Bibliography: leaves 180-199. / xvii, 199, [68] leaves, [1] leaf of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Primary aim was to determine whether levels of the endogenous peptide substance P (SP) would parallel and reflect the reported increased levels of the trophic agent nerve growth factor which is associated with the development of sympathetic hyperinnervation (and ultimately hypertension) in the genetic animal model for hypertension, the spontaneously hypertensive rat. / Thesis (Ph.D.)--University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 1995

Photosynthetic organisms exhibit a variety of responses to changes in light intensity, including differential biosynthesis of chlorophyll-protein complexes. Cultures of Rhodobacter capsulatus grown anaerobically with a low intensity of light (2 W/m²) contained about four times as much B800-850 light harvesting complex as cells grown under high light intensity (140 W/m²). The mRNA transcripts encoding B800-850 beta and alpha peptides were analyzed by Northern blot, S1 nuclease protection and capping with guanylyl transferase. It was found that the steady-state levels of B800-850 mRNAs in high light-grown cultures was about four times as great as in cells grown under low light intensity. Therefore the lesser amounts of mature B800-850 peptide gene products found in cells grown with high light intensity were the result of a posttranscriptional regulatory process. It was also found that there were two polycistronic messages encoding the B800-850 peptides. These messages shared a common 3' terminus but differed in their 5' end segments as a result of transcription initiation at two discrete sites. Moreover the half life of B800-850 mRNAs was about 10 minutes in cells grown with high light and approximately 19 minutes in low light-grown cultures. Transcriptional and translational fusions were constructed between the B800-850 transcription initiation region (from this point on referred to as the puc transcription initiation region; see Fig. 1) and the Escherichia coli lacZ gene. From these studies it was concluded that the rates of transcription initiation of the puc (B800-850) genes was higher in cells grown with high light illumination than in low light-grown cultures, and that the relative amount of B800-850 complexes under these conditions was controlled by a translational or a posttranslational mechanism. The translational and transcriptional fusions were also used for examination of oxygen regulated expression of the puc genes. / Science, Faculty of / Microbiology and Immunology, Department of / Graduate

by Chi Fung Yeung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 83-120). / Abstracts in English and Chinese. / abstract --- p.1 / table of contents --- p.3 / acknowledgments --- p.8 / declaration --- p.9 / list of figures and tables --- p.10 / list of abbreviations --- p.13 / Chapter chapter 1- --- general introduction --- p.15 / Chapter 1.1 --- VASOACTIVE PEPTIDES --- p.18 / Chapter 1.1.1 --- HISTORICAL BACKGROUND --- p.18 / Chapter 1.1.1.1 --- Adrenomedullin --- p.20 / Chapter 1.1.1.2 --- Calcitonin gene-related peptide --- p.21 / Chapter 1.1.1.3 --- Endothelin-3 --- p.22 / Chapter 1.1.2 --- "SYNTHESIS AND RELEASE OF ADRENOMEDULLIN, CALCITONIN GENE RELATED PEPTIDE AND ENDOTHELINS" / Chapter 1.1.2.1 --- SYNTHESIS AND RELEASE OF Adrenomeduulin --- p.24 / Chapter 1.1.2.2 --- SYNTHESIS AND RELEASE OF calcitonin gene related peptide --- p.25 / Chapter 1.1.2.3 --- SYNTHESIS AND RELEASE OF ENDOTHELINS --- p.25 / Chapter 1.1.3 --- "ADRENOMEDULLIN, CALCITONIN GENE RELATED PEPTIDE AND ENDOTHELINS IN THE CNS" --- p.26 / Chapter 1.1.4 --- "RECEPTORS OF ADRENOMEDULLIN, CALCITONIN GENE RELATED PEPTIDE AND ENDOTHELINS AND SIGNAL TRANSDUCTION" --- p.27 / Chapter 1.1.5 --- "BIOLOGICAL ACTIONS OF ADRENOMEDULLIN, CALCITONIN GENE RELATED PEPTIDE AND ENDOTHELINS" / Chapter 1.1.5.1 --- BIOLOGICAL ACTIONS OF ADRENOMEDULLIN --- p.30 / Chapter 1.1.5.1.1 --- haemodynamic effects of adrenomedullin --- p.30 / Chapter 1.1.5.1.2 --- Renal effects of Adrenomedullin --- p.31 / Chapter 1.1.5.1.3 --- Endocrine effects of Adrenomedullin --- p.31 / Chapter 1.1.5.1.4 --- Central effects of Adrenomedullin --- p.32 / Chapter 1.1.5.2 --- CALCITONIN GENE