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Management of Traumatic Brain Injuries at the Kara Regional Hospital
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作者 Tamegnon Dossouvi Tchaa Hodabalo Towoezim +3 位作者 Abdel Kader Moumouni Kokou Kanassoua Iroukora Kassegne Ekoue David Dosseh 《Surgical Science》 2024年第2期19-27,共9页
Introduction: Traumatic Brain Injury (TBI) is a major public health problem causing significant morbidity and mortality in young adults. This study aimed to describe the epidemiological, diagnostic, therapeutic, and e... Introduction: Traumatic Brain Injury (TBI) is a major public health problem causing significant morbidity and mortality in young adults. This study aimed to describe the epidemiological, diagnostic, therapeutic, and evolutionary aspects of TBI. Materials and Methods: This was a prospective, descriptive study conducted from 1 April 2022 to 31 March 2023 on patients admitted to and treated for cranioencephalic trauma in the General Surgery department of Kara Regional Hospital. Results: Eighty-three (83) patients with cranioencephalic trauma were managed out of 773 patients admitted to the department during the study period. The mean age was 34 ± 14.98 years and the sex ratio was 3.6 in favour of men. Motorbike taxi drivers were the social group most affected (n = 33, 40%). The causes of trauma were dominated by public road accidents (n = 80;96%). TBI was mild (n = 40;48%), moderate (n = 35;42%) and severe (n = 8;10%). Cerebral CT scans were performed in 19 patients (23%). Cerebral contusion (n = 4) was the most frequent cerebral lesion. Six patients (7%) with severe head injuries were transferred to Kara University Hospital. Six deaths (7%) occurred in patients with severe head injuries. The main sequelae were intermittent headaches in all patients reviewed, and memory problems (6%). Conclusion: Traumatic brain injuries are common at Kara Regional Hospital. Severe cranial trauma is less frequent but leads to death because of financial difficulties and limited technical facilities. 展开更多
关键词 Traumatic brain Injury Road Accident MOTORCYCLIST Cerebral Contusion TOGO
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The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury 被引量:2
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作者 Yijing Zhao Tong Li +6 位作者 Zige Jiang Chengcheng Gai Shuwen Yu Danqing Xin Tingting Li Dexiang Liu Zhen Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第5期1084-1091,共8页
We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation r... We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury. 展开更多
关键词 chemokine(C-X-C motif)ligand 11 cystathionineβsynthase H2S hypoxic ischemic brain injury inflammation L-CYSTEINE lipopolysaccharide microglia miR-9-5p neuroprotection
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Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury 被引量:1
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作者 Jingzhou Liu Xin Xin +8 位作者 Jiejie Sun Yueyue Fan Xun Zhou Wei Gong Meiyan Yang Zhiping Li Yuli Wang Yang Yang Chunsheng Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期629-635,共7页
Traumatic brain injury results in neuronal loss and glial scar formation.Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury.Neuronal reprogr... Traumatic brain injury results in neuronal loss and glial scar formation.Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury.Neuronal reprogramming is a promising strategy to convert glial scars to neural tissue.However,previous studies have reported inconsistent results.In this study,an AAV9P1 vector incorporating an astrocyte-targeting P1 peptide and glial fibrillary acidic protein promoter was used to achieve dual-targeting of astrocytes and the glial scar while minimizing off-target effects.The results demonstrate that AAV9P1 provides high selectivity of astrocytes and reactive astrocytes.Moreover,neuronal reprogramming was induced by downregulating the polypyrimidine tract-binding protein 1 gene via systemic administration of AAV9P1 in a mouse model of traumatic brain injury.In summary,this approach provides an improved gene delivery vehicle to study neuronal programming and evidence of its applications for traumatic brain injury. 展开更多
关键词 AAV9P1 ASTROCYTES astrocyte-to-neuron conversion GFAP promoter glial scar induced neurons neuronal reprogramming P1 peptide PTBP1 traumatic brain injury
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Transcriptomic and bioinformatics analysis of the mechanism by which erythropoietin promotes recovery from traumatic brain injury in mice 被引量:1
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作者 Weilin Tan Jun Ma +9 位作者 Jiayuanyuan Fu Biying Wu Ziyu Zhu Xuekang Huang Mengran Du Chenrui Wu Ehab Balawi Qiang Zhou Jie Zhang Zhengbu Liao 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第1期171-179,共9页
