Whether the systemic immune response to stroke contributes to long-term disability is unclear. Using deep immune profiling of peripheral blood over a one-year period following ischaemic stroke, Tsai et al. identify three immunological phases characterized by sequential engagement of innate and adaptive immune compartments, which correlate with post-stroke cognitive trajectories.
Antipsychotic drugs may produce adverse effects during development in humans and rodents. However, the extent of these effects has not been systematically characterized nor have molecular mechanisms been identified. Consequently, we sought to evaluate the effects of an extensive panel of antipsychotic drugs in a model organism, C. elegans, whose development is well characterized, and which offers the possibility of identifying novel molecular targets. For these studies, animals were grown from hatching in the presence of vehicle (control) or antipsychotic drugs over a range of concentrations (20-160 μM) and growth was analyzed by measuring head-to-tail length at various intervals. First-generation antipsychotics (e.g., fluphenazine) generally slowed growth and maturation more than second-generation drugs such as quetiapine, and olanzapine. This is consistent with in vitro effects on human neuronal cell lines. Clozapine, a second-generation drug, produced similar growth deficits as haloperidol. Converging lines of evidence, including the failure to rescue growth with high concentrations of agonists, suggested that the drug-induced delay in development was not mediated by the major neurotransmitter receptors recognized by the antipsychotic drugs. Moreover, in serotonin-deficient tph-1 mutants, the drugs dramatically slowed development and led to larval arrest (including dauer formation), and neuronal abnormalities. Evaluation of alternative targets of the antipsychotics revealed a potential role for calmodulin and underscored the significance of Ca 2+ -calmodulin signaling in development. These findings suggest that antipsychotic drugs may interfere with normal developmental processes, and provide a tool for investigating the key signaling pathways involved.
Background Premenstrual dysphoric disorder (PMDD) is a complex and disabling condition that affects women of reproductive age, characterised by severe physical and psychological symptoms that occur cyclically and remit following the onset of menses. As the psychological nature and consequences of PMDD often seem indistinguishable from symptoms of other mental health difficulties, this condition presents distinct diagnostic challenges for healthcare professionals. Therefore, this study aimed to explore women’s experiences of both having PMDD and of receiving this diagnosis. Methods Participant recruitment took place in the United Kingdom during 2018. Seventeen women who had been diagnosed with PMDD by a medical specialist and met the clinical criteria for PMDD on the premenstrual symptoms screening tool were interviewed. The data from these semi-structured interviews were audio-recorded, transcribed and inductively analysed using reflexive thematic analysis. Results Twelve subthemes were identified and organised around four main themes: (1) A broken woman, (2) Misdiagnosis and the lost decades, (3) A life transformed and (4) Negotiating the aftermath. Conclusions The findings of this study highlight the critical importance of the accurate and timely detection of PMDD, with the aim of preventing women from experiencing severe and prolonged psychological distress. In order to achieve this, there needs to be a greater understanding and awareness of PMDD within both the medical and lay communities, alongside training for healthcare practitioners in PMDD assessment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.