ABSTRACT
Background and objectives: Suicidal ideation is a key risk factor for suicidal behaviour among depressed individuals. To explore underlying cognitive patterns associated with suicidal ideation, the present study compared early maladaptive schemas (EMSs) among psychiatric outpatients in treatment for major depressive disorder with and without current suicidal ideation. Methods: The sample consisted of 79 depressed patients who responded to the background questionnaire and completed the Young Schema Questionnaire short form-extended, 21-item Beck Depression Inventory and Beck Hopelessness Scale. Results: Patients with suicidal ideation were more maladaptive in respect to the majority of EMSs compared to those without. After controlling for the concurrent depressive symptom severity and hopelessness Vulnerability to Harm or Illness EMS, which concerns catastrophising beliefs, remained a predictor for suicidal ideation. Conclusion: EMSs may contribute to suicidal ideation among depressed individuals regardless of their mood and future orientation. These results offer implications for the assessment and treatment of suicidality
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Subject(s)
Humans , Male , Female , Adolescent , Young Adult , Adult , Middle Aged , Adaptation, Psychological , Social Isolation , Suicide, Attempted/psychology , Depression/psychology , Psychometrics , Suicide/psychology , Internal-External ControlABSTRACT
BACKGROUND: PEST-domain-enriched tyrosine phosphatase (PEP) is a protein tyrosine phosphatase exclusively expressed in hematopoietic cells. It is a potent negative regulator of T-cell receptor signalling that acts on receptor-coupled protein tyrosine kinases. PEST-domain-enriched tyrosine phosphatase is also expressed in mast cell and is positively regulated by glucocorticoids, but its function is unknown. In this communication, the function of PEP is analysed in mast cells. METHODS: Signal transduction cascades following IgE receptor cross-linking were compared in bone marrow-derived mast cells (BMMC) from PEP(-/-) and PEP(+/+) mice. Furthermore, antigen-induced passive systemic anaphylaxis (PSA) was analysed in PEP(+/+) and PEP(-/-) mice. RESULTS: Bone marrow-derived mast cells from PEP(-/-) mice showed impaired PLCγ1 phosphorylation and Ca(2+) mobilization. Additionally, mice deficient in PEP showed impaired mast cell degranulation and were less susceptible to PSA. Treatment of wild-type BMMC or mice with an Au(I)-phosphine complex that selectively inhibits PEP activity produced defects in Ca(2+) signalling pathway and reduced anaphylaxis similar to that caused by the deletion of the PEP gene. Glucocorticoid that negatively regulates a wide range of mast cell action increased PEP expression and only partially inhibited anaphylaxis. However, glucocorticoid potently inhibited anaphylaxis when combined with the PEP inhibitor. CONCLUSIONS: PEST-domain-enriched tyrosine phosphatase is an important positive regulator of anaphylaxis. Pharmacological inhibition of its activity together with glucocorticoid administration provide an effective rescue for PSA in mice.
