Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic...Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic brain injury by controlled cortical impact. Rat models were intragastrically administered 9 and 18 g/kg Xuefu Zhuyu decoction once a day for 14 or 21 days. Changes in neurological function were assessed by modified neurological severity scores and the Morris water maze. Immunohistochemistry, western blot assay, and re- verse-transcription polymerase chain reaction were used to analyze synapsin protein and mRNA expression at the injury site of rats. Our results showed that Xuefu Zhuyu decoction visibly improved neurological function of rats with traumatic brain injury. These changes were accompanied by increased expression of synaptophysin, synapsin I, and postsynaptic density protein-95 protein and mRNA in a dose-de- pendent manner. These findings indicate that Xuefu Zhuyu decoction increases synapsin expression and improves neurological deficits alder traumatic brain injury.展开更多
Restoring neurological dysfunctions is challenging in patients with the sequels of vertebral and spinal cord lesions.Current guidelines focus on treating the early stage of vertebral and spinal cord lesions,such as te...Restoring neurological dysfunctions is challenging in patients with the sequels of vertebral and spinal cord lesions.Current guidelines focus on treating the early stage of vertebral and spinal cord lesions,such as tethered cord syndrome,syringomyelia,spinal degenerative diseases,spinal infection,ankylosing spondylitis,myelitis,vertebral and spinal cord vascular malformations,and others,whereas the treatments of the sequels of those lesions have received limited attention.Restoring neurological dysfunctions and damaged structures caused by these lesions could improve patient quality of life.The Chinese Association of Neurorestoratology(Preparatory)and the China Committee of International Association of Neurorestoratology therefore proposed and approved this guideline providing the restorative therapeutic rules and references for physicians to treat patients with neurological dysfunction of sequels from vertebral and spinal cord lesions.展开更多
The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurode...The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurodegenerative diseases are characterized by the progressive loss of neuronal structure and function.展开更多
Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic ...Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic brain injury remains poorly understood.In this study,we established rat models of moderate traumatic brain injury using Feeney's weight-dropping method and treated them using rTMS.To help determine the mechanism of action,we measured levels of seve ral impo rtant brain activity-related proteins and their mRNA.On the injured side of the brain,we found that rTMS increased the protein levels and mRNA expression of brain-derived neurotrophic factor,tropomyosin receptor kinase B,N-methyl-D-aspartic acid receptor 1,and phosphorylated cAMP response element binding protein,which are closely associated with the occurrence of long-term potentiation.rTMS also partially reve rsed the loss of synaptophysin after injury and promoted the remodeling of synaptic ultrastructure.These findings suggest that upregulation of synaptic plasticity-related protein expression is the mechanism through which rTMS promotes neurological function recovery after moderate traumatic brain injury.展开更多
Delirium is a transient and acute syndrome of encephalopathy,characterized by disturbances in consciousness,orientation,cognition,perception,and emotional regulation,often accompanied by hallucinations,illusions,psych...Delirium is a transient and acute syndrome of encephalopathy,characterized by disturbances in consciousness,orientation,cognition,perception,and emotional regulation,often accompanied by hallucinations,illusions,psychomotor agitation,and restlessness.Postoperative delirium(POD),a common complication particularly in elderly patients,significantly impacts recovery by prolonging mechanical ventilation,neurosurgical intensive care unit stays,and overall hospitalization durations,while severely diminishing patients’quality of life after discharge.Despite its prevalence,POD remains underrecognized in clinical practice,with significant gaps in its diagnosis and management.This review explores the definition,diagnostic criteria,underlying pathogenesis,and associated risk factors of POD in neurosurgical patients,aiming to offer valuable insights for improving clinical diagnosis and therapeutic strategies.展开更多
