Expert practical operative skills teaching in Trauma and Orthopaedics at a nominal cost.

BACKGROUND AND PURPOSE: The AO Foundation Operative Fracture Management course is the gold standard in training courses currently available for trainees at ST3 level. We have devised a low cost operative skills course comprising instructional lectures, demonstrations and practical dry bone workshops. To assess the quality of teaching, candidates' feedback was analysed in two cohorts for the running of the course over two consecutive years: 2008 and 2009. METHODS: Trainees were given short instructional lectures by consultant surgeons followed by workshops, with a trainer to candidate ratio of 1:4. A trauma inventory was provided by Stryker Trauma UK, ensuring a nominal fee for each candidate (£50). Feedback was anonymously collected according to a Likert scale and analysed using non-parametric methods appropriate for ranked data. MAIN FINDINGS: Twenty one of 22 (95%) candidates gave feedback in 2008 and 18 out of 18 candidates (100%) in 2009. The teaching provided was highly rated consistently for both years, apart from an informal session on theatre tips and tricks in 2008. This was not repeated in 2009 to allow more practical time. Only one session, an intramedullary nailing lecture, had a significant difference in scores between the 2 years (p = 0.044) because of improved scores in 2009. CONCLUSIONS: Due to changes in training, trainees have reduced exposure in theatre and this has implications for the early stages of acquiring practical operative skills. As an adjunct to the AO course, practical skills teaching by consultants in the format of a low cost skills workshop outside of a theatre environment can be achieved with support from a trauma implant supplier.

Specific inhibition of glucocorticoid-induced thymocyte apoptosis by substance P.

Glucocorticoids (GC) are strong inducers of thymocyte apoptosis. In the present study we looked into the possibility that the neuropeptide substance P (SP) might serve as an antagonist to GC-induced apoptosis. Indeed, SP inhibited hydrocortisone (HC)-induced apoptosis of CD4+CD8+ thymocytes in mice, both in vivo and in vitro. It also inhibited HC-induced apoptosis in the T cell hybridoma line 2B4.11, which is sensitive to GC. The inhibitory effect was complete if SP was given with HC or within 1 h after it; partial inhibitory effect could be seen at 2 h and no effect at 3 h. The presence of the SP antagonist nullified SP effect. The effect was specific to both components of the system (i.e., HC as apoptosis inducer and SP as its inhibitor), as judged from comparison to three other apoptosis-inducing means (irradiation, thymic epithelial cells, or retinoic acid), and to two other neuropeptides (somatostatin and vasoactive intestinal peptide). SP/HC antagonism was further demonstrated in two relevant molecular events: 1) HC augmented GC receptor production in our cell system and this was inhibited by SP; and 2) HC reduced the expression of the transcription factor NF-kappaB, SP increased it and when both were present, SP effect dominated. On the other hand, the level of IkappaB (NF-kappaB inhibitory molecule) was decreased by SP, preserved at a relatively high level with HC, and when both SP and HC were present, SP effect dominated. The intensity of SP effect, both in vivo and in vitro, its specificity, its inhibition by SP antagonist, as well as the previously documented presence of SP and its receptor in the thymus suggest that SP might be a physiological antagonist of the potent thymocyte apoptosis induced by GC.

Effect of human recombinant granulocyte-macrophage colony-stimulating factor and IL-3 on the expression of surface markers of human monocyte-derived macrophages in long-term cultures.

Granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-3, which are involved in the maturation of cell precursors in the bone marrow into granulocytes and macrophages, were found also in chronic inflammatory sites, and their production might be enhanced by inflammatory stimulants. These findings led us to examine the effect of human recombinant GM-CSF (hrGM-CSF) and hrIL-3 on the maturation of human peripheral blood monocytes in long-term tissue cultures and on the expression of functional membrane bound molecules. Adherent human peripheral blood monocytes cultured for 2 weeks in the presence of GM-CSF or IL-3 were examined for viability and adherence, expression of membranal HLA-DR, CD-14, and IL-1 alpha, and LPS triggered TNF-alpha production. GM-CSF and IL-3 treatment increased the viability of adherent cells after 2 weeks in culture, and elevated the expression of membranal HLA-DR, CD-14 (LPS receptor), and IL-1 alpha. Such treated macrophage cultures also showed elevated production of TNF-alpha. The results indicate that GM-CSF and IL-3 facilitate the long-term maturation of monocytes into macrophages, augment their capacity to bind LPS, and elevate the release of cytokines involved in inflammatory and granulomatous reactions.