Disease as drama dramatistic constructs and models of redemption in covering illness in Glamour magazine /Pesheva, Ekaterina D., January 2005 (has links)
Thesis (M.A.)--University of Missouri-Columbia, 2005. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file viewed on (December 18, 2006) Vita. Includes bibliographical references.
A cross sectional empirical study of illness conceptualization among lay and professional populationsSiverhus, Scott William. January 1982 (has links)
Thesis (M.S.)--University of Wisconsin--Madison, 1982. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 57-62).
The proximate cause of disease, by induction from the laws of animated nature with an examination of the theories of Townsend, Reich, Darwin, Rush and Wilson /Mace, John. January 3702 (has links)
Thesis (M.D.) -- University of Pennsylvania, 1802. / Microform version available in the Readex Early American Imprints series.
Assessment of the quality of the acute flaccid paralysis (AFP) reporting system, Mpumalanga, South AfricaHarris, Bernice Nerine. January 2003 (has links)
Thesis (MMed. (Faculty of Medicine))--University of Pretoria, 2003. / Summary in Afrikaans and English.
Ontology based personalized modeling for chronic disease risk evaluation and knowledge discovery an integrated approach : a thesis submitted to Auckland University of Technology in fulfilment of the requirements for [the] degree of Doctor of Philosophy (PhD), 2009 /Verma, Anju. January 2009 (has links)
Thesis (PhD) -- AUT University, 2009. / Includes bibliographical references. Also held in print (270 leaves : ill. ; 30 cm.) in the Archive at the City Campus (T 616.0440112 VER)
Thesis (M.D.)--University of Hong Kong, 1992.
Thesis (M.D.)--University of Hong Kong, 1992. / Also available in print.
Liu, Xiao Song.
(has links) (PDF)
Thesis (Ph.D.) - University of Queensland, 2001. / Includes bibliography.
A computational framework for modeling the spread of pathogens and generating effective containment strategies in weakly connected island modelsShaw, Lucas Ray January 2007 (has links)
Thesis (M.S.)--University of Wyoming, 2007. / Title from PDF title page (viewed on June 10, 2009). Includes bibliographical references (p. 97-102).
LAFRANCONI, WALTER MARK.
To study the pulmonary responses to toxic insult, the biochemical and physiological effects of a known pulmonary toxicant (monocrotaline) were investigated. Monocrotaline is a pyrrolizidine alkaloid obtained from the seeds of Crotalaria spectabilis. When this alkaloid is administered to rats in their drinking water (20 mg/1) for 3 weeks, the lung is damaged, resulting in pulmonary hypertension, inhibition of serotonin transport by the pulmonary endothelium, and right heart hypertrophy. Preceeding the hypertrophy is a doubling of the mass of the lung and right ventricle. The change in mass of the lung preceeds that of the right ventricle. The increases in both organs is characterized by elevated RNA but not DNA. The lung mass increase is not accompanied by changes in collagenous proteins but is accompanied by an 86% increase in total lipids. The right ventricle however, responds to monocrotaline with a 400% increase in collagen protein and no change in lipid content, thereby indicating the lung and right ventricle respond differently to monocrotaline. Time course experiments established that the earliest observable event in monocrotaline induced lung damage is pulmonary edema which develops by day 5 and is resolved by day 10. Monocrotaline metabolites generated by an isolated liver and perfused through an isolated lung do not cause pulmonary edema even at concentrations of monocrotaline metabolites near 1 mM. These metabolites do however, alter the pulmonary endothelial transport of serotonin while other endothelial functions such as norepinephrine transport, angiotensin convertining enzyme and 5'-nucleotidase activities are unchanged. The effect of monocrotaline metabolites on pulmonary endothelial cell transport of serotonin is attenuated when the isolated livers are perfused under conditions which inhibit the formation of metabolites. Therefore, one of the pulmonary effects of monocrotaline that takes weeks to develop in vivo, inhibition of pulmonary endothelial transport of serotonin, can be observed under in vitro conditions. These results also directly demonstrate that the pulmonary damage caused by monocrotaline is a result of hepatic metabolism of monocrotaline to a pneumotoxic form.
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