Graduation date: 1961

Statement of purpose: The scope of this dissertation was restricted to exemplary studies on the effects of spectrum, intensity and modulation (as described above) of the photic environment of the common reef coral Pocillopora damicornis and its symbiotic dinoflagellate algae. Various aspects of its biology were investigated. In some cases direct comparison was wade with othar species to emphasize similarities or differences. The central hypothesis of this dissertation can be stated as follows: Subtle changes in the spectrum, intensity and modulation of the natural photic environment can produce a profound effect on growth, reproduction, primary production and general metabolism of the reef corals. / Typescript. Thesis (Ph.D.)--University of Hawaii, 1985. Bibliography: leaves 201-221.

Goals of this investigation were: 1) Differentiate between the effects of turbidity and sedimentation on corals. 2) Differentiate the effects of carbonate and terrigenous sediments on coral growth and metabolism. 3) Develop a predictive model relating increased sediment loading to the photosynthetic rate, growth and survival of corals. 4) Evaluate the validity of the widely cited "10 mg cut-off point" and determine the levels of turbidity and sedimentation that are tolerated by corals. Earlier studies suggest that coral reefs decline when sediment loading levels exceed a sediment trapping rate of 10 mg cm-2 d-1 or a turbidity of 10 mg I-1. An integrated experimental design linked field and laboratory experiments. In the field, corals were transplanted to sites with varying levels of sedimentation. Turbidity, as linked to reduced light availability, had a significant affect on coral growth and metabolism in laboratory experiments but not coral growth or survival in field experiments. Turbidity in the field was highly variable and influenced greatly by wind velocity and rainfall. Terrigenous (or land-derived) sediments influenced light extinction more than carbonate (reef-derived) sediments. In laboratory experiments turbidity was more important than sediment trapping rate in affecting the photosynthetic ability and growth rates of corals. The predictive model stated that the lower the light level (as caused by increased turbidity) the lower the photosynthetic production of corals. The model was supported by results of laboratory experiments where conditions were precisely controlled and monitored. Under field conditions, the predictive model did not hold due to extreme natural variability in sediment loading and variation in a wide range of other environmental factors encountered at the experimental sites. Corals tolerated turbidity exceeding 120 mg I-1 and sediment trapping rates in excess of 11 mg cm2 d-1. Sediment loading is correlated with other environmental factors such as nutrient loading and reduced salinity. Composition of sediment varies widely between different locations. The "10 mg cutoff may prove to be useful in setting limits to vigorous coral reef development, although individual corals or coral assemblages may be able to survive and grow at levels exceeding this value. / Thesis (Ph. D.)--University of Hawaii at Manoa, 2001. Includes bibliographical references (leaves 235-264).

