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Risk factors for brain injury in patients with exertional heatstroke:A 5-year experience

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Chinese Journal of Traumatology 2024年第2期27卷 91-96页

作者： Li Zhong Ming Wu Zhe-Ying Liu Yan Liu Zhi-Feng Liu Department of Traditional Chinese Medicine The First Affiliated HospitalGuizhou University of Chinese MedicineGuiyang550001China Department of Infection and Critical Care Medicine The Second People's Hospital of Shenzhen&First Affiliated Hospital of Shenzhen UniversityHealth Science CenterShenzhenGuangdong province518035China Department of Medical Critical Care Medicine General Hospital of Southem Theatre Command of PLA.Guangzhou510010China Guangdong Branch Center National Clinical Research Center for Geriatric Diseases(Chinese PLA General Hospital)Guangzhou510010China

Purpose:Minimal data exist on brain injury in patients with exertional heatstroke(EHS)in developing country.In this study,we explored the risk factors for brain injury induced by EHS 90-day after onset.Methods:A retrospective cohort study of patients with EHS was conducted in the intensive care unit of the General Hospital of Southern Theater Command of PLA in China from April 2014 to June 2019.Patients were divided into non-brain injury(fully recovered)and brain injury groups(comprising deceased patients or those with neurological sequelae).The brain injury group was further subdivided into a death group and a sequela group for detailed analysis.General information,neurological performance and information on important organ injuries in the acute stage were recorded and analysed.Multivariable logistic regression was used to identify risk factors for brain injury after EHS and mortality risk factors for brain injury,and Kaplan-Meier survival curve was used to evaluate the effect of the neurological dysfunction on survival.Results:Out of the 147 EHS patients,117 were enrolled,of which 96(82.1%)recovered,13(11.1%)died,and 8(6.8%)experienced neurological sequelae.Statistically significant differences were found between non-brain injury and brain injury groups in age,hypotension,duration of consciousness disorders,time to drop core body temperature below 38.5℃,lymphocyte counts,platelet counts,procalcitonin,alanine aminotransferase,aspartate aminotransferase,creatinine,cystatin C,coagulation parameters,international normalized ratio,acute physiology and chronic health evaluation II scores,sequential organ failure assessment(SOFA)scores,and Glasgow coma scale scores(all pbrain injury induced by EHS.The Kaplan-Meier curves suggest significantly prolonged survival(p<0.001)in patients with

关键词： Exertional heatstroke brain injury Sequela Risk factors Disorders of consciousness

Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury

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Neural Regeneration Research 2022年第3期17卷 577-586页

作者： Wei Tang Zong-Duo Guo Wei-Na Chai Dong-Lin Du Xiao-Min Yang Lang Cao Hong Chen Chao Zhou Chong-Jie Cheng Xiao-Chuan Sun Zhi-Jian Huang Jian-Jun Zhong Department of Neurosurgery First Affiliated Hospital of Chongqing Medical UniversityChongqingChina Department of Ophthalmology First Affiliated Hospital of Chongqing Medical UniversityChongqingChina

Micro RNA-491-5 p(miR-491-5 p) plays an important role in regulating cell proliferation and migration;however,the effect of miR-491-5 p on neovascularization after traumatic brain injury remains poorly understood.In this study,a controlled cortical injury model in C57 BL/6 mice and an oxygen-glucose deprivation model in microvascular endothelial cells derived from mouse brain were established to simulate traumatic brain injury in vivo and in vitro,respectively.In the in vivo model,quantitative real-time-polymerase chain reaction results showed that the expression of miR-491-5 p increased or decreased following the intracerebroventricular injection of an miR-491-5 p agomir or antagomir,respectively,and the expression of miR-491-5 p decreased slightly after traumatic brain injury.To detect the neuroprotective effects of miR-491-p,neurological severity scores,Morris water maze test,laser speckle techniques,and immunofluorescence staining were assessed,and the results revealed that miR-491-5 p downregulation alleviated neurological dysfunction,promoted the recovery of regional cerebral blood flow,increased the number of lectin-stained microvessels,and increased the survival of neurons after traumatic brain injury.During the in vitro experiments,the potential mechanism of miR-491-5 p on neovascularization was explored through quantitative real-time-polymerase chain reaction,which showed that miR-491-5 p expression increased or decreased in brain microvascular endothelial cells after transfection with an miR-491-5 p mimic or inhibitor,respectively.Dual-luciferase reporter and western blot assays verified that metallothionein-2 was a target gene for miR-491-5 p.Cell counting kit 8(CCK-8) assay,flow cytometry,and 2′,7′-dichlorofluorescein diacetate(DCFH-DA) assay results confirmed that the downregulation of miR-491-5 p increased brain microvascular endothelial cell viability,reduced cell apoptosis,and alleviated oxidative stress under oxygen-glucose deprivation conditions.Cell scratch assay,Transwell assay,tube formation