Recent studies have found that erythropoietin promotes the recovery of neurological function after traumatic brain injury.However,the precise mechanism of action remains unclea r.In this study,we induced moderate trau... Recent studies have found that erythropoietin promotes the recovery of neurological function after traumatic brain injury.However,the precise mechanism of action remains unclea r.In this study,we induced moderate traumatic brain injury in mice by intrape ritoneal injection of erythro poietin for 3 consecutive days.RNA sequencing detected a total of 4065 differentially expressed RNAs,including 1059 mRNAs,92 microRNAs,799 long non-coding RNAs,and 2115circular RNAs.Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses revealed that the coding and non-coding RNAs that were differentially expressed after traumatic brain injury and treatment with erythropoietin play roles in the axon guidance pathway,Wnt pathway,and MAPK pathway.Constructing competing endogenous RNA networks showed that regulatory relationship between the differentially expressed non-coding RNAs and mRNAs.Because the axon guidance pathway was repeatedly enriched,the expression of Wnt5a and Ephb6,key factors in the axonal guidance pathway,was assessed.Ephb6 expression decreased and Wnt5a expression increased after traumatic brain injury,and these effects were reversed by treatment with erythro poietin.These findings suggest that erythro poietin can promote recove ry of nerve function after traumatic brain injury through the axon guidance pathway. 展开更多
关键词 axon guidance bioinformatics analysis competing endogenous RNA ERYTHROPOIetIN Gene Ontology Kyoto Encyclopedia of Genes and Genomes non-coding RNA RNA sequencing transcriptomics traumatic brain injury
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Structural and functional connectivity of the whole brain and subnetworks in individuals with mild traumatic brain injury:predictors of patient prognosis
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作者 Sihong Huang Jungong Han +4 位作者 Hairong Zheng Mengjun Li Chuxin Huang Xiaoyan Kui Jun Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1553-1558,共6页
Patients with mild traumatic brain injury have a diverse clinical presentation,and the underlying pathophysiology remains poorly understood.Magnetic resonance imaging is a non-invasive technique that has been widely u... Patients with mild traumatic brain injury have a diverse clinical presentation,and the underlying pathophysiology remains poorly understood.Magnetic resonance imaging is a non-invasive technique that has been widely utilized to investigate neuro biological markers after mild traumatic brain injury.This approach has emerged as a promising tool for investigating the pathogenesis of mild traumatic brain injury.G raph theory is a quantitative method of analyzing complex networks that has been widely used to study changes in brain structure and function.However,most previous mild traumatic brain injury studies using graph theory have focused on specific populations,with limited exploration of simultaneous abnormalities in structural and functional connectivity.Given that mild traumatic brain injury is the most common type of traumatic brain injury encounte red in clinical practice,further investigation of the patient characteristics and evolution of structural and functional connectivity is critical.In the present study,we explored whether abnormal structural and functional connectivity in the acute phase could serve as indicators of longitudinal changes in imaging data and cognitive function in patients with mild traumatic brain injury.In this longitudinal study,we enrolled 46 patients with mild traumatic brain injury who were assessed within 2 wee ks of injury,as well as 36 healthy controls.Resting-state functional magnetic resonance imaging and diffusion-weighted imaging data were acquired for graph theoretical network analysis.In the acute phase,patients with mild traumatic brain injury demonstrated reduced structural connectivity in the dorsal attention network.More than 3 months of followup data revealed signs of recovery in structural and functional connectivity,as well as cognitive function,in 22 out of the 46 patients.Furthermore,better cognitive function was associated with more efficient networks.Finally,our data indicated that small-worldness in the acute stage could serve as a predictor of longitudinal changes in connectivity in patients with mild traumatic brain injury.These findings highlight the importance of integrating structural and functional connectivity in unde rstanding the occurrence and evolution of mild traumatic brain injury.Additionally,exploratory analysis based on subnetworks could serve a predictive function in the prognosis of patients with mild traumatic brain injury. 展开更多
关键词 cognitive function CROSS-SECTION FOLLOW-UP functional connectivity graph theory longitudinal study mild traumatic brain injury prediction small-worldness structural connectivity subnetworks whole brain network
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Mitophagy in acute central nervous system injuries:regulatory mechanisms and therapeutic potentials
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作者 Siyi Xu Junqiu Jia +2 位作者 Rui Mao Xiang Cao Yun Xu 《Neural Regeneration Research》 SCIE CAS 2025年第9期2437-2453,共17页
