Physicians' Characteristics Associated with Exploring Suicide Risk among Patients with Depression: A French Panel Survey of General Practitioners

Background

General practitioners (GPs) have a key role to play in suicide prevention, but the rates at which they question patients with depression about suicidal thoughts and plans are rather low. Little is known about GPs'' characteristics associated with such inquiries. Our objectives were to describe GPs'' attitudes, perceived barriers, and self-reported practices in this questioning of these patients and to analyze factors associated with these practices.

Methodology

This cross-sectional survey was conducted among participants in a panel of randomly selected French GPs (1249/1431 participated: 87.3%). GPs were interviewed with a standardized questionnaire covering their professional and personal characteristics, attitudes, and practices in exploring the suicide risk of their patients with depression. We built a suicide inquiry score by summing the responses to 5 items and used a multiple linear regression analysis to explore the characteristics associated with this score.

Principal Findings

Most GPs reported inquiring about the presence of suicidal ideation often or very often; less than 30% reported that they frequently explored signs of a specific suicide plan. The mean suicide inquiry score was 12.4 (SD, 2.9; range, 5–20). False ideas, such as thinking that patients who report suicidal ideas do not often commit suicide, were frequent (42.3%). Previous continuing medical education on suicide, participation in a formal mental health network, and patients who committed suicide in the past 5 years were associated with a higher score. Reluctance to question patients about suicide and perception of insufficient skill were associated with a lower score.

Conclusions/Significance

This study showed great variability in French GPs'' practices in exploring suicide risk in patients with depression. Interventions aiming at improving GPs'' initial training and continuing medical education in suicide and/or depression, and their collaboration with mental health specialists should be developed, and their impacts assessed.     

Functional Limitations of Plasmacytoid Dendritic Cells Limit Type I Interferon,T Cell Responses and Virus Control in Early Life

Infant mortality from viral infection remains a major global health concern: viruses causing acute infections in immunologically mature hosts often follow a more severe course in early life, with prolonged or persistent viral replication. Similarly, the WE strain of lymphocytic choriomeningitis virus (LCMV-WE) causes acute self-limiting infection in adult mice but follows a protracted course in infant animals, in which LCMV-specific CD8⁺ T cells fail to expand and control infection. By disrupting type I IFNs signaling in adult mice or providing IFN-α supplementation to infant mice, we show here that the impaired early life T cell responses and viral control result from limited early type I IFN responses. We postulated that plasmacytoid dendritic cells (pDC), which have been identified as one major source of immediate-early IFN-I, may not exert adult-like function in vivo in the early life microenvironment. We tested this hypothesis by studying pDC functions in vivo during LCMV infection and identified a coordinated downregulation of infant pDC maturation, activation and function: despite an adult-like in vitro activation capacity of infant pDCs, the expression of the E2-2 pDC master regulator (and of critical downstream antiviral genes such as MyD88, TLR7/TLR9, NF-κB, IRF7 and IRF8) is downregulated in vivo at baseline and during LCMV infection. A similar pattern was observed in response to ssRNA polyU, a model ligand of the TLR7 viral sensor. This suggests that the limited T cell-mediated defense against early life viral infections is largely attributable to / regulated by infant pDC responses and provides incentives for novel strategies to supplement or stimulate immediate-early IFN-α responses.     

Protection of Neuronal Diversity at the Expense of Neuronal Numbers during Nutrient Restriction in the Drosophila Visual System

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Highlights? Diet sensitivity of neural proliferation is a property of developmental timing ? Early diet-dependent neural proliferation determines neural stem cell pool size ? Late diet-independent neural proliferation preserves steroid-induced neurogenesis ? Reveals strategy for adapting the size of the developing brain to nutritional conditions     

Bcl10 controls TCR- and FcgammaR-induced actin polymerization

Bcl10 plays an essential role in the adaptive immune response, because Bcl10-deficient lymphocytes show impaired Ag receptor-induced NF-kappaB activation and cytokine production. Bcl10 is a phosphoprotein, but the physiological relevance of this posttranslational modification remains poorly defined. In this study, we report that Bcl10 is rapidly phosphorylated upon activation of human T cells by PMA/ionomycin- or anti-CD3 treatment, and identify Ser(138) as a key residue necessary for Bcl10 phosphorylation. We also show that a phosphorylation-deficient Ser(138)/Ala mutant specifically inhibits TCR-induced actin polymerization yet does not affect NF-kappaB activation. Moreover, silencing of Bcl10, but not of caspase recruitment domain-containing MAGUK protein-1 (Carma1) induces a clear defect in TCR-induced F-actin formation, cell spreading, and conjugate formation. Remarkably, Bcl10 silencing also impairs FcgammaR-induced actin polymerization and phagocytosis in human monocytes. These results point to a key role of Bcl10 in F-actin-dependent immune responses of T cells and monocytes/macrophages.     

Does FSH signaling have a gender?

FSH is the main endocrine control of mammalian reproduction. FSH triggers somatic cells of the gonads which support germ cells metabolically, i.e. Sertoli cells of the seminiferous tubules, and granulosa cells harboring the oocyte, within the ovarian follicle. FSH leads to similar biological responses in both cell types since it stimulates proliferation and differentiation, according to the developmental stage. However, FSH receptor knock-out female mice are infertile, unlike male mice. Hence, FSH is not equally important in both sexes. Nevertheless, does FSH induce distinct signalling mechanisms in its target cells ? Here, we compare the signalling mechanisms induced by FSH in ovarian and testicular physiology.