Background: Traumatic brain injury (TBI) has become the most common cause of death and disability in persons between 15 and 30 years of age, and about 10-15% of patients affected by TBI will end up in a coma. Coma caused by TBI presents a significant challenge to neuroscientists. Right median nerve electrical stimulation has been reported as a simple, inexpensive, non-invasive technique to speed recovery and improve outcomes for traumatic comatose patients.Methods/design: This multicentre, prospective, randomised (1:1) controlled trial aims to demonstrate the efficacy and safety of electrical right median nerve stimulation (RMNS) in both accelerating emergence from coma and promoting long-term outcomes. This trial aims to enrol 380 TBI comatose patients to partake in either an electrical stimulation group or a non-stimulation group. Patients assigned to the stimulation group will receive RMNS in addition to standard treatment at an amplitude of 15-20 mA with a pulse width of 300 μs at 40 Hz ON for 20 s and OFF for 40 s. The electrical treatment will last for 8 h per day for 2 weeks. The primary endpoint will be the percentage of patients regaining consciousness 6 months after injury. The secondary endpoints will be Extended Glasgow Outcome Scale, Coma Recovery Scale-Revised and Disability Rating Scale scores at 28 days, 3 months and 6 months after injury; Glasgow Coma Scale, Glasgow Coma Scale Motor Part and Full Outline of Unresponsiveness scale scores on day 1 and day 7 after enrolment and 28 days, 3 months and 6 months after injury; duration of unconsciousness and mechanical ventilation; length of intensive care unit and hospital stays; and incidence of adverse events.Discussion: Right median nerve electrical stimulation has been used as a safe, inexpensive, non-invasive therapy for neuroresuscitation of coma patients for more than two decades, yet no trial has robustly proven the efficacy and safety of this treatment. The Asia Coma Electrical Stimulation (ACES) trial has the following novel features compared with other major RMNS trials: (1) the ACES trial is an Asian multicentre randomised controlled trial; (2) RMNS therapy starts at an early stage 7-14 days after the injury; and (3) various assessment scales are used to evaluate the condition of patients. We hope the ACES trial will lead to optimal use of right median nerve electrical treatment.Trial Registration: ClinicalTrials.gov, NCT02645578 . Registered on 23 December 2015. [ABSTRACT FROM AUTHOR]- Published
- 2017
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14. Glutamate carboxypeptidase II gene knockout attenuates oxidative stress and cortical apoptosis after traumatic brain injury.
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Yang Cao, Yang Gao, Siyi Xu, Jingang Bao, Yingying Lin, Xingguang Luo, Yong Wang, Qizhong Luo, Jiyao Jiang, Neale, Joseph H., Chunlong Zhong, Cao, Yang, Gao, Yang, Xu, Siyi, Bao, Jingang, Lin, Yingying, Luo, Xingguang, Wang, Yong, Luo, Qizhong, and Jiang, Jiyao
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CARBOXYPEPTIDASES ,GLUTAMIC acid ,OXIDATIVE stress ,BRAIN injuries ,PEPTIDES ,SUPEROXIDE dismutase ,CYTOCHROMES ,PROTEIN metabolism ,ANIMAL experimentation ,APOPTOSIS ,CEREBRAL cortex ,MICE ,MITOCHONDRIA ,PROTEOLYTIC enzymes - Abstract
Background: Glutamate carboxypeptidase II (GCPII) inactivates the peptide co-transmitter N-acetylaspartylglutamate following synaptic release. Inhibition of GCPII elevates extracellular levels of the peptide, inhibits glutamate release and is neuroprotective in an animal model of traumatic brain injury. GCPII gene knockout mice were used to examine the cellular mechanisms underlying the neuroprotective efficacy of this transmitter system.Results: Following controlled cortical impact injury, GCPII knockout (KO) mice exhibited reduced TUNEL-positive nuclei in the contusion margin of the cerebral cortex relative to wild type mice. Impact injury reduced glutathione levels and superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde. Each of these effects was moderated in KO mice relative to wild type. Similarly, the injury-induced increases in cleaved caspase-3, cytosolic cytochrome c levels and Bcl-2/Bax ratio observed in wild type mice were attenuated in the knockout mice.Conclusions: These data support the hypothesis that the neuroprotective efficacy of GCPII KO in traumatic brain injury is mediated via a reduction in oxidative stress. [ABSTRACT FROM AUTHOR]- Published
- 2016
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15. Surgical management and outcomes of non-missile open head injury: Report of 44 cases from a single trauma centre.