Acute central nervous system injuries,including ischemic stro ke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal co rd injury,are a major global health challenge.Identifying optimal ... Acute central nervous system injuries,including ischemic stro ke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal co rd injury,are a major global health challenge.Identifying optimal therapies and improving the long-term neurological functions of patients with acute central nervous system injuries are urgent priorities.Mitochondria are susceptible to damage after acute central nervous system injury,and this leads to the release of toxic levels of reactive oxygen species,which induce cell death.Mitophagy,a selective form of autophagy,is crucial in eliminating redundant or damaged mitochondria during these events.Recent evidence has highlighted the significant role of mitophagy in acute central nervous system injuries.In this review,we provide a comprehensive overview of the process,classification,and related mechanisms of mitophagy.We also highlight the recent developments in research into the role of mitophagy in various acute central nervous system injuries and drug therapies that regulate mitophagy.In the final section of this review,we emphasize the potential for treating these disorders by focusing on mitophagy and suggest future research paths in this area. 展开更多
关键词 autophagy intracerebral hemorrhage ischemic stroke mitochondria mitochondrial biogenesis mitochondrial quality control MITOPHAGY spinal cord injury subarachnoid hemorrhage traumatic brain injury
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Placenta-derived mesenchymal stem cells attenuate secondary brain injury after controlled cortical impact in rats by inhibiting matrix metalloproteinases
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作者 PING YANG YUANXIANG LAN +2 位作者 ZHONG ZENG YAN WANG HECHUN XIA 《BIOCELL》 SCIE 2024年第1期149-162,共14页
Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-t... Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-target and multi-pathway mode of action.Material&Methods:This study investigates the protective mechanisms and benefits of PDMSCs in mitigating the effects of controlled cortical impact(CCI)in rats and glutamate-induced oxidative stress injury in HT22 cells in vitro.Our primary objective is to provide evidence supporting the clinical application of PDMSCs.Results:In the in vivo arm of our investigation,we observed a swift elevation of matrix metalloproteinase-9(MMP-9)in the proximal cortex of injured brain tissues after CCI.PDMSCs,distinguished by their heightened expression of metalloproteinase tissue inhibitors-1 and-2(TIMP-1 and TIMP-2):were intravenously administered via the caudal vein.This intervention yielded significant reductions in the permeability of the blood-brain barrier(BBB):the extent of brain edema,the levels of inflammatory cytokines IL-1βand TNF-αin damaged brain tissue,and the activation status of microglia in CCI-afflicted rats.In the realm of in vitro experiments,PDMSC-conditioned media demonstrated substantial reductions in mortality rates and cleaved caspase-3 levels in glutamate-induced HT22 cells compared with conventional media.Notably,this advantage was negated upon the introduction of neutralizing antibodies targeting TIMP-1 and TIMP-2.Conclusion:Collectively,our findings underscore the potential of PDMSCs in alleviating oxidative stress injury and secondary brain injury in the pathological process of TBI. 展开更多
关键词 Traumatic brain injury Mesenchymal stem cells Oxidative stress Matrix metalloproteinases
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Impact of increasing one-carbon metabolites on traumatic brain injury outcome using pre-clinical models
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作者 Sanika M.Joshi Theresa Currier Thomas Nafisa M.Jadavji 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第8期1728-1733,共6页
Traumatic brain injury is a major cause of death and disability worldwide,affecting over 69 million individuals yearly.One-carbon metabolism has been shown to have beneficial effects after brain damage,such as ischemi... Traumatic brain injury is a major cause of death and disability worldwide,affecting over 69 million individuals yearly.One-carbon metabolism has been shown to have beneficial effects after brain damage,such as ischemic stroke.However,whether increasing one-carbon metabolite vitamins impacts traumatic brain injury outcomes in patients requires more investigation.The aim of this review is to evaluate how one-carbon metabolites impact outcomes after the onset of traumatic brain injury.PubMed,Web of Science,and Google Scholar databases were searched for studies that examined the impact of B-vitamin supplementation on traumatic brain injury outcomes.The search terms included combinations of the following words:traumatic brain injury,dietary supplementation,one-carbon metabolism,and B-vitamins.The focus of each literature search was basic science data.The year of publication in the literature searches was not limited.Our analysis of the literature has shown that