Addendum attached to back facing leaves. / Includes bibliographical references (leaves 172-199). / 199 leaves, 5 photographic plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / The findings establish leukemia inhibitory factor, and possibly oncostatin M, as new members of a small but growing class of cytokines produced in an intracellularly active form and also suggest that the production of alternate transcripts and intercellularly-retained proteins may be a common and important feature of cytokines of the IL-6 and other families. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 2000

Diss. (sammanfattning) Uppsala : Univ., 2001. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Regional pulmonary blood flow and volume was measured in ten rabbits anesthetized with pentobarbital (30 mg/kg). Tracheostomy was performed and catheters were placed into the jugular vein and carotid artery. The cardiac ⁹⁹mtc output was measured using the indicator-dilution technique using Tc labelled RBC followed by an injection of radiolabelled macroaggregates (MAA) to mark regional blood flow. Measurements were made both before and after either exposure to cigarette smoke (3 cigarettes for ten minutes at 4 puffs/minute) or sham exposure to air. The animals were sacrificed and the lungs were removed with the vessels tied. The lungs were then inflated and rapidly frozen over liquid nitrogen. The lungs were sampled into slices by vertical height, each slice was further sampled and then gamma counted for the injected isotopes. Regional pulmonary blood flow was calculated by setting the total lung MAA counts for each MAA equal to the cardiac output so that the sample flow was calculated as the fraction of sample counts to total counts times the cardiac output. The blood volume was marked by the labelled RBC and RBC transit was calculated as blood volume (ml) divided by blood flow (ml/sec). In a second series of experiments (N=10) , ⁵¹Cr PMN were injected as a bolus along with ⁹⁹mtc RBC in an indicator-dilution run. Following the injection of the cells, the blood flow was marked with MAAs and then the same sham or smoke treatments were given as in the previous experiments. At the end of ten minutes, the animals were sacrificed and the lungs were processed the same as before. Regional PMN retention was calculated as the [formula omitted]. The data show that smoke exposure increased pulmonary blood volume (p<.01), pulmonary transit time (p<C.05) and the ratio of lung blood volume to central blood volume (p <C-05) without changing central blood volume or cardiac output. Smoke exposure also caused a redistribution of blood flow from upper to lower lung regions (p <C-05). This lengthened the regional RBC transit times in all regions but particularly in the upper zones. These changes in RBC transit had no effect on PMN retention. We conclude that acute smoke exposure lengthens the RBC transit through the pulmonary circulation by increasing blood volume and redistributing blood flow. This change in red cell behavior was not associated with a consistent change in PMN retention in the lungs. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

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The objective of this thesis was to delineate aspects of the control mechanisms of mammalian pepsinogen secretion. In order to accomplish this goal, a comprehensive study was undertaken which would establish an historical perspective of the subject, validate appropriate methodology and then seek to answer specific questions regarding the physiology and pathophysiology of pepsinogen secretion. More specifically, the objectives of this thesis were: 1. To review the historical background of the subject of pepsinogen in the context of the physiology of digestion with specific emphasis on the work and lives of the two major initial proponents of pepsinogen research (Schwann and Langley). 2. To provide a contemporary overview and evaluation of the current status of pepsinogen pathophysiology. 3. To modify and adapt experimental models necessary for the study of pepsinogen and acid secretion in mammalian gastric mucosa and cells. 4. To establish and validate a pepsinogen assay sensitive and reproducible enough for use in mammalian mucosa! and cellular secretory systems. 5. To delineate the fundamental (second messenger) control mechanisms (cyclic AMP and calcium calmodulin) of pepsinogen secretion in the isolated gastric gland model. 6. To define whether the process of pepsinogen secretion is independent of acid secretion in intact mucosa! preparations. 7. To identify different classes of pharmacological agents which would inhibit pepsinogen secretion and/or release. 8. To identify whether conditions present in critically ill patients liable to mucosal "stress ulceration" might influence the release of pepsinogen.

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1) Test the accuracy of the Welch Allyn Microtympanometer against standard tympanometry. 2) Correlate preoperative clinical findings with: • Microtympanometry • Standard tympanometry 3) Assess influence of induction by gas anaesthesia on: • Post-induction microtympanometry • Intraoperative myringotomy findings 4) Assess the practicality of using the Welch Allyn Microtympanometer as a screening tool in Pre-School audiological testing.

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