The primary goal of my studies was to elucidate the mechanisms for the well-recognized interaction between two nutrients, vitamins E and K. The outcomes from my studies assess mechanisms for adverse effects of vitamin E and provide novel information on mechanisms for vitamin K homeostasis. These findings will provide information relevant for assessing optimal intakes of vitamins E and K. This dissertation presents studies aimed at evaluating three different mechanisms by which vitamin K status could be decreased by increases in whole body vitamin E concentrations in rats supplemented with vitamin E by subcutaneous injections (100 mg α-tocopherol (α-T)/ kg body weight per day), the model system developed in the Traber lab. The tested mechanisms by which vitamin E leads to reduced vitamin K status were: 1) increasing vitamin K metabolism, 2) decreasing menaquinone-4 (MK-4) synthesis from dietary phylloquinone (PK) and 3) potentiating vitamin K excretion through xenobiotic pathways. Two approaches were undertaken to evaluate the hypothesis that vitamin E increases vitamin K metabolism. In Aim 1.1, the in vitro omega-hydroxylation of vitamin K by human cytochrome P450 CYP4F2 (expressed in insect microsomes) was tested because CYP4F2 is considered the limiting step in the catabolism of both vitamins. Chapter 2 shows that CYP4F2 more rapidly hydroxylated vitamin K compared with vitamin E. Moreover, vitamin E did not stimulate vitamin K metabolism in vitro. Thus, it is unlikely vitamin E stimulates vitamin K metabolism in vivo by direct interaction with the CYP4F2 enzyme-substrate complex. In Aim 1.2, the in vivo urinary and biliary excretion of vitamin K metabolites was investigated. Chapter 3 shows that α-T-injected rats significantly increased urinary excretion of vitamin E catabolites, but no increases in urinary vitamin K catabolites were found. Chapter 4 shows that α-T-injected rats increased biliary excretion of 5C-aglycone, a major vitamin K catabolite shared by MK-4 and PK. However, the overall in vivo excretion of vitamin K catabolites was not changed when urinary excretion was also taken into account. Aim 2 evaluated the hypothesis that α-T interferes with the conversion of PK to MK-4 because α-T and PK have similar side-chains. In Aim 2.1, conversion of PK or MN to MK-4 was tested in vivo. Rats were fed semi-purified diets containing equimolar concentrations of either PK or MN for 10 days, then α-T injections were undertaken. Chapter 3 shows that extra-hepatic tissues from α-T injected rats contained significantly lower MK-4 concentrations irrespective of whether the rats were fed PK or MN. These findings show that if vitamin E is interfering with the metabolic mechanism of MK-4 synthesis, then it is not specific to the cleavage of PK's side chain. In Aim 2.2, conversion of deuterium-labeled PK (d₄-PK) to d₄-MK-4 was used to evaluate the extra-hepatic tissue uptake of d₄-PK in α-T-injected rats. Rats were fed semi-purified diets containing equimolar concentrations of d₄-PK similar to my previous study for 10 days then α-T injections were undertaken for 7 days. Chapter 5 shows that total (labeled and unlabeled) vitamin K concentrations decreased in extra-hepatic tissues from α-T injected rats fed d₄-PK. Both d₄-MK-4 and d₄-PK concentrations decreased, suggesting that MK-4 concentrations were dependent upon those of d₄-PK. These findings suggest that PK, and not MN, is the primary substrate for MK-4 synthesis in extra-hepatic tissues. Moreover, both d₄-MK-4 and d₄-PK decreased in α-T-injected rats demonstrating that vitamin E's untoward effect on vitamin K status is likely a mechanism that is shared by both vitamin K forms and not specific to MK-4 synthesis. Recycling of vitamin K from the epoxide was not examined in this study and interference with the recycling mechanism for either PK or MK-4 in α-T injected rats has not been examined. Vitamin E metabolism is greatly increased in α-T-injected rats by increasing various xenobiotic pathways. Thus, vitamin K status was hypothesized to decrease in α-T-injected rats as a result of the up-regulation of these pathways. As shown in Aim 1, urinary vitamin K metabolite excretion was not increased in α-T-injected rats. In Aim 3.1, the biliary excretion of vitamins E and K were examined to evaluate whether the increased expression in biliary transporters, such as MDR1, led to increased vitamin K and E excretion via the bile. Chapter 4 shows that α-T increased in bile over the week of vitamin E injections and α-CEHC was the major vitamin E form excreted in bile. Although biliary PK secretion was unchanged and biliary MK-4 was undetectable, increased excretion of a major catabolite of both PK and MK-4, 5C-aglycone, was observed. In Aim, 3.2, the gene expression of enzymes and transporters in liver and extra-hepatic tissues as mechanisms involved in regulating their concentrations in these tissues was assessed. In Chapters 3 and 5, increased expression of biliary transporters were observed, one of which is known to bind the vitamin K intermediate MN as its substrate. It is possible other vitamin K catabolites, in addition to 5C-and 7C-aglycone, may have been excreted that were unaccounted for, e.g. MN or vitamin K epoxide metabolites. In summary, my studies have shown vitamin K status is decreased in α-T-injected rats because PK and MK-4 concentrations are decreased in many extra-hepatic tissues. Although metabolism of vitamin K was not stimulated in response to α-T injections, increased excretion of a vitamin K catabolite was measured in the bile; however it may not account for all of the vitamin K loss observed in tissues. Alternatively, transport of PK and MN to extra-hepatic tissues or MK-4 recycling may have been inhibited in response to vitamin E. Further studies are needed to distinguish between these mechanisms. / Graduation date: 2013