dietary supplementation of B-vitamins has significantly improved the functional and behavioral recove ry of animals with traumatic brain injury compared to controls.Howeve r,this improvement is dosage-dependent and is contingent upon the onset of supplementation and whether there is a sustained or continuous delive ry of vitamin supplementation post-traumatic brain injury.The details of supplementation post-traumatic brain injury need to be further investigated.Overall,we conclude that B-vitamin supplementation improves behavioral outcomes and reduces cognitive impairment post-traumatic brain injury in animal model systems.Further investigation in a clinical setting should be stro ngly considered in co njunction with current medical treatments for traumatic brain injury-affected individuals. 展开更多
关键词 folic acid NICOTINAMIDE one-carbon metabolism RIBOFLAVIN traumatic brain injury vitamin B12 vitamin B2 vitamin B3
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Repetitive traumatic brain injury–induced complement C1–related inflammation impairs long-term hippocampal neurogenesis
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作者 Jing Wang Bing Zhang +9 位作者 Lanfang Li Xiaomei Tang Jinyu Zeng Yige Song Chao Xu Kai Zhao Guoqiang Liu Youming Lu Xinyan Li Kai Shu 《Neural Regeneration Research》 SCIE CAS 2025年第3期821-835,共15页
Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In ... Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction. 展开更多
关键词 complement C1 dendrite dentate gyrus hippocampus neural stem cell NEUROGENESIS NEUROINFLAMMATION neurological function neuron traumatic brain injury
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Reduction of epinephrine in the lumbar spinal cord following repetitive blast-induced traumatic brain injury in rats
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作者 Shigeharu Tsuda Mustafa Golam +3 位作者 Jiamei Hou Kevin K.W.Wang Floyd J.Thompson Prodip Bose 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1548-1552,共5页
Traumatic brain inju ry-induced unfavorable outcomes in human patients have independently been associated with dysregulated levels of monoamines,especially epinephrine,although few preclinical studies have examined th... Traumatic brain inju ry-induced unfavorable outcomes in human patients have independently been associated with dysregulated levels of monoamines,especially epinephrine,although few preclinical studies have examined the epinephrine level in the central nervous system after traumatic brain injury.Epinephrine has been shown to regulate the activities of spinal motoneurons as well as increase the heart rate,blood pressure,and blood flow to the hindlimb muscles.Therefore,the purpose of the present study was to determine the impact of repeated blast-induced traumatic brain injury on the epinephrine levels in seve ral function-s pecific central nervous system regions in rats.Following three repeated blast injuries at 3-day intervals,the hippocampus,motor cortex,locus coeruleus,vestibular nuclei,and lumbar spinal cord were harvested at post-injury day eight and processed for epinephrine assays using a high-sensitive electrochemical detector cou pled with high-performance liquid chromatography.Our results showed that the epinephrine levels were significantly decreased in the lumbar spinal cord tissues of blast-induced traumatic brain injury animals compared to the levels detected in age-and sex-matched sham controls.In other function-specific central nervous system regions,although the epinephrine levels were slightly altered following blast-induced tra u matic brain injury,they were not statistically significant.These results suggest that blast injury-induced significant downregulation of epinephrine in the lumbar spinal cord could negatively impact the motor and cardiovascular function.This is the first repo rt to show altered epinephrine levels in the spinal cord following repetitive mild blast-induced traumatic brain injury. 展开更多
关键词 balance blood flow cardiovascular system central nervous system EPINEPHRINE ischemic damage lumbar spinal cord muscle tone repeated blast SPASTICITY traumatic brain injury
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High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury
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作者 Mengshi Yang Miao Bai +10 位作者 Yuan Zhuang Shenghua Lu Qianqian Ge Hao Li Yu Deng Hongbin Wu Xiaojian Xu Fei Niu Xinlong Dong Bin Zhang Baiyun Liu 《Neural Regeneration Research》 SCIE CAS 2025年第9期2611-2623,共13页
Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-i... Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet known.In the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action.In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization.Lipopolysaccharide,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were administered.RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone.The Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our hypothesis.High-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain injury.Thus dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in vivo.Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury.Additionally,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway.Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia,which plays an antiinflammatory role.In contrast,inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury.Dexamethasone may exe rt its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway. 展开更多