关键词： brain injury cell migration cell proliferation endothelial cell hypoxia-inducible factor-1 alpha metallothionein 2 microRNA neovascularization neurons vascular endothelial growth factor

Decellularized extracellular matrix and mesenchymal stem cells promote recovery in traumatic brain injury by synergistically enhancing neurogenesis and attenuating neuroinflammation

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Journal of Materials Science & Technology 2023年第7期138卷 17-28页

作者： Xuewei Zhang Bixue Wang Hua Hong Ying Wang Jiashang Liu Changsheng Liu Xi Chen Key Laboratory for Ultrafine Materials of Ministry of Education Frontiers Science Center for Materiobiology and Dynamic ChemistryEngineering Research Center for Biomaterials of Ministry of EducationSchool of Materials Science and EngineeringEast China University of Science and TechnologyShanghai 200237China

Damaged neurons and harsh microenvironments contribute to the injury cascades following traumatic brain injury(TBI).Mesenchymal stem cell(MSC)therapy is considered a viable choice for brain in-jury treatment;however,its clinical use is hindered by limited engraftment,low survival ratio,and uncontrolled differentiation.Herein,the decellularized brain extracellular matrix(dBECM)was prepared through a new method as a delivery system for MSCs.dBECM-based hydrogel with favorable biochem-ical and biomechanical features provides a microenvironment for MSCs in nerve repair.The MSCs-encapsulated dBECM-based hydrogel is shown to improve neuron compensation and structural regen-eration,alleviate neuroinflammation,and promote M1-to-M2 polarization of microglia.Our results first demonstrate that the combination of dBECM and MSCs is a critical vehicle to promote TBI repair from neurogenesis and immunoregulation,showing promise for the physiological recovery of neurogenic dis-eases and injuries.

关键词： ECM Stem cells brain injury Neurogenesis Neuroinflammation

Diffusion tensor tractography characteristics of axonal injury in concussion/mild traumatic brain injury

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Neural Regeneration Research 2022年第5期17卷 978-982页

作者： Sung Ho Jang You Sung Seo Department of Physical Medicine and Rehabilitation College of MedicineYeungnam UniversityDaeguRepublic of Korea

The main advantage of diffusion tensor tractography is that it allows the entire neural tract to be evaluated.In addition,configurational analysis of reconstructed neural tracts can indicate abnormalities such as tearing,narrowing,or discontinuations,which have been used to identify axonal injury of neural tracts in concussion patients.This review focuses on the characteristic features of axonal injury in concussion or mild traumatic brain injury(m TBI)patients through the use of diffusion tensor tractography.Axonal injury in concussion(m TBI)patients is characterized by their occurrence in long neural tracts and multiple injuries,and these characteristics are common in patients with diffuse axonal injury and in concussion(m TBI)patients with axonal injury.However,the discontinuation of the corticospinal tract is mostly observed in diffuse axonal injury,and partial tearing and narrowing in the subcortical white matter are frequently observed in concussion(m TBI)patients with axonal injury.This difference appears to be attributed to the observation that axonal injury in concussion(m TBI)patients is the result of weaker forces than those producing diffuse axonal injuries.In addition,regarding the fornix,in diffuse axonal injury,discontinuation of the fornical crus has been frequently reported,but in concussion(m TBI)patients,many collateral branches form in the fornix in addition to these findings in many case studies.It is presumed that the impact on the brain in TBI is relatively weaker than that in diffuse axonal injury,and that the formation of collateral branches occurs during the fornix recovery process.Although the occurrence of axonal injury in multiple areas of the brain is an important feature of diffuse axonal injury,case studies in concussion(m TBI)have shown that axonal injury occurs in multiple neural tracts.Because axonal injury lesions in m TBI patients may persist for approximately 10 years after injury onset,the characteristics of axonal injury in concussion(m TBI)patients,which are reviewed and c

关键词： axonal injury brain injury concussion diffusion tensor imaging diffusion tensor tractography mild traumatic brain injury neural tract

Overexpression of mitogen-activated protein kinase phosphatase-1 in endothelial cells reduces blood-brain barrier injury in a mouse model of ischemic stroke

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Neural Regeneration Research 2023年第8期18卷 1743-1749页

作者： Xiu-De Qin Tai-Qin Yang Jing-Hui Zeng Hao-Bin Cai Shao-Hua Qi Jian-Jun Jiang Ying Cheng Long-Sheng Xu Fan Bu Department of Neurology&Psychology Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Cardiothoracic Surgery Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Neurology The University of Texas Health Science Center at HoustonHoustonTXUSA Department of Nephrology Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Anesthesiology and Pain Medicine The Affiliated Hospital of Jiaxing UniversityJiaxingZhejiang ProvinceChina

