The impact of regulation, ownership and business culture on managing corporate risk within the water industry

Although the specifics of water utility ownership, regulation and management culture have been explored in terms of their impact on economic and customer value, there has been little meaningful engagement with their influence on the risk environment and risk management. Using a literature review as the primary source of information, this paper maps the existing knowledge base onto two critical questions: what are the particular features of regulation, ownership and management culture which influence the risk dynamic, and what are the implications of these relationships in the context of ambitions for resilient organizations? In addressing these queries, the paper considers the mindful choices and adjustments a utility must make to its risk management strategy to manage strategic tensions between efficiency, risk and resilience. The conclusions note a gap in understanding of the drivers required for a paradigm shift within the water sector from a re-active to a pro-active risk management culture. A proposed model of the tensions between reactive risk management and pro-active, adaptive risk management provides a compelling case for measured risk management approaches which are informed by an appreciation of regulation, ownership and business culture. Such approaches will support water authorities in meeting corporate aspirations to become "high reliability" services while retaining the capacity to out-perform financial and service level targets

Colony Stimulating Factor-1 Is Required to Recruit Macrophages into the Mammary Gland to Facilitate Mammary Ductal Outgrowth

AbstractMammary gland development initiates postnatally with the development of terminal end buds (TEBs) at the end of the rudimentary ducts. These grow out through the fat pad and bifurcate to lay down the rudimentary ductal tree. At the initiation of their development, TEBs recruit to their surrounding stroma a substantial population of macrophages. Using mice homozygous for a null mutation in the gene for the macrophage growth factor, colony stimulating factor-1 (CSF-1), that are severely depleted in macrophages, we demonstrated that CSF-1-regulated macrophages are required for normal branching morphogenesis in the mammary gland. However, these mice have a pleiotropic phenotype as a result of the generalized macrophage deficiency. To test that the effect of the mutation observed in the mammary gland was organ-autonomous, we developed a tetracycline-binary system whereby CSF-1 was specifically expressed in the mammary epithelium under the regulation of the MMTV-promoter. This restored mammary macrophage populations but not those in other tissues and corrected the branching morphogenesis defect. Inhibition of CSF-1 expression by tetracycline treatment for varying periods suggested that CSF-1-regulated macrophages are required throughout early mammary gland development. These data show that macrophages acting locally are required for branching morphogenesis of the mammary gland

Erythro-myeloid progenitors contribute endothelial cells to blood vessels

The earliest blood vessels in mammalian embryos are formed when endothelial cells differentiate from angioblasts and coalesce into tubular networks. Thereafter, the endothelium is thought to expand solely by proliferation of pre-existing endothelial cells. Here we show that a complementary source of endothelial cells is recruited into pre-existing vasculature after differentiation from the earliest precursors of erythrocytes, megakaryocytes and macrophages, the erythro-myeloid progenitors (EMPs) that are born in the yolk sac. A first wave of EMPs contributes endothelial cells to the yolk sac endothelium, and a second wave of EMPs colonizes the embryo and contributes endothelial cells to intraembryonic endothelium in multiple organs, where they persist into adulthood. By demonstrating that EMPs constitute a hitherto unrecognized source of endothelial cells, we reveal that embryonic blood vascular endothelium expands in a dual mechanism that involves both the proliferation of pre-existing endothelial cells and the incorporation of endothelial cells derived from haematopoietic precursors