Graduation date: 1992

Passive and active heat loading causes cardiovascular strain, which can have diverse and substantial effects. Thus, cardiovascular function is integral to work and heat stress tolerance, but recent hyperthermia and exercise literature has not emphasised this relationship, instead focusing on the roles of upper �critical� core temperature or rate of heat storage as primary mechanisms of fatigue. Therefore, the aim of this thesis was to examine some potential causes and effects of cardiovascular strain under heat stress, including potential strategies for attenuating that strain. Body precooling before exercise increases heat storage capacity; the primary mechanism by which attenuations in thermal and cardiovascular strain, and improved work capacity is thought to occur. However, no precooling study has utilised realistic airflow in the laboratory, possibly inflating its purported benefits. Therefore, Study One examined the cardiovascular, thermal, psychophysical and ergogenic effects of precooling with and without airflow in the heat (30�C, 50% rh). Ten males completed four trials in balanced order, comprising 60- min immersion in thermoneutral (35�C) or cool (24�C) water before cycling at 95% ventilatory threshold with airflow (~4.8 m�s⁻�) or no airflow, until exhaustion. Heart rate and mean core, body, and skin temperatures were attenuated for 15 min into cycling after precooling. Endurance time was extended by 30 � 23 min with airflow, and 16 � 15 min with precooling relative to control (28 � 12 min) but not further extended with strategies combined (29 � 21 min). Precooling removed 784 � 223 kJ�m⁻� (calorimetrically); less than the effect of airflow alone (1323 � 1128 kJ�m⁻�). Competition for blood between tissues is pronounced during exercise in the heat: skin and gut have marked increases and decreases, respectively. Gut ischemia affects epithelial tight junction integrity, allowing lippopolysaccharide ingress and immune responses. Bovine colostrum may attenuate gut permeability. Study Two (double-blind, placebo controlled) investigated the effects of aerobic fitness (7 highly fit, 8 moderately fit) and bovine colostrum on physiological and perceived strain, and performance during mixed-mode exercise; cycle 15 min at 50% maximal heart rate range (HRR), run 30 min at 80% HRR then 30 min self-selected paced before another 15 min cycle at the same work-rate. Airflow was graded to running speed. During the last cycle, blood pressure, stroke volume and total peripheral resistance were lower, heart rate and skin blood flow increased, and skin temperature was unchanged compared to the first cycle. Indices of fever response (IL-1β, TNF-α) were not evident during exercise, nor were those of blood-brain barrier permeability (S100β) or cognitive impairment (Stroop test). Neither bovine colostrum, nor higher fitness modified these measures. Moving to upright posture is orthostatically stressful and can initially decrease cerebral perfusion. Compression garments are used to assist venous return; while their effectiveness is unknown, they could reduce heat or orthostatic-induced hypoperfusion. Study Three investigated the cardiovascular and cerebrovascular responses to orthostatic stress with and without passive heating (+0.5�C). Fifteen participants completed two trials (compression v placebo garments) in balanced order. Cerebral autoregulation was assessed via 3-min stand, and via thigh cuff inflation. All participants experienced initial orthostatic hypotension upon standing in one or more trials, with 4/15 individuals experiencing presyncopal symptoms, aborting the standing protocol. In those who "fainted", reductions in blood pressure and partial pressure of end-tidal CO₂ reduced middle cerebral artery velocity. Neither training status nor compression trousers modified the responses. Collectively, cardiovascular strain to heat stress is attenuated when realistic airflow is provided. Increased cardiovascular strain does not inevitably result in clinical outcomes to heat stress. Higher fitness does not necessarily attenuate cardiovascular responses or higher tolerance to heat stress.

Bibliography: leaves 132-159. / xv, 159 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Boron efficiency in oilseed rape (Brassica napua L. and B. juncea L.) was investigated in a wide range of genotypes. Using a solution culture screening of 10 day old seedlings, root length best described shoot growth response, and was used to characterise a total of 65 genotypes. Varieties and breeders lines tolerant of B-deficient growing conditions were identified, and the screening process validated through field trials. B responses in plants sampled at the 'green bud' stage indicated that vegetative growth is important in B efficiency. Studies were conducted to investigate the mechanism of B efficiency in oilseed rape. Results suggest no association between B efficiency and the capacity to acidify the root rhizosphere, or an increased translocation of B from root to shoot. Boron retranslocation was also studied as a mechanism of B efficiency. / Thesis (Ph.D.)--University of Adelaide, Dept. of Plant Science, 1999?

Addenda and corrigenda are tipped-in & numbered leaves 281-282. / Copies of author's previously published articles are inserted back end paper. / Bibliography: leaves 222-279. / xiv, 282 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Studies were performed in the Langendorff-perfused isolated rat heart, using a paradigm in which atrial distension was prevented. The release of natriuretic peptides and endothelin-1, along with cardiac function was monitored during periods of transient ischaemia or hypoxia. Additional studies were performed in patients undergoing cardiac catheterization. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999?

Bibliography: leaves 89-104. / vi, 104 leaves, [15] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / In this study an EMS-mutated Arabidopsis mutant pho2, which accumulates Pi in leaves, was used to study Pi uptake and transport by comparing it to wild-type seedlings. The study aimed to define the physiological lesions in pho2 mutant and to obtain evidence regarding the function of the PHO2 gene in P nutrition in higher plants. Accumulation of Pi in leaves of pho2 was found to reside in the symplast and was not related to Zn-deficiency. The physiology of the pho2 mutant is consistent with either a block in Pi transport in phloem from shoots to roots or an inability of shoot cells to regulate internal Pi concentration. Southern block analysis revealed that the two transporter genes, APT1 and APT2 were not responsible for the pho2 mutant. Data from the mapping of the PHO2 gene along with information from the Arabidopsis genome sequencing will form the basis for cloning the PHO2 gene in the future. / Thesis (Ph.D.)--University of Adelaide, Dept. of Plant Science, 1999

xvii, 215 leaves : ill. ; 30 cm.0 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Agronomy, 1974