Ischemic stroke can cause blood-brain barrier(BBB)injury,which worsens brain damage induced by stroke.Abnormal expression of tight junction proteins in endothelial cells(ECs)can increase intracellular space and BBB leakage.Selective inhibition of mitogen-activated protein kinase,the negative regulatory substrate of mitogen-activated protein kinase phosphatase(MKP)-1,improves tight junction protein function in ECs,and genetic deletion of MKP-1 aggravates ischemic brain injury.However,whether the latter affects BBB integrity,and the cell type-specific mechanism underlying this process,remain unclear.In this study,we established an adult male mouse model of ischemic stroke by occluding the middle cerebral artery for 60 minutes and overexpressed MKP-1 in ECs on the injured side via lentiviral transfection before stroke.We found that overexpression of MKP-1 in ECs reduced infarct volume,reduced the level of inflammatory factors interleukin-1β,interleukin-6,and chemokine C-C motif ligand-2,inhibited vascular injury,and promoted the recovery of sensorimotor and memory/cognitive function.Overexpression of MKP-1 in ECs also inhibited the activation of cerebral ischemia-induced extracellular signal-regulated kinase(ERK)1/2 and the downregulation of occludin expression.Finally,to investigate the mechanism by which MKP-1 exerted these functions in ECs,we established an ischemic stroke model in vitro by depriving the primary endothelial cell of oxygen and glucose,and pharmacologically inhibited the activity of MKP-1 and ERK1/2.Our findings suggest that MKP-1 inhibition aggravates oxygen and glucose deprivation-induced cell death,cell monolayer leakage,and downregulation of occludin expression,and that inhibiting ERK1/2 can reverse these effects.In addition,co-inhibition of MKP-1 and ERK1/2 exhibited similar effects to inhibition of ERK1/2.These findings suggest that overexpression of MKP-1 in ECs can prevent ischemia-induced occludin downregulation and cell death via deactivating ERK1/2,thereby protecting the integrity of BBB

关键词： blood-brain barrier brain injury cerebral ischemia endothelial cells extracellular signal-regulated kinase 1/2 functional recovery mitogenactivated protein kinase phosphatase 1 occludin oxygen and glucose deprivation transient middle cerebral artery occlusion

Status of precision medicine approaches to traumatic brain injury

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Neural Regeneration Research 2022年第10期17卷 2166-2171页

作者： Sahithi Reddi Smita Thakker-Varia Janet Alder Anna O.Giarratana Department of Neuroscience and Cell Biology Rutgers Robert Wood Johnson Medical SchoolPiscatawayNJUSA

Traumatic brain injury(TBI)is a serious condition in which trauma to the head causes damage to the brain,leading to a disruption in brain function.This is a significant health issue worldwide,with around 69 million people suffering from TBI each year.Immediately following the trauma,damage occurs in the acute phase of injury that leads to the primary outcomes of the TBI.In the hours-to-days that follow,secondary damage can also occur,leading to chronic outcomes.TBIs can range in severity from mild to severe,and can be complicated by the fact that some individuals sustain multiple TBIs,a risk factor for worse long-term outcomes.Although our knowledge about the pathophysiology of TBI has increased in recent years,unfortunately this has not been translated into effective clinical therapies.The U.S.Food and Drug Administration has yet to approve any drugs for the treatment of TBI;current clinical treatment guidelines merely offer supportive care.Outcomes between individuals greatly vary,which makes the treatment for TBI so challenging.A blow of similar force can have only mild,primary outcomes in one individual and yet cause severe,chronic outcomes in another.One of the reasons that have been proposed for this differential response to TBI is the underlying genetic differences across the population.Due to this,many researchers have begun to investigate the possibility of using precision medicine techniques to address TBI treatment.In this review,we will discuss the research detailing the identification of genetic risk factors for worse outcomes after TBI,and the work investigating personalized treatments for these higher-risk individuals.We highlight the need for further research into the identification of higher-risk individuals and the development of personalized therapies for TBI.