Since the discovery of the coronavirus disease 2019 outbreak,a vast majority of studies have been carried out that confirmed the worst outcome of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection in...Since the discovery of the coronavirus disease 2019 outbreak,a vast majority of studies have been carried out that confirmed the worst outcome of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection in people with preexisting health conditions,including diabetes,obesity,hypertension,cancer,and cardiovascular diseases.Likewise,diabetes itself is one of the leading causes of global public health concerns that impose a heavy global burden on public health as well as socio-economic development.Both diabetes and SARS-CoV-2 infection have their independent ability to induce the pathogenesis and severity of multi-system organ failure,while the co-existence of these two culprits can accelerate the rate of disease progression and magnify the severity of the disease.However,the exact pathophysiology of multi-system organ failure in diabetic patients after SARS-CoV-2 infection is still obscure.This review summarized the organ-specific possible molecular mechanisms of SARS-CoV-2 and diabetesinduced pathophysiology of several diseases of multiple organs,including the lungs,heart,kidneys,brain,eyes,gastrointestinal system,and bones,and subsequent manifestation of multi-system organ failure.展开更多
AIM:To propose an alternative model of hepatic encephalopathy(HE) in mice,resembling the human features of the disease.METHODS:Mice received two consecutive intraperitoneal injections of thioacetamide(TAA) at low dosa...AIM:To propose an alternative model of hepatic encephalopathy(HE) in mice,resembling the human features of the disease.METHODS:Mice received two consecutive intraperitoneal injections of thioacetamide(TAA) at low dosage(300 mg/kg).Liver injury was assessed by serum transaminase levels(ALT) and liver histology(hematoxylin and eosin).Neutrophil infiltration was estimated by confocal liver intravital microscopy.Coagulopathy was evaluated using prolonged prothrombin and partial thromboplastin time.Hemodynamic parameters were measured through tail cuff.Ammonia levels were quantified in serum and brain samples.Electroencephalography(EEG) and psychomotor activity score were performed to show brain function.Brain edema was evaluated using magnetic resonance imaging.RESULTS:Mice submitted to the TAA regime developed massive liver injury,as shown by elevation of serum ALT levels and a high degree of liver necrosis.An intense hepatic neutrophil accumulation occurred in response to TAA-induced liver injury.This led to mice mortality and weight loss,which was associated with severe coagulopathy.Furthermore,TAA-treated mice presented with increased serum and cerebral levels of ammonia,in parallel with alterations in EEG spectrum and discrete brain edema,as shown by magnetic resonance imaging.In agreement with this,neuropsychomotor abnormalities ensued 36 h after TAA,fulfilling several HE features observed in humans.In this context of liver injury and neurological dysfunction,we observed lung inflammation and alterations in blood pressure and heart rate that were indicative of multiple organ dysfunction syndrome.CONCLUSION:In summary,we describe a new murine model of hepatic encephalopathy comprising multiple features of the disease in humans,which may provide new insights for treatment.展开更多
Background:Neurological dysfunction is a common complication of traumatic brain injury(TBI),and early treatments are critical for the long-term prognosis.This study aimed to investigate whether hypidone hydrochloride(...Background:Neurological dysfunction is a common complication of traumatic brain injury(TBI),and early treatments are critical for the long-term prognosis.This study aimed to investigate whether hypidone hydrochloride(YL-0919)improves neurological function impairment in mice with TBI.Methods:TBI was induced in adult male C57BL/6J mice using the controlled cortical impact(CCI)method.First,the modified neurological severity score(mNSS),rotarod test,and Morris water maze(MWM)test were conducted to assess the impact of YL-0919 on neurological function in mice with TBI.Next,immunofluorescence and laser speckle contrast imaging were utilized to measure the number and activation of microglia and cerebral blood flow(CBF)after TBI.Enzyme-linked immunosorbent assay(ELISA)was employed to assess the inflammatory factors.Finally,Western blotting was performed to measure the expression of proteins.Golgi–Cox staining was utilized to investigate