Background: The co-production and co-facilitation of recovery-focused education programmes is one way in which service users may be meaningfully involved as partners.
Objectives: To evaluate the impact of a clinician and peer co-facilitated information programme on service users' knowledge, confidence, recovery attitudes, advocacy and hope, and to explore their experience of the programme.
Methods: A sequential design was used involving a pre-post survey to assess changes in knowledge, confidence, advocacy, recovery attitudes and hope following programme participation.
Aim: Current monitoring practices fail to diagnose patients with post-transplant hyperglycaemia and tend to delay initiation of treatment, which potentially results in adverse graft and morbidity outcomes. This real-world study set out to assess the impact on insulin resistance indices of a new clinical pathway for diagnosis and treatment of hyperglycaemia following renal transplantation.
Methods: A hundred and forty-seven adult renal transplant recipients, without pre-existing diabetes, from a single centre were included.
Health policy is increasingly advocating for involvement of service users and family members in service development. In the present study, we evaluated the impact of a 4-day education programme in co-facilitation skills on clinician and peer (service users and family members) knowledge, confidence, and subsequent experience as co-facilitators. The programme was designed to train peers and clinicians as co-facilitators on a clinician and peer-led information programme for people experiencing mental health problems.
View Article and Find Full Text PDFCP-64131 (CP), an aminobenzazepine with cytokine-like, physiologic effects similar to granulocyte-colony stimulating factor (G-CSF) and granulocyte macrophage (GM)-CSF, increases the number of neutrophils and stimulates marrow recovery after doxirubicin ablation. CP can also function as a neutrophil agonist, like formyl-Met-leu-Phe (fMLP). In these studies, we show that CP is unique in that it stimulates the p38-mitogen-activated protein kinase (MAPK) pathway but not extracellular signal-regulated kinase (ERK)1/2 or c-jun N-terminal kinase MAPKs in human neutrophils from peripheral blood.
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