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Chen, Lei, Bao, Yinghui, Liang, Yumin, Wang, Yong, and Jiang, Jiyao
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COMPLICATIONS of brain injuries ,ACADEMIC medical centers ,BRAIN abscess ,BRAIN injuries ,COMPUTED tomography ,CONVALESCENCE ,SEIZURES (Medicine) ,DEBRIDEMENT ,FOREIGN bodies ,HEMATOMA ,HYDROCEPHALUS ,LIFE skills ,LONGITUDINAL method ,NEUROPSYCHOLOGICAL tests ,EVALUATION of medical care ,NEUROSURGERY ,PENETRATING wounds ,RESEARCH funding ,SPASMS ,SURGICAL site infections ,SURVIVAL analysis (Biometry) ,TRAUMA centers ,RETROSPECTIVE studies ,DECOMPRESSIVE craniectomy ,DESCRIPTIVE statistics ,ANTIBIOTIC prophylaxis ,PERIOPERATIVE care ,GLASGOW Coma Scale - Abstract
Objective: To retrospectively analyse the surgical management and outcomes of non-missile open head injuries (NMOHI). Methods: Forty-four patients who suffered from NMOHI were included. The Glasgow outcome score (GOS), computed tomography (CT), aetiology and outcomes and complications at discharge and during a 6-month follow-up were analysed. All patients underwent debridement. Intracranial haematoma evacuation, decompressive craniectomy (DC) or replacement were performed. Results: Motor vehicle accident and struck by/against were the most common causes (43.2% each). At admission, 33 patients had Glasgow coma scores (GCS) > 8 and 27 of them had a GCS score of > 13. Mean follow-up was 8.7 ± 4.3 months. All patients underwent debridement, 20 underwent bone fracture replacement and 27 underwent haematoma evacuation; 11 patients underwent haematoma evacuation and DC and one had bilateral DC. Twenty-seven patients showed good recovery; 11 patients had moderate disability; three patients had severe disability; and three patients died. After 6 months, 32 patients had good recovery and the morbidity of severe disability had decreased to 13.6%. Thirteen patients developed intracranial infection. Post-traumatic epilepsy and hydrocephalus was detected in three patients. Cerebrospinal fluid fistula was found in five patients. Only one patient developed a brain abscess after 6 months. Conclusions: NMOHI yielded satisfactory recovery and achieved good outcomes. [ABSTRACT FROM AUTHOR]
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- 2016
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16. Right Median Nerve Electrical Stimulation for Acute Traumatic Coma Patients.
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Lei, Jin, Wang, Lei, Gao, Guoyi, Cooper, Edwin, and Jiang, Jiyao
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- 2015
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17. Glial fibrillary acidic protein as a biomarker in severe traumatic brain injury patients: a prospective cohort study.