关键词 apoptosis BV2 microglia DEXAMetHASONE glucocorticoid receptor GLUCOCORTICOIDS innate immune system microglial polarization neuroinflammation primary microglia traumatic brain injury
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Safety and efficiency of Wharton’s Jelly-derived mesenchymal stem cell administration in patients with traumatic brain injury:First results of a phase I study
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作者 Serdar Kabatas ErdinçCivelek +6 位作者 Osman Boyalı Gülseli Berivan Sezen Omer Ozdemir Yeliz Bahar-Ozdemir Necati Kaplan Eyüp Can Savrunlu Erdal Karaöz 《World Journal of Stem Cells》 SCIE 2024年第6期641-655,共15页
BACKGROUND Traumatic brain injury(TBI)is characterized by a disruption in the normal function of the brain due to an injury following a trauma,which can potentially cause severe physical,cognitive,and emotional impair... BACKGROUND Traumatic brain injury(TBI)is characterized by a disruption in the normal function of the brain due to an injury following a trauma,which can potentially cause severe physical,cognitive,and emotional impairment.Stem cell transplantation has evolved as a novel treatment modality in the management of TBI,as it has the potential to arrest the degeneration and promote regeneration of new cells in the brain.Wharton’s Jelly-derived mesenchymal stem cells(WJ-MSCs)have recently shown beneficial effects in the functional recovery of neurological deficits.AIM To evaluate the safety and efficiency of MSC therapy in TBI.METHODS We present 6 patients,4 male and 2 female aged between 21 and 27 years who suffered a TBI.These 6 patients underwent 6 doses of intrathecal,intramuscular(i.m.)and intravenous transplantation of WJ-MSCs at a target dose of 1×106/kg for each application route.Spasticity was assessed using the Modified Ashworth scale(MAS),motor function according to the Medical Research Council Muscle Strength Scale,quality of life was assessed by the Functional Independence Measure(FIM)scale and Karnofsky Performance Status scale.RESULTS Our patients showed only early,transient complications,such as subfebrile fever,mild headache,and muscle pain due to i.m.injection,which resolved within 24 h.During the one year follow-up,no other safety issues or adverse events were reported.These 6 patients showed improvements in their cognitive abilities,muscle spasticity,muscle strength,performance scores and fine motor skills when compared before and after the intervention.MAS values,which we used to assess spasticity,were observed to statistically significantly decrease for both left and right sides(P<0.001).The FIM scale includes both motor scores(P<0.05)and cognitive scores(P<0.001)and showed a significant increase in pretest posttest analyses.The difference observed in the participants’Karnofsky Performance Scale values pre and post the intervention was statistically significant(P<0.001).CONCLUSION This study showed that cell transplantation has a safe,effective and promising future in the management of TBI. 展开更多
关键词 Traumatic brain injury Wharton Jelly Stem cell therapy TRANSPLANTATION Mesenchymal stem cell
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Resting-state brain network remodeling after different nerve reconstruction surgeries:a functional magnetic resonance imaging study in brachial plexus injury rats
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作者 Yunting Xiang Xiangxin Xing +6 位作者 Xuyun Hua Yuwen Zhang Xin Xue Jiajia Wu Mouxiong Zheng He Wang Jianguang Xu 《Neural Regeneration Research》 SCIE CAS 2025年第5期1495-1504,共10页
Distinct brain remodeling has been found after different nerve reconstruction strategies,including motor representation of the affected limb.However,differences among reconstruction strategies at the brain network lev... Distinct brain remodeling has been found after different nerve reconstruction strategies,including motor representation of the affected limb.However,differences among reconstruction strategies at the brain network level have not been elucidated.This study aimed to explore intranetwork changes related to altered peripheral neural pathways after different nerve reconstruction surgeries,including nerve repair,endto-end nerve transfer,and end-to-side nerve transfer.Sprague–Dawley rats underwent complete left brachial plexus transection and were divided into four equal groups of eight:no nerve repair,grafted nerve repair,phrenic nerve end-to-end transfer,and end-to-side transfer with a graft sutured to the anterior upper trunk.Resting-state brain functional magnetic resonance imaging was obtained 7 months after surgery.The independent component analysis algorithm was utilized to identify group-level network components of interest and extract