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Status epilepticus is a neurological emergency with unknown pathogenesis, controversial treatment options, and poor prognosis. In recent years, with the development of 18F-flurodeoxyglucose positron emission tomography ( 18F-FDG PET) imaging technology, further studies on status epilepticus have been carried out from the perspective of molecular metabolism. This article reviews the current role of 18F-FDG PET in patients with status epilepticus on etiology, disease activity, electric activity, location of epileptogenic foci, and prognosis evaluation.
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BACKGROUND@#Excessive inflammatory responses play a critical role in the development of severe acute pancreatitis (SAP), and controlling such inflammation is vital for managing this often fatal disease. Dexmedetomidine has been reported to possess protective properties in inflammatory diseases. Therefore, this study aimed to investigate whether dexmedetomidine pre-treatment exerts an anti-inflammatory effect in rats with SAP induced by sodium taurocholate, and if so, to determine the potential mechanism.@*METHODS@#SAP was induced with sodium taurocholate. Rats received an intraperitoneal injection of dexmedetomidine 30 min before sodium taurocholate administration. α-bungarotoxin, a selective alpha-7 nicotinic acetylcholine receptor (α7nAchR) antagonist, was injected intra-peritoneally 30 min before dexmedetomidine administration. The role of the vagus nerve was evaluated by performing unilateral cervical vagotomy before the administration of dexmedetomidine. Efferent discharge of the vagal nerve was recorded by the BL-420F Data Acquisition & Analysis System. Six hours after onset, serum pro-inflammatory cytokine (tumor necrosis factor α [TNF-α] and interleukin 6 [IL-6]) levels and amylase levels were determined using an enzyme-linked immunosorbent assay and an automated biochemical analyzer, respectively. Histopathological changes in the pancreas were observed after hematoxylin and eosin staining and scored according to Schmidt criteria.@*RESULTS@#Pre-treatment with dexmedetomidine significantly decreased serum levels of TNF-α, IL-6, and amylase, strongly alleviating pathological pancreatic injury in the rat model of SAP (TNF-α: 174.2 ± 30.2 vs. 256.1±42.4 pg/ml; IL-6: 293.3 ± 46.8 vs. 421.7 ± 48.3 pg/ml; amylase: 2102.3 ± 165.3 vs. 3186.4 ± 245.2 U/L). However, the anti-inflammatory and pancreatic protective effects were abolished after vagotomy or pre-administration of α-bungarotoxin. Dexmedetomidine also significantly increased the discharge frequency and amplitude of the cervical vagus nerve in the SAP rat model (discharge frequency: 456.8 ± 50.3 vs. 332.4 ± 25.1 Hz; discharge amplitude: 33.4 ± 5.3 vs. 20.5 ± 2.9 μV).@*CONCLUSIONS@#Dexmedetomidine administration attenuated the systemic inflammatory response and local pancreatic injury caused by SAP in rats through the cholinergic anti-inflammatory pathway involving vagus- and α7nAChR-dependent mechanisms.
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Abundant clinical and basic studies in recent years reported the high association of Wnt/β-catenin signaling pathway with the incidence and development of multiple neurological disorders. In order to improve the attention about the relationship between Wnt/β-catenin signaling pathway and neurological disorders, and to provide new therapy target, this article reviews the research progress on the relationship between wnt/β-catenin signaling pathway and Parkinson′s disease, Alzheimer′s disease, epilepsy, multiple sclerosis and myasthenia gravis.