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Jin Lei, Guoyi Gao, Junfeng Feng, Yichao Jin, Chuanfang Wang, Qing Mao, Jiyao Jiang, Lei, Jin, Gao, Guoyi, Feng, Junfeng, Jin, Yichao, Wang, Chuanfang, Mao, Qing, and Jiang, Jiyao
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BRAIN injuries ,CYTOSKELETAL proteins ,LONGITUDINAL method ,NEUROLOGIC examination ,PROGNOSIS ,GLASGOW Coma Scale ,DIAGNOSIS - Abstract
Introduction: Glial fibrillary acidic protein (GFAP) may serve as a serum marker of traumatic brain injury (TBI) that can be used to monitor biochemical changes in patients and gauge the response to treatment. However, the temporal profile of serum GFAP in the acute period of brain injury and the associated utility for outcome prediction has not been elucidated.Methods: We conducted a prospective longitudinal cohort study of consecutive severe TBI patients in a local tertiary neurotrauma center in Shanghai, China, between March 2011 and September 2014. All patients were monitored and managed with a standardized protocol with inclusion of hypothermia and other intensive care treatments. Serum specimens were collected on admission and then daily for the first 5 days. GFAP levels were measured using enzyme-linked immunosorbent assay techniques. Patient outcome was assessed at 6 months post injury with the Glasgow Outcome Scale and further grouped into death versus survival and unfavorable versus favorable.Results: A total of 67 patients were enrolled in the study. The mean time from injury to admission was 2.6 hours, and the median admission Glasgow Coma Scale score was 6. Compared with healthy subjects, patients with severe TBI had increased GFAP levels on admission and over the subsequent 5 days post injury. Serum GFAP levels showed a gradual reduction from admission to day 3, and then rebounded on day 4 when hypothermia was discontinued with slow rewarming. GFAP levels were significantly higher in patients who died or had an unfavorable outcome across all time points than in those who were alive or had a favorable outcome. Results of receiver operating characteristic curve analysis indicated that serum GFAP at each time point could predict neurological outcome at 6 months. The areas under the curve for GFAP on admission were 0.761 for death and 0.823 for unfavorable outcome, which were higher than those for clinical variables such as age, Glasgow Coma Scale score, and pupil reactions.Conclusions: Serum GFAP levels on admission and during the first 5 days of injury were increased in patients with severe TBI and were predictive of neurological outcome at 6 months. [ABSTRACT FROM AUTHOR]- Published
- 2015
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18. Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury.
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Gao, Yang, Xu, Siyi, Cui, Zhenwen, Zhang, Mingkun, Lin, Yingying, Cai, Lei, Wang, Zhugang, Luo, Xingguang, Zheng, Yan, Wang, Yong, Luo, Qizhong, Jiang, Jiyao, Neale, Joseph H., and Zhong, Chunlong
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BRAIN injuries ,GLUTAMIC acid ,CARBOXYPEPTIDASES ,DISEASE susceptibility ,SPATIAL memory ,GENE knockout ,NEUROTRANSMITTERS ,LABORATORY mice - Abstract
Glutamate carboxypeptidase II (GCPII) is a transmembrane zinc metallopeptidase found mainly in the nervous system, prostate and small intestine. In the nervous system, glia-bound GCPII mediates the hydrolysis of the neurotransmitter N-acetylaspartylglutamate (NAAG) into glutamate and N-acetylaspartate. Inhibition of GCPII has been shown to attenuate excitotoxicity associated with enhanced glutamate transmission under pathological conditions. However, different strains of mice lacking the GCPII gene are reported to exhibit striking phenotypic differences. In this study, a GCPII gene knockout (KO) strategy involved removing exons 3-5 of GCPII. This generated a new GCPII KO mice line with no overt differences in standard neurological behavior compared to their wild-type (WT) littermates. However, GCPII KO mice were significantly less susceptible to moderate traumatic brain injury (TBI). GCPII gene KO significantly lessened neuronal degeneration and astrocyte damage in the CA2 and CA3 regions of the hippocampus 24 h after moderate TBI. In addition, GCPII gene KO reduced TBI-induced deficits in long-term spatial learning/memory tested in the Morris water maze and motor balance tested via beam walking. Knockout of the GCPII gene is not embryonic lethal and affords histopathological protection with improved long-term behavioral outcomes after TBI, a result that further validates GCPII as a target for drug development consistent with results from studies using GCPII peptidase inhibitors. [ABSTRACT FROM AUTHOR]
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- 2015
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19. Residual hemifacial spasm after microvascular decompression: prognostic factors with emphasis on preoperative psychological state.
