Organizational change-key to capacity building and effective health promotion

Contemporary health promotion is now a well-defined discipline with a strong (albeit diverse) theoretical base, proven technologies (based on program planning) for addressing complex social problems, processes to guide practice and a body of evidence of efficacy and increasingly, effectiveness. Health promotion has evolved principally within the health sector where it is frequently considered optional rather than core business. To maximize effectiveness, quality health promotion technologies and practices need to be adopted as core business by the health sector and by organizations in other sectors. It has proven difficult to develop the infrastructure, workforce and resource base needed to ensure the routine introduction of high-quality health promotion into organizations. Recognizing these problems, this paper explores the use of organizational theory and practice in building the capacity of organizations to design, deliver and evaluate health promotion effectively and efficiently. The paper argues that organizational change is an essential but under-recognized function for the sustainability of health promotion practice and a necessary component of capacity-building frameworks. The interdependence of quality health promotion with organizational change is discussed in this paper through three case studies. While each focused on different aspects of health promotion development, the centrality of organizational change in each of them was striking. This paper draws out elements of organizational change to demonstrate that health promotion specialists and practitioners, wherever they are located, should be building organizational change into both their practice and capacity-building frameworks because without it, effectiveness and sustainability are at risk. (AU)

Delayed treatment with 1,3-butanediol reduces loss of CA1 neurons in the hippocampus of rats following brief forebrain ischemia.

This study examined the effect of 1,3-butanediol on the selective loss of CA1 pyramidal neurons following a short period of near-complete forebrain ischemia. Injection of 55 mmol 1,3-butanediol/kg body weight at 24 h of recirculation and again at 36 h following 10 min of forebrain ischemia markedly reduced damage to CA1 neurons examined at 72 h of recirculation compared with that in saline-treated rats. Comparable treatment with ethanol did not cause significant protection. Neuronal loss was also not reduced by 1,3-butanediol treatment when the ischemic period was extended to 15 min or by single treatments at 24 h or 36 h following 10 min of ischemia. However, a single treatment 5 min after reversal of 10 min of ischemia was effective in ameliorating cell loss. The difference in effectiveness of 1,3-butanediol following 10 min and 15 min of ischemia is consistent with a number of previous studies, indicating that the processes leading to loss of CA1 neurons are modified when the ischemic period is extended. Previous findings that 1,3-butanediol reduced damage in other ischemia-susceptible neuronal subpopulations but not in CA1 neurons most likely reflected the longer period of ischemia which was used. The results of the present investigation demonstrate that administration of 1,3-butanediol offers a novel approach for interfering with post-ischemic loss of CA1 neurons following a brief ischemic period which is effective even when initiated after prolonged recirculation periods.