Brain network abnormalities in emotional response exist in bipolar mania. However, few studies have been published on network degree centrality of first-episode, drug-naive bipolar mania, and healthy controls. This study aimed to assess the utility of neural activity values analyzed via degree centrality methods. Sixty-six first-episode, drugnaive patients with bipolar mania and 60 healthy controls participated in resting-state functional magnetic resonance rescanning and scale estimating. The degree centrality and receiver operating characteristic (ROC) curve methods were used for an analysis of the imaging data. Relative to healthy controls, first-episode bipolar mania patients displayed increased degree centrality values in the left middle occipital gyrus, precentral gyrus, supplementary motor area, Precuneus, and decreased degree centrality values in the left parahippocampal gyrus, right insula and superior frontal gyrus, medial. ROC results exhibited degree centrality values in the left parahippocampal gyrus that could distinguish first-episode bipolar mania patients from healthy controls with 0.8404 for AUC. Support vector machine results showed that reductions in degree centrality values in the left parahippocampal gyrus can be used to effectively differentiate between bipolar disorder patients and healthy controls with respective accuracy, sensitivity, and specificity values of 83.33%, 85.51%, and 88.41%. Increased activity in the left parahippocampal gyrus may be a distinctive neurobiological feature of firstepisode, drug-naive bipolar mania. Degree centrality values in the left parahippocampal gyrus might be served as a potential neuroimaging biomarker to discriminate firstepisode, drug-naive bipolar mania patients from healthy controls.

Introduction Few studies of the effect of cardiac abnormalities on acute intracerebral hemorrhage (ICH) outcomes have been published. We sought to determine whether the left ventricular ejection fraction (LVEF) is associated with the functional outcome and mortality of acute ICH patients. Methods We conducted a retrospective study on 364 acute ICH patients from January to December 2016. The primary outcome was defined by the modified Rankin Scale and mortality at 3 months. The associations between LVEF and outcome were investigated using univariable and multivariable logistic regression models. Results Depressed LVEF was significantly associated with a poor functional outcome with an odds ratio [OR] of 0.966, 95% confidence interval (CI) 0.942–0.991, p = .008, and high mortality (OR 0.968 [95% CI 0.943–0.994], p = .015) at 3 months for acute ICH patients by univariate analysis. Multivariable logistic regression analysis indicated that LVEF was an independent predictor of a poor functional outcome (OR 0.961 [95% CI 0.935–0.988], p = .005) and mortality (OR 0.949 [95% CI 0.918–0.981], p = .002). The percentage of acute ICH patients with poor functional outcome ( p = .005) and mortality ( p = .002) was obviously higher in the group of patients with a LVEF of <50%. Conclusions LVEF is an independent predictor of functional outcome and mortality at 3 months for acute ICH patients. These findings could provide the evidence needed for prognosis prediction in acute ICH patients.

No abstract

Objective: To explore the relationship between pro-inflammatory factor high-mobility group box 1 (HMGB1) and glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the development of epilepsy. Methods: Thalamic reticular nucleus (TRN) slice was treated with kainic acid (KA) to simulate seizure. Seizure-like spikes and spontaneous inhibitory postsynaptic currents (sIPSCs) were recorded within TRN slices using whole-cell patch clamp techniques. The translocation of HMGB1 were detected by Immunofluorescence. HMGB1/TLR4 signaling pathway and its downstream inflammatory factors (IL-1β and NF-κB) were detected by RT-PCR, Western blot and ELISA. Results: KA-evoked seizure-like spikes were observed in the TRN slices and blocked by perampanel. sIPSCs in the TRN were enhanced by KA and blocked by perampanel. The translocation of HMGB1 in TRN were promoted by KA and inhibited by perampanel. The expression of HMGB1/TLR4 signaling pathway were promoted by KA and suppressed by perampanel. Conclusion: The AMPA receptor and HMGB1/TLR4 signaling pathway interaction jointly contribute to the development of epilepsy.

No abstract