1,202 research outputs found

    Preoptic Inputs and Mechanisms that Regulate Maternal Responsiveness

    Get PDF
    The preoptic area is a well-established centre for the control of maternal behaviour. An intact medial preoptic area (mPOA) is required for maternal responsiveness because lesion of the area abolishes maternal behaviours. Although hormonal changes in the peripartum period contribute to the initiation of maternal responsiveness, inputs from pups are required for its maintenance. Neurones are activated in different parts of the mPOA in response to pup exposure. In the present review, we summarise the potential inputs to the mPOA of rodent dams from the litter that can activate mPOA neurones. The roles of potential indirect effects through increased prolactin levels, as well as neuronal inputs to the preoptic area, are described. Recent results on the pathway mediating the effects of suckling to the mPOA suggest that neurones containing the neuropeptide tuberoinfundibular peptide of 39 residues in the posterior thalamus are candidates for conveying the suckling information to the mPOA. Although the molecular mechanism through which these inputs alter mPOA neurones to support the maintenance of maternal responding is not yet known, altered gene expression is a likely candidate. Here, we summarise gene expression changes in the mPOA that have been linked to maternal behaviour and explore the idea that chromatin remodelling during mother-infant interactions mediates the long-term alterations in gene expression that sustain maternal responding

    Retrospective case note review of chronic spontaneous urticaria outcomes and adverse effects in patients treated with omalizumab or ciclosporin in UK secondary care.

    Get PDF
    BACKGROUND: Omalizumab is approved in the UK as add-on treatment for chronic spontaneous urticaria (CSU) in patients with inadequate response to H1-antihistamines. Ciclosporin is an established but unlicensed 3rd line option for CSU. Two parallel retrospective observational studies were conducted to describe outcomes of treatment and adverse events with omalizumab or ciclosporin for CSU treatment. METHODS: Data from UK specialist centres prescribing omalizumab (five centres) or ciclosporin (three centres) in CSU patients were collected from hospital records by clinical staff and pooled for analysis. RESULTS: Forty-six patients prescribed omalizumab and 72 patients prescribed ciclosporin were included. Twenty-two (48%) omalizumab-treated patients had paired Urticaria Activity Scores (UAS7), showing a 25.4 point improvement during treatment (P < 0.0001). Paired Dermatology Life Quality Index (DLQI) was available in 28 (61%) omalizumab-treated and 17 (24%) ciclosporin-treated patients. At least a 75% improvement in DLQI score was observed in 79% of omalizumab-treated and 41% of ciclosporin-treated patients, and 65% of omalizumab-treated patients had complete resolution of their quality-of-life impairment (DLQI 0-1) versus 21% of ciclosporin-treated patients. Clinician comments reported symptom clearance in 15/36 (42%) omalizumab-treated and 10/60 (17%) ciclosporin-treated patients. Proportions of patients with adverse events were similar but those for omalizumab resembled CSU symptoms, making causality assignment difficult, whereas those for ciclosporin were consistent with its known adverse effect profile. CONCLUSIONS: Validated patient-reported measures of disease severity and quality of life should be used routinely in CSU management. Based on clinician comments and DLQI scores, symptoms and quality of life showed a greater improvement in the omalizumab-treated cohort than in the ciclosporin-treated cohort
    corecore