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OBJECTIVE To investigate the protective effect and mechanisms of luteolin-7-O-β-d-glucuronide (LGU) on oxygen glucose deprivation (OGD)-induced H9C2 cardiomyocytes injury. METH-ODS The protective effect of LGU on OGD-induced H9C2 cardiomyocytes death were investigated by MTT assay. The microfilament change of H9C2 cardiomyocytes was detected by phalloidin staining and the lactate dehydrogenase (LDH) leakage rate was also detected by LDH kit. In order to explore the possible mechanisms of LGU, ATP content, intracellular Ca2+fluorescent intensity and concentra-tion, mitochondrial membrane potential (MMP)and the expressions of apoptosis-related proteins were detected by ATP kit,CLSM(Fluo-3/AM probe),Ca2+kit,CLSM(JC-1 probe)and western blotting meth-od, respectively. RESULTS The inhibition of H9C2 cardiomyocyte survival rate inducedby OGD was improvedby pretreated with LGU in a concentrationdependent manner. The microfilaments injury as well as the increase of LDH leakage rate were also improvedby pretreated with LGU.The ATP content was significantly decreased,intracellular Ca2+fluorescent intensity and concentration were significantly increased and the MMP was significantly decreased 4 hafter OGD. LGU significantly reversed the de-crease of intracellular ATP content,the increase of Ca2+fluorescent intensity and concentration and the decrease of MMP.The release of cytochrome C,the expressionsof caspase-9 and caspase-3 in H9C2 cardiomyocytes were increased 16 h after OGD.LGUsignificantly inhibited the changes of these apop-tosis-related proteins. CONCLUSION LGU has a significant protective effect against OGD-induced H9C2 cardiomyocytes injury through inhibiting calcium overload,increasing ATP content,improving mi-tochondrial function and inhibiting apoptosis.
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OBJECTIVE To investigate the neuroprotective effect and possible mechanisms of lute-olin-7-O-β-D-glucuronide (LGU) against focalcerebral ischemic injury. METHODS The focal cerebral ischemic injury model was established by middle cerebral artery occlusion (MCAO). Male Sprague Dawley rats were randomly divided into sham group,model group(MCAO),LGU group(0.24,0.72 and 2.16 mg·kg-1)and positive control group(Edaravone at 5 mg·kg-1).LGU was injected intravenously 30 min after MCAO.Neurological severity score,infarct volume and brain water content were detected 24 h after MCAO and the levels of Na+-K+ATPase,Ca2+ATPase,TNF-α and IL-1β were detected to explore the possible mechanisms.For the therapeutic time window test,LGU(0.72 mg·kg-1)was injected intrave-nously 0.5, 2, 4, 6, 8, 10 and 12 h respectively after MCAO. To evaluate motion behavior, LGU were injected intravenously 30 min after MCAO and once per day during detection period. The changes of motor coordination were detected by rotating rod method and grip strength analysis, and the changes of gaits were detected using DigiGait Imaging System. RESULTS LGU improved the neurological severity score, infarct volume ratio and brain water content. The therapeutic time window of LGU for cerebral infarction and brain edema was at least 6 h and for neurological dysfunction was 12 h.LGU also prolonged the latency on rotarod, increased the forelimb tension and improved 8 gait parameters, including stance duration,stride length,stance width,paw area,paw area variability,gait symmetry,ataxia coefficient and tau propulsion.Furthermore,LGU increased Na+-K+-ATPase and Ca2+-ATPase levels in the cortex and hippocampus in the ischemic side,reduced the levels of TNF-α and IL-1β in the serum. CONCLUSION LGU has a significant neuroprotective effect against cerebral ischemic injury via improving energy metabolism and reducing inflammation.