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Jin, Yichao, Zhao, Changyi, Su, Shanshan, Zhang, Xiaohua, Qiu, Yongming, and Jiang, Jiyao
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SPASMS ,MICROCIRCULATION disorders ,NEUROMUSCULAR diseases ,FACIAL hemiatrophy ,FACIAL nerve diseases - Abstract
Residual hemifacial spasm (HFS) after microvascular decompression (MVD) is common, and the factors associated with residual HFS are still controversial. In the present study, we analyzed the outcome of 212 patients with hemifacial spasm after a single microvascular decompression and evaluated the prognostic factors involved in residual hemifacial spasm. Based on our study, possible prognostic factors included indentation of the root exit zone (REZ), preoperative illness duration, and preoperative psychological state. We suggest that MVD should be performed as early as possible for it may decrease the rate of residual HFS. Preoperative assessment of psychological state in HFS patients is a timely intervention that should be implemented to minimize the residual HFS. [ABSTRACT FROM AUTHOR]
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- 2015
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20. Blockade of N-acetylaspartylglutamate peptidases: a novel protective strategy for brain injuries and neurological disorders.
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Zhong, Chunlong, Luo, Qizhong, and Jiang, Jiyao
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BRAIN injury treatment ,NEUROLOGICAL disorders ,THERAPEUTICS ,ASPARTYL peptides ,N-Acetylglutamate ,PEPTIDASE ,GLUTAMATE receptors ,NEUROPROTECTIVE agents - Abstract
The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) is reported to suppress glutamate release mainly through selective activation of presynaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3). Therefore, strategies of inhibition of NAAG peptidases and subsequent NAAG hydrolysis to elevate levels of NAAG could reduce glutamate release under pathological conditions and be neuroprotective by attenuating excitotoxic cell injury. A series of potent inhibitors of NAAG peptidases has been synthesized and demonstrated efficacy in experimental models of ischemic-hypoxic brain injury, traumatic brain injury, inflammatory pain, diabetic neuropathy, amyotrophic lateral sclerosis and phencyclidine-induced schizophrenia-like behaviors. The excessive glutamatergic transmission has been implicated in all of these neurological disorders. Thus, blockade of NAAG peptidases may augment an endogenous protective mechanism and afford neuroprotection in the brain. This review aims to summarize and provide insight into the current understanding of the novel neuroprotective strategy based on limiting glutamate excitotoxicity for a wide variety of brain injuries and neurological disorders. [ABSTRACT FROM AUTHOR]
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- 2014
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21. The neuroprotective effects of intravascular low level laser irradiation on cerebral ischemia rats.
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Qiu, Yongming, Lu, Zhaofeng, Wang, Zhongguang, and Jiang, Jiyao
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- 2005
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22. Atorvastatin increases endothelial progenitor cells in balloon-injured mouse carotid artery.
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Zhou, Jianpo, Chen, Lei, Fan, Yiling, Jiang, Jiyao, and Wan, Jieqing
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ATORVASTATIN ,PROGENITOR cells ,NITRIC-oxide synthases ,MESSENGER RNA ,VASCULAR endothelial growth factor receptors ,TREATMENT of carotid artery diseases ,ENDOTHELIAL cells ,HYPERPLASIA ,PREVENTION - Abstract
Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 2014
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23. Acute Traumatic Brain Injury: Is Current Management Evidence Based? An Empirical Analysis of Systematic Reviews.
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Lei, Jin, Gao, Guoyi, and Jiang, Jiyao
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- 2013
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24. ID1 affects the efficacy of radiotherapy in glioblastoma through inhibition of DNA repair pathways.
