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Introduction: Childhood trauma (CT) has been recognized as a risk factor for psychosis. Among the pathways implicated in the CT-psychosis association, attributional biases (ABs) hold a prominent position. ABs disrupt reality testing, thus laying a conducive ground for the emergence of paranoid symptoms. Paranoid patients have been theorized to externalize the causality of negative life events (externalizing bias; EB), mainly by blaming other people (personalizing bias; PB), in an attempt to maintain their self-esteem. Objectives: We sought to investigate the presence and intercorrelations of CT and ABs in a group of patients with schizophreniaspectrum psychosis (SSP). Methods: We compared 63 SSP inpatients to a healthy control group (HC) on measures of CT and attributional style. CT was assessed with the Childhood Experience of Care and Abuse Questionnaire (CECA.Q), and attributional style with the Internal, Personal and Situational Attributions Questionnaire (IPSAQ). Results: SSP inpatients displayed higher levels of CT (X2 (1, N = 124) = 34.5, p < .001) and PB (U = 1309, p = .002) than HCs. EB was not detected in the SSP group. Within the SSP group, PB was negatively correlated to the severity of maternal antipathy (rs = - 0.380, p = .002) and neglect (rs = - 0.300, p = .017). Conclusions: SSP inpatients do not favor external attributions for negative events. However, when they do externalize causality for negative events, they tend to personalize the blame. If PB serves the purpose of preserving an intact self-image in paranoid patients, negative maternal rearing behaviors appear to reduce this defensive capacity. [ABSTRACT FROM AUTHOR]

Endothelial cells (ECs) grant access of disseminated cancer cells to distant organs. However, the molecular players regulating the activation of quiescent ECs at the premetastatic niche (PMN) remain elusive. Here, we find that ECs at the PMN coexpress tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its cognate death receptor 5 (DR5). Unexpectedly, endothelial TRAIL interacts intracellularly with DR5 to prevent its signaling and preserve a quiescent vascular phenotype. In absence of endothelial TRAIL, DR5 activation induces EC death and nuclear factor κB/p38-dependent EC stickiness, compromising vascular integrity and promoting myeloid cell infiltration, breast cancer cell adhesion, and metastasis. Consistently, both down-regulation of endothelial TRAIL at the PMN by proangiogenic tumor-secreted factors and the presence of the endogenous TRAIL inhibitors decoy receptor 1 (DcR1) and DcR2 favor metastasis. This study discloses an intracrine mechanism whereby TRAIL blocks DR5 signaling in quiescent endothelia, acting as gatekeeper of the vascular barrier that is corrupted by the tumor during cancer cell dissemination.

A male patient aged 43 presented with psychotic symptomatology after a traumatic event involving accidental mutilation of the fingers. Initial presentation was uncommon although the patient responded well to pharmacotherapy. The theoretical framework, management plan and details of the treatment are presented.