Relic Neutralino Densities and Detection Rates with Nonuniversal Gaugino Masses

We extend previous analyses on the interplay between nonuniversalities in the gaugino mass sector and the thermal relic densities of LSP neutralinos, in particular to the case of moderate to large tan beta. We introduce a set of parameters that generalizes the standard unified scenario to cover the complete allowed parameter space in the gaugino mass sector. We discuss the physical significance of the cosmologically preferred degree of degeneracy between charginos and the LSP and study the effect this degree of degeneracy has on the prospects for direct detection of relic neutralinos in the next round of dark matter detection experiments. Lastly, we compare the fine tuning required to achieve a satisfactory relic density with the case of universal gaugino masses, as in minimal supergravity, and find it to be of a similar magnitude. The sensitivity of quantifiable measures of fine-tuning on such factors as the gluino mass and top and bottom masses is also examined.Comment: Uses RevTeX; 14 pages, 16 figure

Genetically diabetic animals.

Several animal species, mostly rodents, were described to exhibit spontaneously diabetes mellitus on a hereditary basis. These findings were highly appreciated with the expectation to get more insight into the pathogenesis of diabetes in humans. During the last few years since the discovery of leptin (Zhang et al. 1994) and its downstream signal transduction cascade (Friedman and Halaas 1998), tremendous new insight of the genetics of diabetic and obese animal disease models was derived. Up to now, at least six genetically diabetic animal models exhibit defects in the leptin pathway: the ob mutation in the mouse resulted in leptin deficiency. The db mutation in the mouse and the cp and fa mutations in the rat are different mutations of the leptin receptor gene. The fat mutation in the mouse results in a biologically inactive carboxypeptidase E, which processes the prohormone conversion of POMC into α-MSH, which activates the hypothalamic MC4 receptor. Finally the Agouti yellow (y) mouse exhibit a ubiquitous expression of the Agouti protein which represents an antagonist of the hypothalamic MC4 receptor