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Guo, Qinhua, Guo, Pin, Mao, Qing, Lan, Jin, Lin, Yingying, Jiang, Jiyao, and Qiu, Yongming
- Abstract
Glioblastoma multiforme (GBM) is characterized by poor therapeutic response and poor overall survival. It is crucial that more effective therapies be developed for the treatment of GBM. Inhibitor of DNA binding protein-1 (ID1) has been shown to maintain the self-renewal capacity of neural stem cells and might be involved in the therapeutic resistance of GBM. In the present study, we explored survival data from the The Cancer Genome Atalas database that were based on ID1 expression for patients diagnosed with primary GBMs. Interestingly, patients with high ID1 expression had better survival than patients with low ID1 expression, and a strong correlation was found between radiotherapy efficacy, ID1 expression, and overall survival. We further investigated the relationship between ID1 expression and the radiosensitivity of glioblastoma using glioblastoma cell lines. The clonogenic formation assay showed that U87 ID1-shRNA cells were much less sensitive to radiation. Moreover, both the results of the γH2AX foci staining assay and the comet assay further revealed that ID1 negatively regulates DNA repair processes by downregulating the expression of genes such as DNA ligase IV (LIG4) and ataxia-telangiectasia-mutated. Additionally, ID1 induces G2/M arrest in U87 cells. Taken together, these results suggest that ID1 may be a new prognostic marker for GBM and have important implications for the therapeutic strategies used to treat GBM patients. [ABSTRACT FROM AUTHOR]
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- 2013
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25. Role of intraoperative microvascular Doppler in the microsurgical management of intracranial aneurysms.
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Cui, Hua, Wang, Yong, Yin, Yuhua, Wan, Jieqing, Fei, Zhimin, Gao, Weizhen, and Jiang, Jiyao
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Background: The outcome of surgical treatment of intracranial aneurysms may be influenced by incomplete exclusion of the aneurysm or stenosis of the parent vessels. The goal of this study was to evaluate the usefulness and reliability of intraoperative microvascular Doppler (IMD) in guiding optimal clip placement in aneurysm surgery.Methods: We conducted a retrospective analysis of 79 patients, with a total of 85 intracranial aneurysms, operated between January 2004 and April 2009, who were evaluated with IMD using a 20-MHz probe before and after clip application. IMD was used to examine the aneurysmal sac and adjacent vessels.Results: The findings of IMD helped in adjusting the clip placement. In 9 (10.6%) of the 85 aneurysms, IMD revealed a persistent blood flow through the aneurysmal sac after clip application and the clip was repositioned. IMD showed relevant stenosis of adjacent vessels induced by the clip positioning in 10 of 79 (12.7%) cases. In six cases (7.6%), a blood flow reduction in the artery feeding the aneurysm was evident after clipping; in the other four cases (5.1%), the clip produced a severe blood flow reduction in other adjacent vessels. In addition, in two of these cases, an initial stenosis induced by clip positioning that had escaped detection by visual inspection through the operating microscope was identified by IMD. There were no complications related to the use of IMD.Conclusions: IMD is a safe, feasible, and very reliable technique and should be used routinely in intracranial aneurysm surgery. [ABSTRACT FROM AUTHOR]- Published
- 2011
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26. Extracranial Microanatomic Study of Supraorbital Keyhole Approach.
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Lin, Yixin, Zhang, Weiqiao, Luo, Qizhong, Jiang, Jiyao, and Qiu, Yongming
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- 2009
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27. The expression of glutamate transporters in chest compression-induced audiogenic epilepsy: a comparative study.