RELATED PEPTIDE / Chapter 1.1.5.2.1 --- haemodynamic effects of calcitonin gene related peptide --- p.33 / Chapter 1.1.5.2.2 --- Renal effects of calcitonin gene related peptide --- p.34 / Chapter 1.1.5.2.3 --- Endocrine effects of calcitonin gene related peptide --- p.34 / Chapter 1.1.5.2.4 --- Central effects of calcitonin gene related peptide --- p.35 / Chapter 1.1.5.3 --- ENDOTHELINS / Chapter 1.1.5.3.1 --- haemodyamic effects of endothelins --- p.36 / Chapter 1.1.5.3.2 --- Renal effects of Endothelins --- p.36 / Chapter 1.1.5.3.3 --- endocrine effects of endothelins --- p.37 / Chapter 1.1.5.3.4 --- Central effects of Endothelins --- p.37 / Chapter 1.1.6. --- PROLIFERATIVE OR ANTI-PROLIFERATIVE EFFECTS --- p.38 / Chapter 1.1.7 --- CLINICAL RELEVANCE OF VASOACTIVE PEPTIDES / Chapter 1.1.7.1 --- Clinical relevance of Adrenomedullin --- p.39 / Chapter 1.1.7.2 --- Clinical relevance of calcitonin gene related peptide --- p.40 / Chapter 1.1.7.3 --- Clinical relevance of Endothelins --- p.41 / Chapter 1.2 --- ASTROCYTES / Chapter 1.2.1 --- Historical background and astrocyte morphology --- p.42 / Chapter 1.2.2 --- Physiological roles of astrocytes --- p.44 / Chapter 1.2.3 --- Pathology of astrocytes --- p.45 / Chapter 1.3 --- NEUROPEPTIDE RECEPTORS AND ASTROCYTES / Chapter 1.3.1 --- Neuropeptide receptors on astrocytes --- p.47 / Chapter 1.3.2 --- Consequences of receptor activation --- p.49 / Chapter 1.4 --- AIMS OF THE THESIS --- p.50 / Chapter CHAPTER 2 --- "GENERAL MATERIALS AND METHODS, AND DATA ANALYSIS" / Chapter 2.1 --- MATERIALS / Chapter 2.1.1 --- ANIMALS --- p.54 / Chapter 2.1.2 --- PEPTIDE HORMONES --- p.54 / Chapter 2.1.3 --- ISOTOPES AND RADIOIMMUNOASSAY KITS --- p.54 / Chapter 2.1.4 --- CULTURE MATERIALS AND CHEMICALS --- p.55 / Chapter 2.1.5 --- PREPARATION OF MATERIALS / Chapter 2.1.5.1 --- Preparation of primary cultures of astrocytes --- p.55 / Chapter 2.1.5.2 --- Preparation of medium and binding buffer --- p.56 / Chapter 2.1.5.3 --- Preparation of 125I-labelled vasoactive peptides --- p.56 / Chapter 2.1.6 --- MEASUREMENT OF CELLULAR CYCLIC AMP --- p.57 / Chapter 2.1.7 --- DETERMINATION OF PROTEIN CONTENT OF CULTURED ASTROCYTES --- p.60 / Chapter 2.2 --- METHODS --- p.61 / Chapter 2.2.1 --- LIGAND BINDING: MEASUREMENT OF 125I-AM AND 125I-CGRP BINDING / Chapter 2.2.1.1 --- Binding kinetics --- p.61 / Chapter 2.2.1.2 --- Determination of specific binding of 125I-AM and 125I-CGRP --- p.61 / Chapter 2.2.1.3 --- Competition binding studies --- p.62 / Chapter 2.2.2 --- "BIOCHEMICAL INTERACTIONS BETWEEN ET3, AM, CGRP AND PKC-ANALOG" / Chapter 2.2.2.1 --- Determination of the production of cAMP in response to AM and CGRP --- p.62 / Chapter 2.2.2.2 --- Determination of the effect of PMA on AM and CGRP-dependent CAMP production --- p.63 / Chapter 2.2.2.3 --- Determination of the effect of the phorbol esters on AM and CGRP-dependent cAMP production --- p.63 / Chapter 2.2.2.4 --- Elucidation of antagonistic effect of staurosporine and Ro31-8220 --- p.64 / Chapter 2.2.2.5 --- Determination of the effects of ET-3 on AM and CGRP- dependent CAMP accumulation --- p.64 / Chapter 2.2.2.6 --- Determination of the effects of PKC inhIBition on ET-3 suppression of AM- and CGRP-induced CAMP responses --- p.64 / Chapter 2.2.2.7 --- Elucidation of antagonistic effect of cycloheximide --- p.65 / Chapter 2.3 --- STATISTIC ANALYSIS --- p.65 / Chapter CHAPTER 3 --- RESULTS / Chapter 3.1 --- BINDING KINETICS OF 125I-AM AND 125I-CGRP --- p.68 / Chapter 3.2 --- SPECIFIC BINDING OF 125I-AM AND 125I-CGRP --- p.68 / Chapter 3.3 --- COMPETITION BINDING --- p.68 / Chapter 3.4 --- DOSE RESPONSE OF ADRENOMEDULLIN AND CGRP- STIMULATED CAMP PRODUCTION --- p.69 / Chapter 3.5 --- EFFECTS OF PHORBOL ESTERS ON AM AND CGRP DEPENDENT CAMP ACCUMULATION --- p.69 / Chapter 3.6 --- EFFECT OF PMA ON AM AND CGRP-DEPENDENT CAMP ACCUMULATION --- p.70 / Chapter 3.7 --- EFFECT OF ET-3 ON AM AND CGRP-DEPENDENT CAMP ACCUMULATION --- p.70 / Chapter 3.8 --- "THE EFFECTS OF STAUROSPORINE, RO 31-8220" --- p.71 / Chapter 3.9 --- EFFECT OF CYCLOHEXIMIDE ON THE SUPPRESSIVE ACTION OF ET3 --- p.72 / Chapter CHAPTER 4 --- DISCUSSION --- p.73 / Chapter CHAPTER 5 --- GENERAL CONCLUSION --- p.80 / REFERENCES --- p.83 / APPENDIX-PUBLISHED PAPER