the structure of pyramidal neurons.Results:YL-0919 significantly alleviated neurological dysfunction in TBI+YL-0919 mice compared with TBI+Vehicle mice,increased the time spent on the rotarod(F=1.297,P<0.05),and partially relieved cognitive dysfunction in TBI mice(for mNSS,F=5.540,P<0.01;for MWM test,F=30.78,P<0.05).Additionally,YL-0919 effectively inhibited the proliferation and activation of microglia(both P<0.01),promoted the recovery of CBF around the brain injury site and inhibited the expression of tumor necrosis factor-α(F=9.142,P<0.05)and IL-1β(F=4.662,P<0.05),and increased the concentration of IL-4(F=5.172,P<0.05).Furthermore,continuous gavage of YL-0919(2.5mg/kg)for seven days effectively increased the protein expression of brain-derived neurotrophic factor(BDNF),promoted the phosphorylation of mammalian target of rapamycin(mTOR),increased postsynaptic density protein 95(PSD95)and synapsin1 levels,and increased the neuronal dendritic complexity and the dendritic spine density around the brain injury site(all P<0.05).Conclusions:Our findings indicated that YL-0919 can ameliorate neurological dysfunction in mice after TBI through the suppression of inflammation and the stimulation of the BDNF-mTOR signaling pathway.These findings provide an insightful perspective on the potential pharmacological mechanism involved in the neuroprotective effect of YL-0919.展开更多
Acute ischemic stroke(AIS)causes irreversible neurological dysfunction that results from the variable loss of neurons(Campbell et al.,2019).Although reperfusion therapy is a proven treatment of AIS(Mendelson and Prabh...Acute ischemic stroke(AIS)causes irreversible neurological dysfunction that results from the variable loss of neurons(Campbell et al.,2019).Although reperfusion therapy is a proven treatment of AIS(Mendelson and Prabhakaran,2021),many patients do not seek treatment promptly after symptom onset or do not achieve satisfactory recovery despite achieving successful mechanical thrombectomy.Thus,patients require rehabilitation to support recovery.展开更多
基金supported by the National Natural Science Foundation of China,No.81673719,81173175 and 81303074a grant from China Postdoctoral Science Foundation,No.2016M600639 and 2017T100614
文摘Xuefu Zhuyu decoction has been used for treating traumatic brain injury and improving post-traumatic dysfunction, but its mechanism of action needs further investigation. This study established rat models of traumatic brain injury by controlled cortical impact. Rat models were intragastrically administered 9 and 18 g/kg Xuefu Zhuyu decoction once a day for 14 or 21 days. Changes in neurological function were assessed by modified neurological severity scores and the Morris water maze. Immunohistochemistry, western blot assay, and re- verse-transcription polymerase chain reaction were used to analyze synapsin protein and mRNA expression at the injury site of rats. Our results showed that Xuefu Zhuyu decoction visibly improved neurological function of rats with traumatic brain injury. These changes were accompanied by increased expression of synaptophysin, synapsin I, and postsynaptic density protein-95 protein and mRNA in a dose-de- pendent manner. These findings indicate that Xuefu Zhuyu decoction increases synapsin expression and improves neurological deficits alder traumatic brain injury.
文摘Restoring neurological dysfunctions is challenging in patients with the sequels of vertebral and spinal cord lesions.Current guidelines focus on treating the early stage of vertebral and spinal cord lesions,such as tethered cord syndrome,syringomyelia,spinal degenerative diseases,spinal infection,ankylosing spondylitis,myelitis,vertebral and spinal cord vascular malformations,and others,whereas the treatments of the sequels of those lesions have received limited attention.Restoring neurological dysfunctions and damaged structures caused by these lesions could improve patient quality of life.The Chinese Association of Neurorestoratology(Preparatory)and the China Committee of International Association of Neurorestoratology therefore proposed and approved this guideline providing the restorative therapeutic rules and references for physicians to treat patients with neurological dysfunction of sequels from vertebral and spinal cord lesions.
文摘The aging process is an inexorable fact throughout our lives and is considered a major factor in develo ping neurological dysfunctions associated with cognitive,emotional,and motor impairments.Aging-associated neurodegenerative diseases are characterized by the progressive loss of neuronal structure and function.
