In the last few decades, parasitic infections have created a major human health problem across the world. In developing countries the problem is beyond control and the number of new cases is on a continuous rise. Leishmaniasis is a tropical disease affecting large number of population. Development of an effective and inexpensive vaccine represents a practical way to control this disease, as available chemotherapy is always accompanied by sever side effects. The major surface glycoproteins of the Leishmania parasites, gp63 and HASP-B1 have been postulated to be good candidates for vaccine development. In this study Leishmania parasite gp63 and HASP-B1 antigens were screened for potential immunogenic CTL epitopes (peptides) in HLA-A2 (HHD) transgenic mice. Three peptides given the code names of C1, C2 and B8 derived from gp63 were tested in HHDII mice for their immunogenicity. Two peptides (C2 and B8) were shown to be highly immunogenic following one in vivo immunization however, 2 immunizations were needed to improve the immunogenicity of the C1 peptide. These results were also confirmed by INF-γ and IL-4 profiles in cultured spenocytes. In contrast to IL-4, the amount of INF-γ in splenocytes cultured with relevant immunogenic peptides was significantly higher than those in controls.  

Alzheimer's disease (AD) is a uniquely human disorder. Although the pathogenesis of AD is not fully understood, growing evidence indicates that the deposition of beta-amyloid (Aβ) and the local reactions of various cell types to this protein play major roles in the development of the disease. In the present study transgenic mice expressing mutant amyloid precursor protein (APP) has been used. These mice exhibit selective neuronal death in the brain regions that are most affected in AD, suggesting that amyloid plaque formation is directly involved in AD neurons loss. Brains from 12 transgenic animals and 12 age-matched non transgenic littermate controls (1 and 2 years old) were examined histopathologically. One year old transgenic animals (n=6) exhibit deposits of human Aâ in the hippocampus, corpus callosum and cerebral cortex. By 2 years of age, a great number of diffuse and mature plaques were present in the cortex and hippocampus, and subcortical regions like thalamus and striatum. Another major finding was reduction of cholinergic cells in the medial septum, striatum and diagonal band of Broca. The present data are consistent with the hypothesis that the neuropathology begins in the cerebral cortex and hippocampus before spreading in a retrograde fashion to subcortical regions.