Gravitino phenomenology and cosmological implications of supergravity

In this thesis we consider the phenomenology of supergravity, and in particular the particle called "gravitino". We begin with an introductory part, where we discuss the theories of inflation, supersymmetry and supergravity. Gravitino production is then investigated into details, by considering the research papers here included. First we study the scattering of massive W bosons in the thermal bath of particles, during the period of reheating. We show that the process generates in the cross section non trivial contributions, which eventually lead to unitarity breaking above a certain scale. This happens because, in the annihilation diagram, the longitudinal degrees of freedom in the propagator of the gauge bosons disappear from the amplitude, by virtue of the supergravity vertex. Accordingly, the longitudinal polarizations of the on-shell W become strongly interacting in the high energy limit. By studying the process with both gauge and mass eigenstates, it is shown that the inclusion of diagrams with off-shell scalars of the MSSM does not cancel the divergences. Next, we approach cosmology more closely, and study the decay of a scalar field S into gravitinos at the end of inflation. Once its mass is comparable to the Hubble rate, the field starts coherent oscillations about the minimum of its potential and decays pertubatively. We embed S in a model of gauge mediation with metastable vacua, where the hidden sector is of the O'Raifeartaigh type. First we discuss the dynamics of the field in the expanding background, then radiative corrections to the scalar potential V(S) and to the Kähler potential are calculated. Constraints on the reheating temperature are accordingly obtained, by demanding that the gravitinos thus produced provide with the observed Dark Matter density. We modify consistently former results in the literature, and find that the gravitino number density and T_R are extremely sensitive to the parameters of the model. This means that it is easy to account for gravitino Dark Matter with an arbitrarily low reheating temperature.

Associations of gene polymorphisms and nutrition with calcium homeostasis and bone mineral density : Studies on skeletal nutrigenetics

Heredity explains a major part of the variation in calcium homeostasis and bone strength, and the susceptibility to osteoporosis is polygenetically regulated. Bone phenotype results from the interplay between lifestyle and genes, and several nutritional factors modulate bone health throughout life. Thus, nutrigenetics examining the genetic variation in nutrient intake and homeostatic control is an important research area in the etiology of osteoporosis. Despite continuing progress in the search for candidate genes for osteoporosis, the results thus far have been inconclusive. The main objective of this thesis was to investigate the associations of lactase, vitamin D receptor (VDR), calcium sensing receptor (CaSR) and parathyroid hormone (PTH) gene polymorphisms and lifestyle factors and their interactions with bone health in Finns at varying stages of the skeletal life span. Markers of calcium homeostasis and bone remodelling were measured from blood and urine samples. Bone strength was measured at peripheral and central bone sites. Lifestyle factors were assessed with questionnaires and interviews. Genetic lactase non-persistence (the C/C-13910 genotype) was associated with lower consumption of milk from childhood, predisposing females in particular to inadequate calcium intake. Consumption of low-lactose milk and milk products was shown to decrease the risk for inadequate calcium intake. In young adulthood, bone loss was more common in males than in females. Males with the lactase C/C-13910 genotype may be more susceptible to bone loss than males with the other lactase genotypes, although calcium intake predicts changes in bone mass more than the lactase genotype. The BsmI and FokI polymorphisms of the VDR gene were associated with bone mass in growing adolescents, but the associations weakened with age. In young adults, the A986S polymorphism of the calcium sensing receptor gene was associated with serum ionized calcium concentrations, and the BstBI polymorphism of the parathyroid gene was related to bone strength. The FokI polymorphism and sodium intake showed an interaction effect on urinary calcium excretion. A novel gene-gene interaction between the VDR FokI and PTH BstBI gene polymorphisms was found in the regulation of PTH secretion and urinary calcium excretion. Further research should be carried out with more number of Finns at varying stages of the skeletal life span and more detailed measurements of bone strength. Research should concern mechanisms by which genetic variants affect calcium homeostasis and bone strength, and the role of diet-gene and gene-gene interactions in the pathogenesis of osteoporosis.