Stakeholders' role in improving Ghana's construction safety

Health and safety (H&S) management has traditionally been the responsibility of the contractor. Most often, contractors are blamed for the accidents and other ill health that occur on their construction sites. H&S performance is, however, enhanced when there is effective collaboration between those involved in the construction process. This paper therefore explores the role of stakeholders in promoting construction H&S in Ghana through public works procurement. The four main stakeholders identified and evaluated in this study are the government, the client (employer), the contractor and the employee(s). Seven interviewees (comprising procurement managers, consultants and quantity surveyors) from public institutions in Ghana participated in the research. Data were collected using semi-structured interviews and were thematically analysed. Results indicate a conflict in the perceived functions and relation of these stakeholders in the construction process. To address the constraint to improving construction H&S, certain recommendations are offered. These include the identification of specific individuals responsible for supervision and employee training, the development of H&S policies by the government and contracts that clearly outline the contractual obligations of all parties involved. Additionally, the specific roles and involvements of other stakeholders in the procurement process in improving construction H&S are also outlined

Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin

SummaryEndothelial cells in growing tumors express activated Akt, which when modeled by transgenic endothelial expression of myrAkt1 was sufficient to recapitulate the abnormal structural and functional features of tumor blood vessels in nontumor tissues. Sustained endothelial Akt activation caused increased blood vessel size and generalized edema from chronic vascular permeability, while acute permeability in response to VEGF-A was unaffected. These changes were reversible, demonstrating an ongoing requirement for Akt signaling for the maintenance of these phenotypes. Furthermore, rapamycin inhibited endothelial Akt signaling, vascular changes from myrAkt1, tumor growth, and tumor vascular permeability. Akt signaling in the tumor vascular stroma was sensitive to rapamycin, suggesting that rapamycin may affect tumor growth in part by acting as a vascular Akt inhibitor