Returning to health visiting practice: completing the circle.

One strategic health authority, NHS London, initiated a pilot return to health visiting/nursing practice scheme in London in 2010. This paper reports on the experiences of the first three cohorts of returnees on the City University London programme, one of the London programmes, and the adaptations that have been made to the programme to help provide returnees with the theory base and practice experience to equip them to work in today's health visiting. Written evaluation forms were completed by the returnees and information gathered from their application forms. This information was supplemented for Cohort 1 with some interviews with practice teachers and lecturers and a mid-stage questionnaire to the returnees. Of the 54 students in the three cohorts over half were still on one or both Nursing and Midwifery Council registers, which had not been anticipated at the start of the programme and led to modifications to the programme after Cohort 1 with an increase in the health visiting specific content. The returnees had a wide range of experience to bring back to health visiting reflecting the fact that a large number had been out of health visiting for more than 11 years. The evaluation shows that providing support by the university to the practice placement areas; ensuring that the taught element is current and useful to health visiting practice and having a relevant but not too onerous assessment process are critical.

Essential role for hematopoietic prostaglandin D2 synthase in the control of delayed type hypersensitivity.

Hematopoietic prostaglandin D(2) synthase (hPGD(2)S) metabolizes cyclooxygenase-derived prostaglandin (PG) H(2) to PGD(2), which is dehydrated to cyclopentenone PGs, including 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)). PGD(2) acts through two receptors (DP1 and DP2/CRTH2), whereas 15d-PGJ(2) can activate peroxisome proliferator-activated receptors or inhibit a range of proinflammatory signaling pathways, including NF-kappaB. Despite eliciting asthmatic and allergic reactions through the generation of PGD(2), it is not known what role hPGD(2)S plays in T helper (Th)1-driven adaptive immunity. To investigate this question, the severity and duration of a delayed type hypersensitivity reaction was examined in hPGD(2)S knockout and transgenic mice. Compared with their respective controls, knockouts displayed a more severe inflammatory response that failed to resolve, characterized histologically as persistent acute inflammation, whereas transgenic mice had little detectable inflammation. Lymphocytes isolated from inguinal lymph nodes of hPGD(2)S(-/-) animals showed hyperproliferation and increased IL-2 synthesis effects that were rescued by 15d-PGJ(2), but not PGD(2), working through either of its receptors. Crucially, 15d-PGJ(2) exerted its suppressive effects through the inhibition of NF-kappaB activation and not through peroxisome proliferator-activated receptor signaling. In contrast, lymph node cultures from transgenics proliferated more slowly and synthesized significantly less IL-2 than controls. Therefore, contrary to its role in driving Th2-like responses, this report shows that hPGD(2)S may act as an internal braking signal essential for bringing about the resolution of Th1-driven delayed type hypersensitivity reactions. Consequently, hPGD(2)S-derived cyclopentenone PGs may protect against inflammatory diseases, where T lymphocytes play a pathogenic role, as in rheumatoid arthritis, atopic eczema, and chronic rejection.