基金supported by the President Foundation of Nanfang Hospital,Southern Medical University,No.2016Z003(50107021)(to JZF).
文摘Studies have shown that repetitive transcra nial magnetic stimulation(rTMS)can enhance synaptic plasticity and improve neurological dysfunction.Howeve r,the mechanism through which rTMS can improve moderate traumatic brain injury remains poorly understood.In this study,we established rat models of moderate traumatic brain injury using Feeney's weight-dropping method and treated them using rTMS.To help determine the mechanism of action,we measured levels of seve ral impo rtant brain activity-related proteins and their mRNA.On the injured side of the brain,we found that rTMS increased the protein levels and mRNA expression of brain-derived neurotrophic factor,tropomyosin receptor kinase B,N-methyl-D-aspartic acid receptor 1,and phosphorylated cAMP response element binding protein,which are closely associated with the occurrence of long-term potentiation.rTMS also partially reve rsed the loss of synaptophysin after injury and promoted the remodeling of synaptic ultrastructure.These findings suggest that upregulation of synaptic plasticity-related protein expression is the mechanism through which rTMS promotes neurological function recovery after moderate traumatic brain injury.
基金Supported by Science and Technology Program of Nantong City,No.Key003Nantong Young Medical Expert,No.46+2 种基金the Science and Technology Program of Nantong Health Committee,No.MA2019003,No.MA2021017,and No.MSZ2024038Science and Technology Program of Nantong City,No.JCZ2022040Kangda College of Nanjing Medical University,No.KD2021JYYJYB025,No.KD2022KYJJZD022,and No.KD2024KYJJ289.
文摘Delirium is a transient and acute syndrome of encephalopathy,characterized by disturbances in consciousness,orientation,cognition,perception,and emotional regulation,often accompanied by hallucinations,illusions,psychomotor agitation,and restlessness.Postoperative delirium(POD),a common complication particularly in elderly patients,significantly impacts recovery by prolonging mechanical ventilation,neurosurgical intensive care unit stays,and overall hospitalization durations,while severely diminishing patients’quality of life after discharge.Despite its prevalence,POD remains underrecognized in clinical practice,with significant gaps in its diagnosis and management.This review explores the definition,diagnostic criteria,underlying pathogenesis,and associated risk factors of POD in neurosurgical patients,aiming to offer valuable insights for improving clinical diagnosis and therapeutic strategies.
基金Supported by a Predoctoral Fellowship Grant from the American Heart Association,No.835262(to Roy B).
文摘Since the discovery of the coronavirus disease 2019 outbreak,a vast majority of studies have been carried out that confirmed the worst outcome of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection in people with preexisting health conditions,including diabetes,obesity,hypertension,cancer,and cardiovascular diseases.Likewise,diabetes itself is one of the leading causes of global public health concerns that impose a heavy global burden on public health as well as socio-economic development.Both diabetes and SARS-CoV-2 infection have their independent ability to induce the pathogenesis and severity of multi-system organ failure,while the co-existence of these two culprits can accelerate the rate of disease progression and magnify the severity of the disease.However,the exact pathophysiology of multi-system organ failure in diabetic patients after SARS-CoV-2 infection is still obscure.This review summarized the organ-specific possible molecular mechanisms of SARS-CoV-2 and diabetesinduced pathophysiology of several diseases of multiple organs,including the lungs,heart,kidneys,brain,eyes,gastrointestinal system,and bones,and subsequent manifestation of multi-system organ failure.
基金CNPq,Fapemig,PRONEX and CAPES for financial support.
