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Suicide is commonly found in patients with major depressive disorder (MDD), while the associations among depressive symptoms and their relationships with suicidal risk remain unclear. This study identified the symptoms associated with suicidal risk and the most central symptoms in the MDD networks based on both self‐reported and clinical‐interview scales. A total of 446 outpatients with MDD were recruited. The Mini International Neuropsychiatric Interview (MINI) was used to assess the suicidal risk. The 13‐item Beck Depression Inventory (BDI‐13) and 17‐item Hamilton Depression Rating Scale (HAMD‐17) were used to measure the depressive symptoms. Network analysis was used to estimate the network models. Ten symptoms in the BDI‐13 network were related to suicidal risk, among which sadness had the strongest association. Among the six symptoms in the HAMD‐17 network that were associated with suicidal risk, guilty feeling was the strongest. Sense of failure was the most central symptom in the BDI‐13 network, while depressed mood had the highest centrality in the HAMD‐17 network. The depressive symptoms related to suicide risk and the clinical features of MDD showed different characteristics based on different assessment types. Combining self‐reported and clinician‐rated assessments in future studies and clinical practice might lead to some new findings. [ABSTRACT FROM AUTHOR]

Childhood trauma and empathy deficits have been found to be related to borderline personality disorder (BPD), but the mechanisms of action remain unclear. This study aims to investigate the characteristics of empathy in male offenders with BPD tendencies and to test its mediating role in the relationship between childhood trauma and BPD tendencies. Two hundred and fifty-seven male offenders and 43 male nonoffender controls completed the Childhood Trauma Questionnaire Short From (CTQ-SF), the Questionnaire of Cognitive and Affective Empathy (QCAE) and the Chinese version of the computerized Yoni Task. ANOVA, Mixed-model ANOVAs and the PROCESS macro were used to analyze the inventory data and task performances. Compared to male offenders without BPD tendencies and nonoffender controls, offenders with BPD tendencies showed more severe childhood abuse, lower cognitive empathy and poorer task performances in second-order cognitive and second-order affective theory of mind. Furthermore, cognitive empathy was found to play a mediating role in the relationship between childhood trauma and BPD tendencies. Our findings indicate the effects of childhood trauma and empathy impairments on BPD and suggest the possible application value of the precision empathy ability training in the intervention of offenders with BPD. [ABSTRACT FROM AUTHOR]

Although Butylphthalide (BP) has protective effects that reduce ischemia-induced brain damage and neuronal cell death, little is known about the precise mechanisms occurring during cerebral ischemia/reperfusion (I/R). Therefore, the aim of this study was to investigate the neuroprotective mechanisms of BP against ischemic brain injury induced by cerebral I/R through inhibition of the c-Jun N-terminal kinase (JNK)-Caspase3 signaling pathway. BP in distilled non-genetically modified Soybean oil was administered intragastrically three times a day at a dosage of 15 mg/(kg day) beginning at 20 min after I/R in Sprague-Dawley rats. Immunohistochemical staining and Western blotting were performed to examine the expression of related proteins, and TUNEL-staining was used to detect the percentage of neuronal apoptosis in the hippocampal CA1 region. The results showed that BP could significantly protect neurons against cerebral I/R-induced damage. Furthermore, the expression of p-JNK, p-Bcl2, p-c-Jun, FasL, and cleaved-caspase3 was also decreased in the rats treated with BP. In summary, our results imply that BP could remarkably improve the survival of CA1 pyramidal neurons in I/R-induced brain injury and inhibit the JNK-Caspase3 signaling pathway. [ABSTRACT FROM AUTHOR]

Cerebral ischemia/reperfusion (I/R) injury is a leading cause of learning and memory dysfunction. Hydrogen sulfide (H 2 S) has been shown to confer neuroprotection in various neurodegenerative diseases, including cerebral I/R-induced hippocampal CA1 injury. However, the underlying mechanisms have not been completely understood. In the present study, rats were pretreated with SAM/NaHS (SAM, an H 2 S agonist, and NaHS, an H 2 S donor) only or SAM/NaHS combined with CaM (an activator of CaMKII) prior to cerebral ischemia. The Morris water maze test demonstrated that SAM/NaHS could alleviate learning and memory impairment induced by cerebral I/R injury. Cresyl violet staining was used to show the survival of hippocampal CA1 pyramidal neurons. SAM/NaHS significantly increased the number of surviving cells, whereas CaM weakened the protection induced by SAM/NaHS. The immunohistochemistry results indicated that the number of Iba1-positive microglia significantly increased after cerebral I/R. Compared with the I/R group, the number of Iba1-positive microglia in the SAM/NaHS groups significantly decreased. Co-Immunoprecipitation and immunoblotting were conducted to demonstrate that SAM/NaHS suppressed the assembly of CaMKII with the ASK1-MKK3-p38 signal module after cerebral I/R, which decreased the phosphorylation of p38. In contrast, CaM significantly inhibited the effects of SAM/NaHS. Taken together, the results suggested that SAM/NaHS could suppress cerebral I/R injury by downregulating p38 phosphorylation via decreasing the assembly of CaMKII with the ASK1-MKK3-p38 signal module. [ABSTRACT FROM AUTHOR]