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Objective To study the value of epidemiology-based mortality score,a novel scoring system,in in-hospital adult patients with status epilepticus (SE) for predicting mortality,and to compare it with the status epilepticus severity score (STESS).Methods The clinical and electroencephalography data of 54 adult patients with SE admitted from June 2013 to June 2016 were derived from a prospective SE database of Zhejiang Provincial Hospital of Traditional Chinese Medicine.The outcome was defined as inhospital death or survival at discharge.When the receiver-operating characteristic (ROC) curves were made,the area under ROC (AUC) and the optimal cutoff value were calculated.Fisher's linear discriminant function analysis was conducted with the outcome as dependent variable and the scores as independent variables.Results Among 54 patients with SE recruited into the study,13 (24.10 ％) died in the hospital.The ROC curve for prediction of in-hospital death based on the STESS had a AUC of 0.705with an optimal cutoff value for discrimination (best match for both sensitivity (0.77) and specificity (0.56) to be ≥ 3 points.The AUC based on the EMSE was 0.800 with an optimal cutoff value for discrimination (best match for both sensitivity (0.92) and specificity (0.61) to be ≥ 79 points.Three elements added in combination with EMSE system (etiology-age-comorbidity,EMSE-EAC) predicted inhospital mortality with the best match for both sensitivity (1.00) and specificity (0.56) as the optimal cutoff point was ≥32 points,and the AUC was 0.814.Four elements added in combination with EMSE system (etiology-age-comorbidity-EEG,EMSE-EACE) predicted in-hospital mortality with the best match for both sensitivity (0.77) and specificity (0.98) as the optimal cutoff point was ≥71 points with an AUC of 0.925.The AUC of EMSE-EACE was larger than that of both STESS and EMSE (Both P ＜ 0.01).Discriminant equations were found by Fisher linear discriminant analysis.The rates of accuracy of the equation for predicting patients' prognosis were 44.44％ (STESS),62.96％ (EMSE),70.37％ (EMSE-EAC) and 81.48％ (EMSE-EACE) respectively,suggesting that the equations of EMSE,EMSE-EAC and EMSE-EACE have superior stability.Conclusions The EMSE is an effective clinical scoring system that focuses on individual mortality.EMSE-EACE is superior over both STESS and EMSE in the prediction of inhospital death.
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Objective To study the value of epidemiology-based mortality score,a novel scoring system,in in-hospital adult patients with status epilepticus (SE) for predicting mortality,and to compare it with the status epilepticus severity score (STESS).Methods The clinical and electroencephalography data of 54 adult patients with SE admitted from June 2013 to June 2016 were derived from a prospective SE database of Zhejiang Provincial Hospital of Traditional Chinese Medicine.The outcome was defined as inhospital death or survival at discharge.When the receiver-operating characteristic (ROC) curves were made,the area under ROC (AUC) and the optimal cutoff value were calculated.Fisher's linear discriminant function analysis was conducted with the outcome as dependent variable and the scores as independent variables.Results Among 54 patients with SE recruited into the study,13 (24.10 ％) died in the hospital.The ROC curve for prediction of in-hospital death based on the STESS had a AUC of 0.705with an optimal cutoff value for discrimination (best match for both sensitivity (0.77) and specificity (0.56) to be ≥ 3 points.The AUC based on the EMSE was 0.800 with an optimal cutoff value for discrimination (best match for both sensitivity (0.92) and specificity (0.61) to be ≥ 79 points.Three elements added in combination with EMSE system (etiology-age-comorbidity,EMSE-EAC) predicted inhospital mortality with the best match for both sensitivity (1.00) and specificity (0.56) as the optimal cutoff point was ≥32 points,and the AUC was 0.814.Four elements added in combination with EMSE system (etiology-age-comorbidity-EEG,EMSE-EACE) predicted in-hospital mortality with the best match for both sensitivity (0.77) and specificity (0.98) as the optimal cutoff point was ≥71 points with an AUC of 0.925.The AUC of EMSE-EACE was larger than that of both STESS and EMSE (Both P ＜ 0.01).Discriminant equations were found by Fisher linear discriminant analysis.The rates of accuracy of the equation for predicting patients' prognosis were 44.44％ (STESS),62.96％ (EMSE),70.37％ (EMSE-EAC) and 81.48％ (EMSE-EACE) respectively,suggesting that the equations of EMSE,EMSE-EAC and EMSE-EACE have superior stability.Conclusions The EMSE is an effective clinical scoring system that focuses on individual mortality.EMSE-EACE is superior over both STESS and EMSE in the prediction of inhospital death.