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Lu, Zhaofeng, Zhang, Weiqiao, Zhang, Ning, Jiang, Jiyao, Luo, Qizhong, and Qiu, Yongming
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Background: This study was conducted to compare the expression of three glutamate transporter subtypes (GLAST, GLT-1 and EAAC1) in rats undergoing chest compression-induced global cerebral ischemia in the presence and absence of cerebral ischemia-related epilepsy. Material and methods: A reliable rat model of global cerebral ischemia-related epilepsy was established. The rats were divided into the following groups: sham surgery group (Group S), global cerebral ischemia without epilepsy (Group I) and global cerebral ischemia with epilepsy (Group E). The latter two groups were further divided into four subgroups based on time (24 hours, 72 hours, 5 days and 7 days) after 8 minutes of chest compression. Electroencephalographic recordings were obtained in all rats. Hippocampal tissue samples were prepared, and the expression of GLAST, GLT-1 and EAAC1 in the hippocampal CA1 region and the motor cortex area was studied using immunohistochemical methods. Results: Seizure developed in 32 (64%) of 50 rats. Compared with that in group I, the expression of GLT-1 in the hippocampal CA1 region and the motor cortex area in group E was down-regulated, and EAAC1 was up-regulated in those regions. Conclusion: Altering the expression of GLT-1 and EAAC1 through some means might lead them to be potential targets for therapy in cerebral ischemia-related epilepsy. [ABSTRACT FROM AUTHOR]
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- 2008
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28. Primary diffuse large B-cell lymphoma of the dura mimicking a meningioma with intervening skull bone invasion.
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Gao, Yang, Zhong, Chunlong, and Jiang, Jiyao
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- 2014
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29. miRNA Delivery: Tailored Lipoprotein‐Like miRNA Delivery Nanostructure Suppresses Glioma Stemness and Drug Resistance through Receptor‐Stimulated Macropinocytosis (Adv. Sci. 5/2020).
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Jiang, Gan, Chen, Huan, Huang, Jialin, Song, Qingxiang, Chen, Yaoxing, Gu, Xiao, Jiang, Zhenhuan, Huang, Yukun, Lin, Yingying, Feng, Junfeng, Jiang, Jiyao, Bao, Yinghui, Zheng, Gang, Chen, Jun, Chen, Hongzhuan, and Gao, Xiaoling
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DRUG resistance ,MICRORNA ,NANOSTRUCTURES - Published
- 2020
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30. Moderate hypothermia inhibits microglial activation after traumatic brain injury by modulating autophagy/apoptosis and the MyD88-dependent TLR4 signaling pathway.
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Zhang, Fengchen, Dong, Haiping, Lv, Tao, Jin, Ke, Jin, Yichao, Zhang, Xiaohua, and Jiang, Jiyao
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BRAIN injuries ,HYPOTHERMIA treatment ,NEUROGLIA ,TOLL-like receptors ,DOWNREGULATION - Abstract
Background: Complex mechanisms participate in microglial activation after a traumatic brain injury (TBI). TBI can induce autophagy and apoptosis in neurons and glial cells, and moderate hypothermia plays a protective role in the acute phase of TBI. In the present study, we evaluated the effect of TBI and moderate hypothermia on microglial activation and investigated the possible roles of autophagy/apoptosis and toll-like receptor 4 (TLR4).Methods: The TBI model was induced with a fluid percussion TBI device. Moderate hypothermia was achieved under general anesthesia by partial immersion in a water bath for 4 h. All rats were killed 24 h after the TBI.Results: Our results showed downregulation of the microglial activation and autophagy, but upregulation of microglial apoptosis, upon post-TBI hypothermia treatment. The expression of TLR4 and downstream myeloid differentiation primary response 88 (MyD88) was attenuated. Moderate hypothermia reduced neural cell death post-TBI.Conclusions: Moderate hypothermia can reduce the number of activated microglia by inhibiting autophagy and promoting apoptosis, probably through a negative modulation between autophagy and apoptosis. Moderate hypothermia may attenuate the pro-inflammatory function of microglia by inhibiting the MyD88-dependent TLR4 signaling pathway. [ABSTRACT FROM AUTHOR]- Published
- 2018
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31. Eight-year follow-up of a fibromuscular dysplasia patient with multiple fusiform aneurysms.
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Guo, Liemei, Qiu, Yongming, Zhang, Xiaohua, and Jiang, Jiyao
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LETTERS to the editor ,FIBROUS dysplasia of bone ,DYSPLASIA - Abstract
A letter to the editor regarding follow-up of a fibromuscular dysplasia patient with multiple fusiform aneurysms is presented.
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- 2012
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