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    Target temperature management and therapeutic hypothermia in sever neuroprotection for traumatic brain injury: Clinic value and effect on oxidative stress
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    Abstract:
    This study is to explore the application of target temperature management and therapeutic hypothermia in the treatment of neuroprotection patients with severe traumatic brain injury and its effect on oxidative stress. From February 2019 to April 2021, 120 patients with severe traumatic brain injury cured were selected in our hospital. The patients were randomly divided into control and experimental groups. The control group accepted mild hypothermia therapy. The experimental group took targeted temperature management and mild hypothermia therapy. This study compared the prognosis, National Institute of Health Stroke Scale (NIHSS) score, oxidative stress level, brain function index and the incidence of complications in different groups. The prognosis of the experimental group was better (P < .05). After treatment, the NIHSS score lessened. The NIHSS score of the experimental group was lower at 3 and 6 weeks after treatment (P < .05). Following treatment, the level of superoxide dismutase-1 in the experimental group was higher and the level of malondialdehyde was lower (P < .05). After treatment, the brain function indexes of patients lessened. The experimental group's myelin basic protein, neuron specific enolase and glial fibrillary acidic protein indexes were lower (P < .05). The incidences of pendant pneumonia, atelectasis, venous thrombosis of extremities and ventricular arrhythmias in the experimental group were remarkably lower (P < .05). Targeted temperature management and mild hypothermia treatment can improve neurological function, maintain brain cell function, and reduce stress-reactions risk. The incidence of complications during hospitalization was reduced.
    Keywords:
    Enolase
    Malondialdehyde
    Glasgow Outcome Scale
    Therapeutic effect
    Targeted temperature management
    Edaravone
    Brain damage
    Stroke
    Much progress has been made in the study of protective effect of edaravone against brain damage, especially in the prevention and treatment of cerebral ischemic stroke or neonatal hypoxic-ischemic encephalopathy with edaravone. The strategy of combined treatment has gained extensive attention. This review aims at the progress of these fields in recent five years.
    Edaravone
    Brain damage
    Hypoxic-Ischemic Encephalopathy
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    Objective To explore the change of serum neuron specific enolase(NSE)levels in acute cerebral infarction patients and the influence of edaravone on it.Methods Totally 78 patients with acute cerebral infarction(within 48 hours)diagnosed by CT or MRI were at random divided as edaravone group and routine group.The serum NSE levels of the patients in both groups were measured before treatment,and on the 7th,14th,21st day of the treatment.The scores of neurological deficits of the patients in the two groups were before and after treatment also compared.Results The serum NSE levels in the two groups before treatment showed no significantly different(P0.05).The NSE levels on the 7th,14th,21st day of the treatment of the edaravone group were respectively significantly different from those of the routine group(P0.05).There was no significant difference before treatment in score of neurological deficit between the two group(P0.05),but there were on the 7th,14th,21st day of the treatment(P0.05).Conclusion Edaravone can markedly reduce the serum NSE level and promote the recovery of neurological function in patients with acute cerebral infarction.
    Edaravone
    Enolase
    Neurological deficit
    Therapeutic effect
    Citations (0)
    Objective To expore the effect of nerve growth factor(NGF) on hypoxic-ischemic brain damage(HIBD) in neonatal rats. Methods The HIBD models were established with 7-day postnatal SD rats.Right after hypoxic-ischemic insult,NGF 100U per rat or normal saline solution was injected intraperisoneally.At 24 hours and 48 hours after hypoxic-ischemic insult,values of neuron-specific enolase(NSE)in serum were measured by radioimmunoassy and immunohistochemical technique was used to investigate the changes of expression of NSE in cerebral tissues. Results The use of NGF lowered serum NSE and increased the protein expression of NSE in the left cerebral tissues. Conclusion It is suggested that intraperitoneal administration on NGF can protect against hypoxic-ischemic brain damage(HIBD) in neonatal rats.