关键词： apolipoprotein E biomarkers brain injury brain-derived neurotrophic factor clinical trials personalized treatments precision medicine tau translational research traumatic brain injury

TianmaGouteng yin attenuates ischemic stroke-induced brain injury by inhibiting the AGE/RAGE pathway

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BIOCELL 2023年第6期47卷 1345-1352页

作者： LUOJUN ZHENG LUAN WENG DIWEN SHOU Department of TCM Pharmacy The First Affiliated Hospital of Zhejiang Chinese Medical University(Zhejiang Provincial Hospital of Chinese Medicine)Hangzhou310003China

Background:Ischemic stroke is characterized by permanent or transient obstruction of blood flow,leading to a growing risk factor and health burden.Tianmagouteng yin(TMG)is commonly used in Chinese medicine to treat cerebral ischemia.The aim of this study was to investigate the neuroprotective effects of TMG against ischemic stroke.Methods:Either permanent middle cerebral artery occlusion(pMCAO)or sham operation was performed on anesthetized Wistar male rats(n=36).Results:Results demonstrated that TMG administration reduced the infarction volume and mitigated the neurobehavioral deficits.Hematoxylin and eosin(HE)staining and Prussian blue staining revealed that TMG attenuated tissue disruption and microbleeds in hippocampus tissues.In addition,TMG down-regulated the receptor of advanced glycation end products(RAGE)and p-JAK2.It also inhibited the concentrations of advanced glycation end products(AGEs),ferritin,malondialdehyde(MDA),and reactive oxygen species(ROS).Conclusion:As repetitive clinical trials of neuroprotectants targeting stroke have failed previously,our results suggested that the natural product,TMG,can probably help in the vicious cycles of ischemic stroke pathology.

关键词： Ischemic stroke Tianmagouteng yin brain injury Neuroprotection AGE/RAGE pathway pMCAO

Engineering of electrospun nanofiber scaffolds for repairing brain injury

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再生工程(英文)

再生工程(英文) 2023年第3期4卷 289-303页

作者： Wenzhe Du Tong Wang Shuyun Hu Jixin Luan Feng Tian Guolin Ma Jiajia Xue State Key Laboratory of Organic-Inorganic Composites Beijing University of Chemical TechnologyBeijing 100029PR China Beijing Laboratory of Biomedical Materials Beijing University of Chemical TechnologyBeijing 100029PR China Department of Radiology China-Japan Friendship HospitalNo.2 East Yinghua RoadChaoyang DistrictBeijing 100029PR China

Patients with brain injury can suffer disability and accompanying complications.Current clinical treatments have significant limitations to successful repair due to the complexity of the pathological processes and the inhibitory microenvironment that follows brain injury.Here,we conclude recent research progresses in engineering strate-gies based on electrospun nanofibers for promoting neural repair and functional recovery after brain injury.Firstly,we introduce the main pathological mechanisms of current brain injuries,pointing out the prospect of the application of electrospun nanofiber scaffolds compared to current clinical treatment strategies.We then discuss the repair strategies combining the structure and the morphology of nanofiber scaffolds with load therapeutic factors such as cells,drugs and growth factors.All of these strategies show potential for improving the repair of brain injury.Finally,we point out the challenges facing the effective treatment of brain injury,aiming to provide insights into the development of repairing scaffolds for brain function recovery from the perspective of clinical treatment.

关键词： Electrospun nanofibers brain injury Engineering strategies Neural repair Functional recovery

Brief inhalation of sevoflurane can reduce glial scar formation after hypoxic-ischemic brain injury in neonatal rats

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Neural Regeneration Research 2021年第6期16卷 1052-1061页

作者： Qiu-Shi Gao Ya-Han Zhang Hang Xue Zi-Yi Wu Chang Li Ping Zhao Department of Anesthesiology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Previous studies have demonstrated that sevoflurane postconditioning can provide neuroprotection after hypoxic-ischemic injury and improve learning and memory function in developing rodent brains.The classical Rice-Vannucci model was used to induce hypoxic-ischemic injury,and newborn(postnatal day 7)rats were treated with 2.4%sevoflurane for 30 minutes after hypoxic-ischemic injury.Our results showed that sevoflurane postconditioning significantly improved the learning and memory function of rats,decreased astrogliosis and glial scar formation,increased numbers of dendritic spines,and protected the histomorphology of the hippocampus.Mechanistically,sevoflurane postconditioning decreased expression of von Hippel-Lindau of hypoxia-inducible factor-1α and increased expression of DJ-1.Injection of 1.52μg of the hypoxia-inducible factor-1αinhibitor YC-1(Lificiguat)into the left lateral ventricle 30 minutes before hypoxic-ischemic injury reversed the neuroprotection induced by sevoflurane.This finding suggests that sevoflurane can effectively alleviate astrogliosis in the hippocampus and reduce learning and memory impairments caused by glial scar formation after hypoxic-ischemic injury.The underlying mechanism may be related to upregulated DJ-1 expression,reduced ubiquitination of hypoxia-inducible factor-1α,and stabilized hypoxiainducible factor-1αexpression.This study was approved by the Laboratory Animal Care Committee of China Medical University,China(approval No.2016PS337K)on November 9,2016.

关键词： brain injury brain central nervous system in vivo injury model plasticity rat recovery regeneration repair