resting-state functional connectivity values of each voxel within the component.Alterations in intra-network resting-state functional connectivity were compared among the groups.Target muscle reinnervation was assessed by behavioral observation(elbow flexion)and electromyography.The results showed that alterations in the sensorimotor and interoception networks were mostly related to changes in the peripheral neural pathway.Nerve repair was related to enhanced connectivity within the sensorimotor network,while end-to-side nerve transfer might be more beneficial for restoring control over the affected limb by the original motor representation.The thalamic-cortical pathway was enhanced within the interoception network after nerve repair and end-to-end nerve transfer.Brain areas related to cognition and emotion were enhanced after end-to-side nerve transfer.Our study revealed important brain networks related to different nerve reconstructions.These networks may be potential targets for enhancing motor recovery. 展开更多
关键词 brain functional networks end-to-end nerve transfer end-to-side nerve transfer independent component analysis nerve repair peripheral plexus injury resting-state functional connectivity
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Exosomes derived from microglia overexpressing miR-124-3p alleviate neuronal endoplasmic reticulum stress damage after repetitive mild traumatic brain injury
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作者 Yan Wang Dai Li +12 位作者 Lan Zhang Zhenyu Yin Zhaoli Han Xintong Ge Meimei Li Jing Zhao Shishuang Zhang Yan Zuo Xiangyang Xiong Han Gao Qiang Liu Fanglian Chen Ping Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2010-2018,共9页
We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repet... We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repetitive mild traumatic brain injury remains unclear.In this study,we first used an HT22 scratch injury model to mimic traumatic brain injury,then co-cultured the HT22 cells with BV2 microglia expressing high levels of miR-124-3p.We found that exosomes containing high levels of miR-124-3p attenuated apoptosis and endoplasmic reticulum stress.Furthermore,luciferase reporter assay analysis confirmed that miR-124-3p bound specifically to the endoplasmic reticulum stress-related protein IRE1α,while an IRE1αfunctional salvage experiment confirmed that miR-124-3p targeted IRE1αand reduced its expression,thereby inhibiting endoplasmic reticulum stress in injured neurons.Finally,we delivered microglia-derived exosomes containing miR-124-3p intranasally to a mouse model of repetitive mild traumatic brain injury and found that endoplasmic reticulum stress and apoptosis levels in hippocampal neurons were significantly reduced.These findings suggest that,after repetitive mild traumatic brain injury,miR-124-3 can be transferred from microglia-derived exosomes to injured neurons,where it exerts a neuroprotective effect by inhibiting endoplasmic reticulum stress.Therefore,microglia-derived exosomes containing miR-124-3p may represent a novel therapeutic strategy for repetitive mild traumatic brain injury. 展开更多
关键词 apoptosis C/EBP homologous protein endoplasmic reticulum stress EXOSOME inositol-requiring enzyme MICROGLIA miR-124-3p neuron repetitive mild traumatic brain injury X-box binding protein 1
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Optic nerve sheath diameters in nontraumatic brain injury:A scoping review and role in the intensive care unit
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作者 Madhura Bhide Deven Juneja +1 位作者 Omender Singh Shakya Mohanty 《World Journal of Critical Care Medicine》 2024年第3期75-90,共16页
BACKGROUND Neuromonitoring in medical intensive care units is challenging as most patients are unfit for invasive intracranial pressure(ICP)modalities or unstable to transport for imaging.Ultrasonography-based optic n... BACKGROUND Neuromonitoring in medical intensive care units is challenging as most patients are unfit for invasive intracranial pressure(ICP)modalities or unstable to transport for imaging.Ultrasonography-based optic nerve sheath diameter(ONSD)is an attractive option as it is reliable,repeatable and easily performed at the bedside.It has been sufficiently validated in traumatic brain injury(TBI)to be incorporated into the guidelines.However,currently the data for non-TBI patients is inconsistent for a scientific recommendation to be made.AIM To compile the existing evidence for understanding the scope of ONSD in measuring ICP in adult non-traumatic neuro-critical patients.METHODS PubMed,Google Scholar and research citation analysis databases were searched for studies in adult patients with non-traumatic causes of raised ICP.Studies from 2010 to 2024 in English languages were included.RESULTS We found 37 articles relevant to our search.The cutoff for ONSD in predicting ICP varied from 4.1 to 6.3 mm.Most of the articles used cerebrospinal fluid opening pressure followed by raised ICP on computed tomography/magnetic resonance imaging as the comparator parameter.ONSD was also found to be a reliable outcome measure in cases of acute ischaemic stroke,intracerebral bleeding and intracranial infection.However,ONSD is of doubtful utility in septic metabolic encephalopathy,dysnatremias and aneurysmal subarachnoid haemorrhage.CONCLUSION ONSD is a useful tool for the diagnosis of raised ICP in non-traumatic neuro-critically ill patients and may also have a role in the prognostication of a subset of patients. 展开更多
