Thesis (Ph. D.)--Freie Universität Berlin, 1989. / Includes bibliographical references (p. 231-262).

Thesis (Ph. D.)--Illinois State University, 1990. / Title from title page screen, viewed December 2, 2005. Dissertation Committee: H. Tak Cheung (chair), Herman Brockman, Harry Huizinga, Anthony Otsuka, Brian Wilkinson. Includes bibliographical references (leaves 116-127) and abstract. Also available in print.

Originally presented as the author's thesis, Hamburg, 1967.

No description available.

by Ming-chiu Fung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1980. / Includes bibliographies.

L'objectif de ce travail était l'identification de nouveaux facteurs influençant la capacité des protéines à s'agréger ou ayant un i mpact sur l'agrégation d'autres protéines. Nous avons étudié l'influence des ligands anti-amyloïdes, interactions protéine-protéine et la glycation sur l'agrégation des protéine prion. La protéine prion a activée l'agrégation amyloïde d ans d'autres protéines habituellement stables. La glycation de la protéine prion entraîne une diminution de son amyloïdogénicité. En même temps, cette modification facilite légèrement l'agrégation amorphe de la protéine prion. Dans ce cas, l'effet antiagrégant total de la curcumine et de l'acide 3,4-diméthoxycinnamique a été affaibli, car a près la modification, l'agrégation s'est faite d avantage par la moyen non spécifique. L a présence de bêta-caséine avec une activité semblable à celle du chaperon supprime significative tout type d'agrégation des protéines prions, et combinaison de bêta-caséine et de ligands anti-amyloïdes est une méthode efficace d e suppression complète de l'amylose de la protéine prion. La bêta-caséine glyquée a montré s a capacité à s'agréger par elle-même et à f ormer des agrégats ordonnés fluorescent spécifiques avec un colorant thioflavine T. La présence de protéine prion a grandement facilité l a formation de ces agrégats, au contraire les ligands anti-amyloïdes l'ont supprimé. L'interaction de la protéine prion glyquée et de la b êta-caséine conduit à la formation des agrégats sphériques, que sont enrichis en structures a myloïdes pendant le traitement thermique. Dans ce cas, l’effet antiamyloïde de la curcumine et de l’acide 3,4-diméthoxycinamique disparaît presque complètement. / The main aim of this work was a search of new factors influencing the ability of proteins for aggregation themselves or impact the a ggregation of other proteins. We investigated the i nfluence of anti-amyloid ligands, protein-protein i nteractions and glycation on prion protein a ggregation. The prion protein activated amyloid a ggregation in other usually stable proteins. The glycation of the prion protein causes a decrease in its amyloidogenicity. At the same time, this m odification slightly facilitates the amorphous a ggregation of the prion protein. Also, the total a nti-aggregating effect of curcumin and 3,4- dimethoxycinnamic acid in this case was weakened, since after the modification the a ggregation was done more by non-specific m eans. T he presence of beta-casein with chaperone-like a ctivity significantly suppresses all types of prion protein aggregation, and a combination of beta- casein and anti-amyloid ligands was decided to b e an effective method of total prion protein a myloidosis suppression. The glycated beta- casein showed its ability to aggregate by itself and to form specific fluorescent ordered a ggregates with a thioflavin T dye. The presence of prion protein greatly facilitated the formation of t hese aggregates, unlike the anti-ligands, which i nhibits it. The interaction of glycated prion protein and beta-casein leads to the formation of s pherical aggregates, which are being enriched b y amyloid structures during heat treatment. In this case, the antiamyloid effect of curcumin and 3,4-dimethoxycinamic acid disappears almost completely.

T cells are one of the key cells in the immune system. Although they are not the first line of defense against a pathogen, their functions can greatly enhance the phagocytosis and destruction of pathogens as well as the development of antibody responses. Furthermore, even when responding T cells have facilitated the clearance of the pathogen, they can avoid death to become long-lived cells that "remember" encountering the pathogen for years afterward. This long-term memory allows subsequent immune responses to improve with each exposure, ultimately preventing disease upon reinfection. The activation of these T cells depends on specific recognition of antigen along with a costimulatory signal. This activation process is well studied, but not completely understood. Additionally, the mechanism behind memory T cell development is still very much unknown. In the work presented in this thesis, delivery of costimulatory signals via CD4O and 0X40 were studied using an in vivo superantigen (SAg) model of T cell stimulation. In the context of this two-signal (SAg + costimulation) model, both CD4O and OX40 could deliver signals that enhanced SAg-reactive T cell clonal expansion, but they could only partially prevent T cell death. Coadministration of the inflammatory agent lipopolysaccharide (LPS), however, could keep increased responder T cell populations alive for at least two months. Interestingly, this three-signal (SAg + costimulation + LPS) induced survival was not dependent on proinflammatory cytokines or activation of the transcription factor NF-KB, but was sensitive to the immunosuppressant cyclosporin A (CsA). The mode of action of CsA may point to the mechanism driving long-term T cell survival. Additionally, examination of early time points after three-signal stimulation suggested more clues to the mechanism of survival induction. The cytokines IL-2 and TNF-�� seem to be involved early on, but for now, little is known about their complete role. Thus, the goal of this work was to investigate the costimulatory and adjuvant-mediated signals required for memory T cell development. Ultimately, an understanding of how memory T cells can be generated could be used to enhance vaccine efficacy or shut off autoimmune conditions. / Graduation date: 2002

Personality of stutterers

Thèse d'exercice : Médecine vétérinaire : Toulouse 3 : 2008. / Titre provenant de l'écran titre. Bibliogr. p. 81-87.

Inaug.-diss.--Munich. / Lebenslauf. "Literaturverzeichnis"; p. 85-87.