The associated factors of suicide attempts in patients with major depressive disorder (MDD) comorbid with anxiety remains unclear. To the best of our knowledge, this is the first study with a large sample size that examines the risk factors of suicide attempts in first-episode drug-naïve (FEND) MDD patients comorbid with anxiety and includes clinical correlates, metabolic parameters, and thyroid hormone levels. A total of 1718 FEDN MDD patients were enrolled. The Hamilton Depression Scale (HAMD), Hamilton Anxiety Scale (HAMA), and Positive and Negative Syndrome Scale (PANSS) were used to assess the symptoms of patients. Metabolic parameters and thyroid hormone levels were measured. The prevalence of suicide attempts in MDD patients comorbid anxiety symptoms was 24.28%, which was 9.51 times higher than that in MDD patients without anxiety symptoms (3.25%). Compared to non-attempters, MDD patients with anxiety symptoms who attempted suicide scored higher on HAMD and HAMA, and had higher systolic blood pressure, higher levels of thyroid stimulating hormone (TSH), and thyroid peroxidases antibody (TPOAb), which were also correlated with suicide attempts in MDD patients comorbid anxiety symptoms. The combination of HAMA score, HAMD score, and TSH could differentiate suicide attempters from non-suicide attempters. Further, the age of onset, illness duration, BMI, TSH, and TPOAb were associated with the times of suicide attempts in MDD patients comorbid anxiety symptoms. Our results demonstrate high prevalence of suicide attempts in MDD patients comorbid anxiety symptoms. Several clinical correlates, metabolic parameters, and thyroid hormones function contribute to the suicide attempts in MDD patients comorbid anxiety symptoms.

Although many studies have examined executive functions and facial emotion recognition in people with schizophrenia, few of them focused on the correlation between them. Furthermore, their relationship in the siblings of patients also remains unclear. The aim of the present study is to examine the correlation between executive functions and facial emotion recognition in patients with first-episode schizophrenia and their siblings. Thirty patients with first-episode schizophrenia, their twenty-six siblings, and thirty healthy controls were enrolled. They completed facial emotion recognition tasks using the Ekman Standard Faces Database, and executive functioning was measured by Wisconsin Card Sorting Test (WCST). Hierarchical regression analysis was applied to assess the correlation between executive functions and facial emotion recognition. Our study found that in siblings, the accuracy in recognizing low degree ‘disgust’ emotion was negatively correlated with the total correct rate in WCST (r = −0.614, p = 0.023), but was positively correlated with the total error in WCST (r = 0.623, p = 0.020); the accuracy in recognizing ‘neutral’ emotion was positively correlated with the total error rate in WCST (r = 0.683, p = 0.014) while negatively correlated with the total correct rate in WCST (r = −0.677, p = 0.017). People with schizophrenia showed an impairment in facial emotion recognition when identifying moderate ‘happy’ facial emotion, the accuracy of which was significantly correlated with the number of completed categories of WCST (R2 = 0.432, P < .05). There were no correlations between executive functions and facial emotion recognition in the healthy control group. Our study demonstrated that facial emotion recognition impairment correlated with executive function impairment in people with schizophrenia and their unaffected siblings but not in healthy controls.

The association between BDNF gene functional Val66Met polymorphism rs6265 and the schizophrenia is far from being consistent. In addition to the heterogeneous in schizophrenia per se leading to the inconsistent results, the interaction among multi-genes is probably playing the main role in the pathogenesis of schizophrenia, but not a single gene. Neurotrophic tyrosine kinase receptor 2 (NTRK2) is the high-affinity receptor of BDNF, and was reported to be associated with mood disorders, though no literature reported the association with schizophrenia. Thus, in the present study, total 402 patients with paranoid schizophrenia (the most common subtype of schizophrenia) and matched 406 healthy controls were recruited to investigate the role of rs6265 in BDNF, three polymorphisms in NTRK2 gene (rs1387923, rs2769605 and rs1565445) and their interaction in the susceptibility to paranoid schizophrenia in a Chinese Han population. We did not observe significant differences in allele and genotype frequencies between patients and healthy controls for all four polymorphisms separately. The haplotype analysis also showed no association between haplotype of NTRK2 genes (rs1387923, rs2769605, and rs1565445) and paranoid schizophrenia. However, we found the association between the interaction of BDNF and NTRK2 with paranoid schizophrenia by using the MDR method followed by conventional statistical analysis. The best gene-gene interaction model was a three-locus model (BDNF rs6265, NTRK2 rs1387923 and NTRK2 rs2769605), in which one low-risk and three high-risk four-locus genotype combinations were identified. Our findings implied that single polymorphism of rs6265 rs1387923, rs2769605, and rs1565445 in BDNF and NTRK2 were not associated with the development of paranoid schizophrenia in a Han population, however, the interaction of BDNF and NTRK2 genes polymorphisms (BDNF-rs6265, NTRK2-rs1387923 and NTRK2-rs2769605) may be involved in the susceptibility to paranoid schizophrenia.

Atypical antipsychotics are highly effective antischizophrenic medications but their clinical utility is limited by adverse metabolic sequelae. We investigated whether upregulation of macrophage migration inhibitory factor (MIF) underlies the insulin resistance that develops during treatment with the most commonly prescribed atypical antipsychotic, olanzapine. Olanzapine monotherapy increased BMI and circulating insulin, triglyceride, and MIF concentrations in drug-naive schizophrenic patients with normal MIF expression, but not in genotypic low MIF expressers. Olanzapine administration to mice increased their food intake and hypothalamic MIF expression, which led to activation of the appetite-related AMP-activated protein kinase and Agouti-related protein pathway. Olanzapine also upregulated MIF expression in adipose tissue, which reduced lipolysis and increased lipogenic pathways. Increased plasma lipid concentrations were associated with abnormal fat deposition in liver and skeletal muscle, which are important determinants of insulin resistance. Global MIF-gene deletion protected mice from olanzapine-induced insulin resistance, as did intracerebroventricular injection of neutralizing anti–MIF antibody, supporting the role of increased hypothalamic MIF expression in metabolic dysfunction. These findings uphold the potential pharmacogenomic value of MIF genotype determination and suggest that MIF may be a tractable target for reducing the metabolic side effects of atypical antipsychotic therapy.

Although interleukin-18 (IL-18) has been implicated in the pathophysiology of stroke, research findings concerning IL-18 level in stroke have been inconsistent. Thus, we performed a cross-sectional study in patients with first-episode ischemic stroke and then extracted relevant data from databases to validate our results. A total of 252 patients and 259 healthy subjects were recruited, and serum IL-18 level was evaluated in a cross-sectional study. Then, we extracted data and conducted a meta-analysis, including 2,928 patients and 3,739 controls to support our results. A 95% confidence interval for standardized mean difference (SMD) was calculated using a Z test. We found IL-18 was higher in stroke patients than in controls (2.39 ± 0.25 vs. 2.25 ± 0.28, F=8.60, p=0.004) and was negatively associated with the NIHSS scale (r = -0.14, p=0.028). A subsequent meta-analysis confirmed that IL-18 level was higher in stroke patients than in controls (SMD = 2.14, 95% CI = 1.54 ∼ 2.73, P< 0.001). IL-18 level increased with the severity of the stroke (p< 0.01). These findings revealed increased IL-18 level contributed to the development and severity of ischemic stroke, suggesting the potential of this biomarker to become an important reference for the early monitoring of ischemic stroke.