关键词 Intracranial hypertension Intracranial pressure monitoring Medical intensive care unit Neuro-monitoring Nontraumatic brain injury Optic nerve sheath diameter Optic nerve ultrasound
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Toll-like receptor 4 as a possible therapeutic target for delayed brain injuries after aneurysmal subarachnoid hemorrhage 被引量:24
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作者 Takeshi Okada Hidenori Suzuki 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第2期193-196,共4页
Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage(SAH), and Toll-like receptor(TLR) 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, T... Neuroinflammation is a well-recognized consequence of subarachnoid hemorrhage(SAH), and Toll-like receptor(TLR) 4 may be an important therapeutic target for post-SAH neuroinflammation. Of the TLR family members, TLR4 is expressed in various cell types in the central nervous system, and is unique in that it can signal through both the myeloid differentiation primary-response protein 88-dependent and the toll receptor associated activator of interferon-dependent cascades to coordinate the maximal inflammatory response. TLR4 can be activated by many endogenous ligands having damage-associated molecular patterns including heme and fibrinogen at the rupture of an intracranial aneurysm, and the resultant inflammatory reaction and thereby tissue damages may furthermore activate TLR4. It is widely accepted that the excreted products of TLR4 signaling alter neuronal functions. Previous studies have focused on the pathway through nuclear factor(NF)-κΒ signaling among TLR4 signaling pathways as to the development of early brain injury(EBI) such as neuronal apoptosis and blood-brain barrier disruption, and cerebral vasospasm. However, many findings suggest that both pathways via NF-κΒ and mitogen-activated protein kinases may be involved in EBI and cerebral vasospasm development. To overcome EBI and cerebral vasospasm is important to improve outcomes after SAH, because both EBI and vasopasm are responsible for delayed brain injuries or delayed cerebral ischemia, the most important preventable cause of poor outcomes after SAH. Increasing evidence has shown that TLR4 signaling plays an important role in SAH-induced brain injuries. Better understanding of the roles of TLR4 signaling in SAH will facilitate development of new treatments. 展开更多
关键词 cerebral aneurysm cerebral vasospasm early brain injury delayed brain injury delayed cerebral ischemia inflammation subarachnoid hemorrhage Toll-like receptor 4
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Homer signaling pathways as effective therapeutic targets for ischemic and traumatic brain injuries and retinal lesions 被引量:3
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作者 Xiu-Quan Wu Ning Su +1 位作者 Zhou Fei Fei Fei 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第7期1454-1461,共8页
Ischemic and traumatic insults to the central nervous system account for most serious acute and fatal brain injuries and are usually characterized by primary and secondary damage.Secondary damage presents the greatest... Ischemic and traumatic insults to the central nervous system account for most serious acute and fatal brain injuries and are usually characterized by primary and secondary damage.Secondary damage presents the greatest challenge for medical staff;however,there are currently few effective therapeutic targets for secondary damage.Homer proteins are postsynaptic scaffolding proteins that have been implicated in ischemic and traumatic insults to the central nervous system.Homer signaling can exert either positive or negative effects during such insults,depending on the specific subtype of Homer protein.Homer 1b/c couples with other proteins to form postsynaptic densities,which form the basis of synaptic transmission,while Homer 1a expression can be induced by harmful external factors.Homer 1c is used as a unique biomarker to reveal alterations in synaptic connectivity before and during the early stages of apoptosis in retinal ganglion cells,mediated or affected by extracellular or intracellular signaling or cytoskeletal processes.This review summarizes the structural features,related signaling pathways,and diverse roles of Homer proteins in physiological and pathological processes.Upregulating Homer 1a or downregulating Homer 1b/c may play a neuroprotective role in secondary brain injuries.Homer also plays an important role in the formation of photoreceptor synapses.These findings confirm the neuroprotective effects of Homer,and support the future design of therapeutic drug targets or gene therapies for ischemic and traumatic brain injuries and retinal disorders based on Homer proteins. 展开更多
