<p> In the practice of resource management conservation, it is common to introduce new members into small inbred populations in order to increase genetic diversity and reduce the negative effects of inbreeding. Although fitness often increases in the F1 generation immediately following intrapopulation hybridization, few studies have focused on the long-term fitness of such populations. The model organisms <i>Drosophila melanogaster</i> and <i> D. simulans</i> were used to investigate if heterosis, an increase in the fitness in the hybrid population, or outbreeding depression, a decline in the fitness in the hybrid population, occurs over an eight generation period. At each generation, a series of fitness related assays were performed to assess relative fitness. Results of this study were mixed. At best, only some hybridized populations showed slightly higher, but often nonsignificant increases in fitness, never in more than one assay. The lack of consistent strong persistent heterosis suggests that conservation efforts such as habitat preservation maybe be a better use of effort and money for assisting endangered species. </p>

<p> Identity and intensity of parasitism have been shown to be correlated to the host genotype at the major histocompatibility complex (MHC), a genomic region involved in the adaptive immune response. However, the evolutionary mechanisms by which parasites exert a selective force on host immune systems are unknown. This thesis investigates the relationship between parasitism and MHC genotype in two bear populations in Southcentral Alaska. We diagnosed infection using the polymerase chain reaction (PCR), targeting the ribosomal subunit of 18S of common blood parasites. Parasitism was detected in half of brown bears and 75% of black bears. We detected <i>Eimeria</i> spp. and several species of apicomplexan and nematode parasites, and we report here the first finding of <i>Trypanosoma cruzi</i> in Alaskan bears. We found no association between MHC genotype and identity or intensity of infection, suggesting that other loci or even non-genetic factors are important covariates in predicting infection status.</p>