Like lemmings over a cliff : a study of Alberta physician burnout

ix, 106 leaves : ill. ; 29 cm. --The prevalence and severity of physician burnout in Alberta was investigated. A total of 1161 out of 6584 (17.6%) practicing physicians, retired physicians, residents, and medical students responded to the survey either by fax, mail, or electronic version. The survey consisted of one demographic section and four burnout measures, one of which was the Modified Maslach Burnout Inventory (MMBI). More specifically, and relative to the Alberta physician population numbers provided by the Alberta Medical Association (AMA), 22 % were practicing physicians; 9.2 % retired; 7.5 % residents, and 1.3 % medical students. Based on the Phase Model, almost ha1f(i.e., 48.6%) of Alberta physicians are found to be in an advanced phase of burnout (i.e., phases VI, VII, & VIII). A comparison of these data with other occupations and countries is also offered

A Drosophila Model of Multiple Endocrine Neoplasia Type 2

Dominant mutations in the Ret receptor tyrosine kinase lead to the familial cancer syndrome multiple endocrine neoplasia type 2 (MEN2). Mammalian tissue culture studies suggest that Ret(MEN2) mutations significantly alter Ret-signaling properties, but the precise mechanisms by which Ret(MEN2) promotes tumorigenesis remain poorly understood. To determine the signal transduction pathways required for Ret(MEN2) activity, we analyzed analogous mutations in the Drosophila Ret ortholog dRet. Overexpressed dRet(MEN2) isoforms targeted to the developing retina led to aberrant cell proliferation, inappropriate cell fate specification, and excessive Ras pathway activation. Genetic analysis indicated that dRet(MEN2) acts through the Ras-ERK, Src, and Jun kinase pathways. A genetic screen for mutations that dominantly suppress or enhance dRet(MEN2) phenotypes identified new genes that are required for the phenotypic outcomes of dRet(MEN2) activity. Finally, we identified human orthologs for many of these genes and examined their status in human tumors. Two of these loci showed loss of heterozygosity (LOH) within both sporadic and MEN2-associated pheochromocytomas, suggesting that they may contribute to Ret-dependent oncogenesis