Identifying support mechanisms to overcome barriers to food safety scheme certification in the food and drink manufacturing industry in Wales, UK.

Obtaining food safety certification is essential for food manufacturers. Potential barriers to obtaining certification are complex, interrelated and broadly relate to, 'knowledge and skills', 'time, cost and resources', and 'communication and access to information'. This study aimed to explore requirements for support to enable food manufacturers in Wales to overcome identified barriers. Food manufacturers (n = 37) participated in group discussions (n = 2) and completed online-questionnaires (n = 29). Support mechanisms, perceived necessary to obtain food safety certification included; funding for training and audit-fees, support for implementing food safety scheme documentation, on-site support through mentoring/coaching and pre-audits. Findings identify the need for a food safety scheme certification support package pathway incorporating online, off-site, on-site and financial support to assist food and drink manufacturers obtain third-party food safety certification. Such assistance would support three critical areas. Findings may inform development of support mechanisms to increase uptake of food safety certification and accelerate food-sector growth.

Replacement of Lost Substance P Reduces Fibrosis in the Diabetic Heart by Preventing Adverse Fibroblast and Macrophage Phenotype Changes.

Reduced levels of the sensory nerve neuropeptide substance P (SP) have been reported in the diabetic rat heart, the consequence being a loss of cardioprotection in response to ischemic post-conditioning. We considered whether this loss of SP also predisposes the heart to non-ischemic diabetic cardiomyopathy in the form of fibrosis and hypertrophy. We report that diabetic Leprdb/db mice have reduced serum SP and that administration of exogenous replacement SP ameliorated cardiac fibrosis. Cardiac hypertrophy did not occur in Leprdb/db mice. Cardiac fibroblasts exposed to high glucose converted to a myofibroblast phenotype and produced excess extracellular matrix proteins; this was prevented by the presence of SP in the culture media. Cardiac fibroblasts exposed to high glucose produced increased amounts of the receptor for advanced glycation end products, reactive oxygen species and inflammatory cytokines, all of which were prevented by SP. Cultured macrophages assumed an M1 pro-inflammatory phenotype in response to high glucose as indicated by increased TNF-α, CCL2, and IL-6. SP promoted a shift to the reparative M2 macrophage phenotype characterized by arginase-1 and IL-10. Leprdb/db mice showed increased left ventricular M1 phenotype macrophages and an increase in the M1/M2 ratio. Replacement SP in Leprdb/db mice restored a favorable M1 to M2 balance. Together these findings indicate that a loss of SP predisposes the diabetic heart to developing fibrosis. The anti-fibrotic actions of replacement SP involve direct effects on cardiac fibroblasts and macrophages to oppose adverse phenotype changes. This study identifies the potential of replacement SP to treat diabetic cardiomyopathy.