    Enolase
    Brain damage
    Hypoxia
    Cerebral hypoxia
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    Objective To investigate the pefinatal infant brain damage in the blcod of neuron specific enolase and long-term changes in the development of nervous system disordem related to the neonatal brain injury prognosis timely predictions for the early intervention and provide a theoretical basis.Methods 40 cases of periatal brain injury in newborns were selected for the study.20 patients over the same period of normal newborns assigned to the control groups.both groups in the 72 hours after birth within the collected blood samples submitted preservation of the neuronspecific enolase enzyme,and rely follow-up of the two groups,so as to cover Gesell development scale statistical analysis of neuron specific enolase and perinatal brain damage in children with long-term development of nervous system disorder relevant.Results Brain injury group blood neurompeeifie enolase concentrations were higher:15-month-old brain-injury group scale evaluation of sale to group health suspicious after three clays of Mood neuronspecific enolase concentrations significantly higher to the development of the normal group.Conclusion Neuronspecific enolase may change as early diagnosis of perinatal brain injury,as well aft the main indicators of the long-term prognosis. Key words: Phosphopyr; Hypoxia-ischemia,brain; Infant,newbomuvate hydratase
    Enolase
    Brain damage
    Objective: To investigate the protective effects of edaravone on hypoxic-ischemic brain in newborn rats. Methods: The hypoxic-ischemic brain damage (HIBD) models were prepared on 7-day-old newborn SD rats. 122 rats were randomly divided into hypoxic-ischemic, high-dose edaravone-treated, low-dose edaravone-treated and sham groups. Edaravone or NS was injected intraperitoneally immediately after hypoxic-ischemia (HI) treatment for 5 days. The contents of MDA and SOD in the brain were assessed 24 h, 48 h, 72 h after HIBD. The hippocampal changes were observed by microscope. The influence of edaravone on apoptosis of neurons in the cortex 72 h after HIBD was assessed by means of TUNEL. The learning and memory functions were evaluated 35 d after HI using Morris water maze test. Results: The contents of MDA and SOD 24 h, 48 h or 72 h after HI treatment were statistically significantly different between the high-dose group and the HI group (P﹤0.01) ,but were not significant between the low-dose group and the HI group (P﹥0.05). TUNEL staining showed that many apoptotic neurons were observed in the cortex of the left brain tissue 72 h after HIBD. Compared with the HI group(317.67 ± 24.27),the number of the apoptotic neurons of the cortex in the high-dose group(206.83 ± 21.94 ) was reduced significantly(P﹤0.01); the number in the low-dose group (301.30 ± 17.61) was decreased, while the difference showed no significance(P﹥0.05). Conclusion: High-dose intraperitoneally injected edaravone has significant protective effect on HIBD in newborn rats.
    Edaravone
    Brain damage
    Free radical scavenger
    Citations (0)
    Objective:To investigate the effect of edaravone injection on the neuron-specific enolase(NSE) concentration in serum from patients with acute cerebral infarction.Methods:The NSE concentrations in serum from 35 patients were measured by an ELISA method.Neurological deficit was scored for clinical effect assessment.Results:Serum NSE levels and neurological deficit scores in edaravone treating group significantly decreased at d 3 compared with those in routine therapy group((P)0.01).The efficiency rate was 62.86 % in edaravone treating group,and 34.29 % in routine therapy group at d 21.Conclusion:Edaravone injection can protect brain tissue from acute cerebral infarction and lessen nerve function impairment.
    Edaravone
    Enolase
    Neurological deficit
    Citations (0)
    Objective To investigate the value of serum neuron-specific enolase(NSE)levels in the diagnosis of neonatal asphyxia Methods 154 late-preterm neonates were enrolled in the study,including 94 with neonatal asphyxia for experimental group,52 with perinatal asphyxia,42 without brain damage and 60 normal ones for control group.For all the research objects blood samples were obtained for NSE detecting and Apgar scores were evaluated on proper time.MRI was performed 3~7 days after birth in experimental group. Results The levels of serum NSE in 52 with perinatal asphyxia were significantly higher than those in ones without brain damage and in control group.There were no significant difference between the levels in ones without brain damage and in control group.Conclusion Serum NSE level can be used as the early objective markers for evaluating the prognosis of brain damage due to late preterm perinatal asphyxia.
    Enolase
    Brain damage
    Perinatal asphyxia
    Neuronal damage
    Apgar score
    Asphyxia Neonatorum
    Citations (0)
    Objective To investigate the changes of serum neuron-specific enolase(NSE),high-sensitivity Creactive protein(hs-CRP) levels and the relationship of NSE,hs-CRP levels w ith neurological function defect in acute cerebral infarction patients,and the influence of edaravone on it.Methods 90 patients w ith acute cerebral infarction w ere randomly divided into control group and edaravone group,the control group w ere given routine treatment,apart from routine therapy,the edaravone group w ere added edaravone 30 mg,tw ice a day,total of 14 d;the serum levels of NSE,hs-CRP and the change of neural function defect w ere investigated before treatment,7 d and 14 d after treatment.Results The serum levels of NSE,hs-CRP were in a positive correlation with the score of neurological function defect(P 0.01).The edaravone group serum levels of NSE and hs-CRP were lower than those of control group(P 0.05) in invasion 7d after treatment.Score of NIHSS in the trial group w as low er than that of control group(P 0.05).Conclusion The serum levels of NSE,hs-CRP increase in the patients with acute cerebral infraction,and they can reflect the degree of cerebral infraction,so they can be regarded as objective indexes judging the degree of brain damage.Edaravone can reduce the serum NSE and hs-CRP levels and promote the recovery of neurological function in patients w ith acute cerebral infarction.
    Edaravone
    Enolase
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