This project is about the mechanisms associated with amyloid induced cytotoxicity. Amyloidoses consist of several diseases where normal or mutated protein precipitates into amyloid fibrils. Dysfunction of organs and toxicity to nervous tissue is triggered by the deposition of fibrils. Presently 24
The development of diabetes mellitus depends on the balance between beta-cell proliferation and death. As mitogen-activated protein kinases (MAPK) may control this balance, the aim of this study was to investigate the events leading to MAPK activation in beta-cells and the consequences of these events.
Apoptosis or programmed cell death is crucial for the resolution of inflammation, and phagocytosis of apoptotic cells initiates the release of actively anti-inflammatory responses from the phagocytes. Eosinophils are one of the most potent inflammatory cells in the body and is involved in a number of diseases, most commonly associated with parasitic infections and allergic diseases.
The aim of this thesis (Apoptosis Regulation via the Mitochondrial Pathway: Membrane Response upon Apoptotic Stimuli) was the investigation of the mitochondrial response mechanisms upon apoptotic stimuli. The specific objectives were the biophysical characterization of membrane dynamics and the specific roles of
Apoptosis, or programmed cell death, is a controlled process by which aged or damages cells are eliminated in multicellular organisms. Neutrophils, short-lived phagocytes of the innate immune system, are highly equipped effectors that can sense, locate, ingest and kill bacterial pathogens. Inflammatory
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