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Objective: Sex differences in schizophrenia have been noted across domains such as sleep and cognitive function； however, how they interact remains unclear. This study aimed to explore sex differences in the relationship between insomnia and cognitive function in patients with chronic schizophrenia., Methods: 718 schizophrenia patients (480 males and 238 females) and 397 healthy controls were recruited. Insomnia was collected by a questionnaire. Insomnia severity index (ISI) was used to evaluate the severity of insomnia. The clinical symptoms and cognition were assessed with the Positive and Negative Syndrome Scale (PANSS) and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), respectively., Results: Schizophrenia patients showed significantly lower scores compared to healthy controls on the RBANS total score and four indexes (all p < 0.05). Male patients had a lower rate of insomnia, higher scores on the RBANS visuospatial/constructional, language, and total score than female patients (all P < 0.05). Insomnia patients had lower RBANS immediate memory, language, and total scores than non-insomnia patients, and the results only appeared in female patients (all P < 0.05). In addition, there were significant negative correlations between ISI and RBANS language and delayed memory in male patients, while ISI was significantly negatively correlated with RBANS immediate memory in female patients (all P < 0.05)., Conclusion: Our findings suggest that there are sex differences in insomnia, cognitive performance, and their association in patients with chronic schizophrenia. These sex differences may have important potential clinical significance for the identification, evaluation, and treatment of insomnia in patients with chronic schizophrenia., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The present study was aimed to reveal the function of extracellular RNAs (exRNAs) in retinal ischemia reperfusion (I/R) injury, and evaluate whether RNase administration can effectivelyreduce I/Rinjury. A retinal I/R injury C57BL/6J wild-type mice model was established by elevating intraocular pressure for 1 h. All mice received 3 doses of RNase or the same dose of normal saline at different time points. After 7 days of reperfusion, retinal damage was quantified by counting retinal ganglion cells and measuring retinal layer thickness. The apoptotic retinal cells were detected by the TUNEL experiment, and the expressions of caspase-3, proinflammatory cytokines in retinal tissues, and glial fibrillary acidic protein (GFAP) protein and mRNA were detected to determine the underlying mechanism. It was found that RNase administration (1) reduced the significant loss of retinal morphology caused by I/R injury; (2) down-regulated the expression of NF-κBp65, IL-6 and GFAP relative to the I/R mice; (3) decreased the apoptosis of retinal cells and the levels of caspase-3; (4) attenuated exRNAs levels in retinal tissues on day 7 after retinal I/R. In short, increased exRNAs may contribute to retinal I/R damages in mice, and RNase therapy can effectively attenuate retinal damage by reducing inflammatory response and apoptosis., Competing Interests: Declaration of Competing Interest Without conflict of interest in the submission of our manuscript., (Copyright © 2020. Published by Elsevier B.V.)

Patients with schizophrenia (SCZ) exhibit higher suicide rates than the general population. However, the molecular mechanism responsible for the high rate of suicidal behavior in SCZ remains poorly understood. MTHFR Ala222Val (C677T; rs 1801133) polymorphism has repeatedly demonstrated to play a pathological role in numerous mental disorders, but none of these studies focused on the susceptibility of suicidal behavior in SCZ. In the present cross-sectional study, we recruited 957 chronic inpatients with SCZ and 576 healthy controls to assess the psychopathological symptoms of SCZ and compare the frequency of the MTHFR Ala222Val genotype in both suicide attempters and non-attempters. Our results demonstrated no significant differences in MTHFR Ala222Val genotype and allele distributions between the SCZ patients and controls (p > 0.05), but showed a statistical significance in the distribution of Ala/Val genotype between suicide attempters and non-attempters (p < 0.05). Further logistic regression analysis showed that MTHFR Ala222Val genotype, psychopathological symptoms, number of cigarettes smoked per day and drinking status were related to suicide attempts in SCZ (p < 0.05). Our study demonstrated that MTHFR Ala222Val polymorphism and some clinical characteristics might confer susceptibility to suicide in patients with SCZ.

The neurotrophic hypothesis of depression is supported by consistent findings of lower serum BDNF levels in depressed patients. Increasing evidence shows different clinical characteristics of patients with psychotic major depression versus nonpsychotic major depression. However, the possible association between BDNF and psychotic symptoms in depression has not been investigated. We recruited 90 treatment-resistant depression (TRD) patients and 90 gender- and age-matched healthy control subjects and examined serum BDNF in both groups. Patients' depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HDRS-17), and psychopathological symptoms by the 18-item Brief Psychiatric Rating Scale (BPRS-18). Our results showed that BDNF levels were significantly lower in patients than controls. Correlation analysis revealed a significantly positive correlation between BDNF and the thought disturbance subscale of BPRS-18 (p < 0.05), and a trend toward a significantly positive correlation between BDNF and the BPRS-18 total score (p = 0.06). Stepwise multiple regression analyses confirmed BDNF as the influencing factor for the thought disturbance subscales of the BPRS-18. Our findings suggest that BDNF may be involved in the pathophysiology of TRD, and its associated psychotic symptoms, especially thought disturbance., (Copyright © 2017 Elsevier B.V. All rights reserved.)

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