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Objective To analyze the correlation between serum monocyte chemotactic protein-2 (MCP-2), growth differentiation factor-15 (GDF-15) and personality characteristics of patients with major depressive disorder (MDD) and their effects on suicidal ideation. Methods A total of 149 MDD patients who were admitted to The First Psychiatric Hospital of Harbin from January 2022 to June 2023 were selected as MDD group, and 75 healthy volunteers who underwent physical examination during the same period were selected as healthy group. Enzyme linked immunosorbent assay was used to detect serum levels of MCP-2 and GDF-15, and the personality traits of MDD patients were evaluated using the Eysenck Personality Questionnaire (EPQ). The Pearson method was used to analyze the correlation between serum MCP-2, GDF-15, and EPQ score. Based on the presence or absence of suicidal ideation, multivariate logistic regression and receiver operating characteristic (ROC) curves were used to analyze the predictive value of each factor on suicidal ideation in MDD patients. Results The levels of serum MCP-2 and GDF-15 in MDD group were higher than those in healthy group (P＜0.05). Among the 149 MDD patients, 56 cases (37.58%) had suicidal ideation. Higher HAMD score, poor sleep quality, severe anxiety, history of attempted suicide, and higher levels of serum MCP-2 and GDF-15 were independent risk factors for suicidal ideation in MDD patients (P＜0.05). The AUC of serum MCP-2, GDF-15 alone and in combination for predicting suicidal ideation in MDD were 0.679, 0.675 and 0.819, respectively. Conclusion The levels of serum MCP-2 and GDF-15 in MDD patients are closely relate to the personality characteristics of MDD patients, higher levels of MCP-2 and GDF-15 are risk factors for suicidal ideation in MDD patients.

Abstract Backgroud This study aimed to explore the clinical value of long - term electroencephalogram (LTM EEG) in seizure-free individuals taking antiepileptic drugs (AEDs) for more than 2 years. We try to look for clinical factors associated with epileptiform activity on LTM EEG in seizure free patients. We hope that the detection of epileptiform activity by the LTM EEG recording can develop the better treatment strategy. Methods The LTM EEG recordings of 770 individuals with a definite diagnosis of epilepsy were assessed. Two hundred sixty-two individuals accorded with the inclusion criteria and exclusion criteria. We collect the demographic and clinical information and LTM EEG data of these 262 individuals. We analysed the data by one-way analysis of variance and Cox proportional hazards models. Results We found that more epileptiform activity were found with LTM EEG recording than regular EEG recording in seizure-free individuals. We found several clinical factors could be associated with epileptiform activity on LTM EEG in seizure free patients by a one-way analysis: symptomatic or cryptogenic epilepsy [hazard ratio (HR) = 2.6], history of cerebral trauma (HR = 7.5), and abnormal imaging findings (HR = 3.1). The following factors suggested a correlation between history of cerebral trauma (HR = 2.4) and history of cerebral surgery (HR = 3.4) with epileptiform activity on LTM EEG presentation by multivariate logistic regression analysis. Conclusions The study indicated a correlation of a number of factors with abnormal LTM EEG presentation: symptomatic or cryptogenic epilepsy, history of cerebral trauma, history of cerebral surgery, and abnormal imaging findings. The LTM EEG recording may help find epileptiform activity in high risk seizure-free individuals. The individuals need be reevaluated the therapeutic strateagies, and increase the hope to reach real seizure-free.

L-3,4-dihydroxyphenylalanine (L-dopa) remains the most effective therapy for Parkinson's disease (PD), but its long-term administration is associated with the development of debilitating motor complications known as L-dopa-induced dyskinesia (LID). Enhanced function of dopamine D1 receptor (D1R) and N-methyl-D-aspartate receptor (NMDAR) is believed to participate in the pathogenesis of LID. Given the existence of physical and functional interactions between D1R and NMDAR, we explored the effects of uncoupling D1R and NMDA GluN1 (GluN1) interaction on LID by using the Tat-conjugated interfering peptide (Tat-D1-t2). In this study, we demonstrated in 6-hydroxydopamine (6-OHDA)-lesioned PD rat model that intrastriatal injection of Tat-D1-t2 alleviated dyskinetic behaviors and downregulated the phosphorylation of DARPP-32 at Thr34 induced by levodopa. Moreover, we also showed intrastriatal administration of Tat-D1-t2 elicited alterations in membranous GluN1 and D1R expression. These findings indicate that D1R/GluN1 complexes may be a molecular target with therapeutic potential for the treatment of dyskinesia in Parkinson's patients.