文摘AIM:To propose an alternative model of hepatic encephalopathy(HE) in mice,resembling the human features of the disease.METHODS:Mice received two consecutive intraperitoneal injections of thioacetamide(TAA) at low dosage(300 mg/kg).Liver injury was assessed by serum transaminase levels(ALT) and liver histology(hematoxylin and eosin).Neutrophil infiltration was estimated by confocal liver intravital microscopy.Coagulopathy was evaluated using prolonged prothrombin and partial thromboplastin time.Hemodynamic parameters were measured through tail cuff.Ammonia levels were quantified in serum and brain samples.Electroencephalography(EEG) and psychomotor activity score were performed to show brain function.Brain edema was evaluated using magnetic resonance imaging.RESULTS:Mice submitted to the TAA regime developed massive liver injury,as shown by elevation of serum ALT levels and a high degree of liver necrosis.An intense hepatic neutrophil accumulation occurred in response to TAA-induced liver injury.This led to mice mortality and weight loss,which was associated with severe coagulopathy.Furthermore,TAA-treated mice presented with increased serum and cerebral levels of ammonia,in parallel with alterations in EEG spectrum and discrete brain edema,as shown by magnetic resonance imaging.In agreement with this,neuropsychomotor abnormalities ensued 36 h after TAA,fulfilling several HE features observed in humans.In this context of liver injury and neurological dysfunction,we observed lung inflammation and alterations in blood pressure and heart rate that were indicative of multiple organ dysfunction syndrome.CONCLUSION:In summary,we describe a new murine model of hepatic encephalopathy comprising multiple features of the disease in humans,which may provide new insights for treatment.
基金supported by grants from the National Natural Science Foundation of China(No.82204360)National Natural Science Foundation of China(No.82270411)National Science and Technology Innovation 2030 Major Program(No.2021ZD0200900).
文摘Background:Neurological dysfunction is a common complication of traumatic brain injury(TBI),and early treatments are critical for the long-term prognosis.This study aimed to investigate whether hypidone hydrochloride(YL-0919)improves neurological function impairment in mice with TBI.Methods:TBI was induced in adult male C57BL/6J mice using the controlled cortical impact(CCI)method.First,the modified neurological severity score(mNSS),rotarod test,and Morris water maze(MWM)test were conducted to assess the impact of YL-0919 on neurological function in mice with TBI.Next,immunofluorescence and laser speckle contrast imaging were utilized to measure the number and activation of microglia and cerebral blood flow(CBF)after TBI.Enzyme-linked immunosorbent assay(ELISA)was employed to assess the inflammatory factors.Finally,Western blotting was performed to measure the expression of proteins.Golgi–Cox staining was utilized to investigate the structure of pyramidal neurons.Results:YL-0919 significantly alleviated neurological dysfunction in TBI+YL-0919 mice compared with TBI+Vehicle mice,increased the time spent on the rotarod(F=1.297,P<0.05),and partially relieved cognitive dysfunction in TBI mice(for mNSS,F=5.540,P<0.01;for MWM test,F=30.78,P<0.05).Additionally,YL-0919 effectively inhibited the proliferation and activation of microglia(both P<0.01),promoted the recovery of CBF around the brain injury site and inhibited the expression of tumor necrosis factor-α(F=9.142,P<0.05)and IL-1β(F=4.662,P<0.05),and increased the concentration of IL-4(F=5.172,P<0.05).Furthermore,continuous gavage of YL-0919(2.5mg/kg)for seven days effectively increased the protein expression of brain-derived neurotrophic factor(BDNF),promoted the phosphorylation of mammalian target of rapamycin(mTOR),increased postsynaptic density protein 95(PSD95)and synapsin1 levels,and increased the neuronal dendritic complexity and the dendritic spine density around the brain injury site(all P<0.05).Conclusions:Our findings indicated that YL-0919 can ameliorate neurological dysfunction in mice after TBI through the suppression of inflammation and the stimulation of the BDNF-mTOR signaling pathway.These findings provide an insightful perspective on the potential pharmacological mechanism involved in the neuroprotective effect of YL-0919.
文摘Acute ischemic stroke(AIS)causes irreversible neurological dysfunction that results from the variable loss of neurons(Campbell et al.,2019).Although reperfusion therapy is a proven treatment of AIS(Mendelson and Prabhakaran,2021),many patients do not seek treatment promptly after symptom onset or do not achieve satisfactory recovery despite achieving successful mechanical thrombectomy.Thus,patients require rehabilitation to support recovery.