关键词 brain injury calcium signaling cerebral ischemia dendritic spine glutamate receptor Homer scaffolding protein neuron NEUROPROTECTION retinal ganglion cell review traumatic brain injury
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Combined Spinal Epidural Catheters for Epidural Cooling, Cerebrospinal Fluid Aspiration and Spinal Intralipid Infusion for Treatment of Spinal and Brain Injuries, Diseases and Protection
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作者 Joseph Eldor 《Open Journal of Anesthesiology》 2014年第1期13-30,共18页
A new proposal for spinal cord and brain treatment and protection due to injuries and diseases is made herein. It is composed of two 20G nylon catheters with 6 lateral holes arranged circumferentially within 3 cm from... A new proposal for spinal cord and brain treatment and protection due to injuries and diseases is made herein. It is composed of two 20G nylon catheters with 6 lateral holes arranged circumferentially within 3 cm from the tip and a closed end. One catheter is inserted into the epidural space and the other catheter is inserted into the spinal space in two different lumbar interspaces using an 18G Tuohy needle 90 mm. The epidural catheter is used for cooled saline injection and infusion. The spinal catheter is used for Intralipid spinal injections and CSF aspiration. The proposal is based on the current studies on spinal cord cooling and CSF aspiration as well as on the Intralipid resuscitation properties and lipid brain protection. A study is needed to evaluate the clinical value of this combined approach. 展开更多
关键词 SPINAL CATHetER EPIDURAL CATHetER EPIDURAL Cooling SPINAL INTRALIPID SPINAL Injury brain Injury SPINAL Disease brain Disease SPINAL PROTECTION brain PROTECTION
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重度创伤性颅脑损伤后凝血功能障碍患者血浆α2-抗纤溶酶、vWF及ET-1水平及其影响因素分析 被引量:1
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作者 冯三江 张秀卿 +3 位作者 王鹏 连烨 金晓 刘善贤 《创伤外科杂志》 2024年第4期279-285,共7页
目的探讨重度创伤性颅脑损伤(TBI)后凝血功能障碍患者血浆α2-抗纤溶酶(α2-AP)、血管性血友病因子(vWF)及内皮素-1(ET-1)水平变化及影响因素。方法回顾性分析2021年1月—2022年12月南阳市第一人民医院神经外科和新乡市中心医院神经外... 目的探讨重度创伤性颅脑损伤(TBI)后凝血功能障碍患者血浆α2-抗纤溶酶(α2-AP)、血管性血友病因子(vWF)及内皮素-1(ET-1)水平变化及影响因素。方法回顾性分析2021年1月—2022年12月南阳市第一人民医院神经外科和新乡市中心医院神经外科收治的106例重度TBI患者。其中男性58例,女性48岁;年龄32~60岁,平均43.7岁。根据TBI后24 h内是否发生凝血功能障碍分为凝血正常组(74例)和凝血障碍组(32例)。比较两组重度TBI患者临床资料和入院次日清晨的凝血功能指标及血浆α2-AP、vWF、ET-1水平;Pearson相关性分析重度TBI后凝血功能障碍患者血浆α2-AP、vWF、ET-1水平与凝血功能指标的关系;Logistic回归性分析影响重度TBI患者发生凝血功能障碍的危险因素;受试者工作特征(ROC)曲线分析血浆α2-AP、vWF、ET-1水平对重度TBI患者发生凝血功能障碍的预测价值。结果两组患者年龄、入院GCS、入院头部最高AIS和入院时平均MAP比较,差异有统计学意义[(45.4±5.7)岁vs.(42.8±4.2)岁、(6.7±1.1)分vs.(7.2±0.9)分、(4.6±0.8)分vs.(3.7±0.6)分、(84.1±11.2)mmHg vs.(91.0±9.7)mmHg],P<0.05。凝血障碍组TBI患者PT、APTT和INR等凝血功能指标水平和血浆α2-AP、vWF、ET-1水平高于凝血正常组,纤维蛋白原(FIB)水平低于凝血正常组[(27.9±3.4)s vs.(12.0±1.9)s、(66.4±5.8)s vs.(36.2±2.3)s、1.6±0.2 vs.1.0±0.1、(67.8±8.2)mg/L vs.(19.3±2.4)mg/L、(162.5±24.6)%vs.(94.8±10.4)%、(65.1±5.2)mg/L vs.(41.6±3.9)mg/L、(2.6±0.3)g/L vs.(3.9±0.5)g/L,差异有统计学意义(P<0.05)。Pearson相关性分析,重度TBI后凝血功能障碍患者血浆α2-AP、vWF、ET-1与PT呈强正相关(r=0.723、0.528、0.586,P<0.05),与APTT呈强正相关(r=0.646、0.572、0.585,P<0.05),与INR呈强正相关(r=0.592、0.507、0.548,P<0.05),与FIB呈强负相关(r=-0.653、-0.672、-0.526,P<0.05);Logistic回归分析显示,入院时GCS降低(OR=2.593,95%CI:1.018~6.606,P<0.05)、α2-AP水平升高(OR=3.019,95%CI:1.107~8.236,P<0.05)和vWF水平升高(OR=2.729,95%CI:1.028~7.243,P<0.05)为重度TBI患者发生凝血功能障碍的相关危险因素;ROC曲线显示,α2-AP、vWF、ET-1预测重度TBI患者发生凝血功能障碍的AUC分别为0.887(95%CI:0.805~0.969,P<0.05)、0.828(95%CI:0.734~0.922,P<0.05)和0.807(95%CI:0.695~0.918,P<0.05),联合检测的AUC为0.912(95%CI:0.854~0.970,P<0.05),灵敏度为91.67%,特异度为87.14%。结论重度TBI后凝血功能障碍患者血浆α2-AP、vWF和ET-1水平均显著升高,其中血浆α2-AP、vWF水平升高为重度TBI患者发生凝血功能障碍的相关危险因素。 展开更多
关键词 创伤性颅脑损伤 凝血功能障碍 血浆α2-抗纤溶酶 血管性血友病因子 内皮素-1 预测价值
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Ferroptosis:a critical player and potential therapeutic target in traumatic brain injury and spinal cord injury 被引量:9
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作者 Qing-Sheng Li Yan-Jie Jia 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第3期506-512,共7页
Ferroptosis,a new non-necrotizing programmed cell death(PCD),is driven by iron-dependent phospholipid peroxidation.Ferroptosis plays a key role in secondary traumatic brain injury and secondary spinal cord injury and ... Ferroptosis,a new non-necrotizing programmed cell death(PCD),is driven by iron-dependent phospholipid peroxidation.Ferroptosis plays a key role in secondary traumatic brain injury and secondary spinal cord injury and is closely related to inflammation,immunity,and chronic injuries.The inhibitors against ferroptosis effectively improve iron homeostasis,lipid metabolism,redox stabilization,neuronal remodeling,and functional recovery after trauma.In this review,we elaborate on the latest molecular mechanisms of ferroptosis,emphasize its role in secondary central nervous trauma,and update the medicines used to suppress ferroptosis following injuries. 展开更多
关键词 ferroptosis immune response INFLAMMATION iron homeostasis lipid metabolism medicine programmed cell death spinal cord injury traumatic brain injury
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