The use of an ocean surface velocity dependent wind stress is examined in the context of a 3-layer double-gyre quasigeostrophic wind-driven ocean circulation model. The new wind stress formulation results in a large reduction of the power input by the wind into the oceanic circulation. This wind stress is proportional to a quadratic function of Ua--u o, where Ua is the wind at 10m above the ocean surface and uo is the ocean surface current. Because the winds are typically faster than the ocean currents, the impact of the ocean surface velocity on the wind stress itself is relatively small. However, the power input is found to be greatly reduced with the new formulation. This is shown by simple scaling argument and numerical simulations in a square basin. Our results suggest that the wind power input may be as much as 35% smaller than is typically assumed. / The ocean current signature is clearly visible in the scatterometer-derived wind stress fields. We argue that because the actual ocean velocity differs from the modeled ocean velocities, care must be taken in directly applying scatterometer-derived wind stress products to the ocean circulation models. This is not to say that the scatterometer-derived wind stress is not useful. Clearly the great spatial and temporal coverage make these data sets invaluable. Our point is that it is better to separate the atmospheric and oceanic contribution to the stresses. / Finally, the new wind stress decreases the sensitivity of the solution to the (poorly known) bottom friction coefficient. The dependence of the circulation strength on different values of bottom friction is examined under the standard and the new wind stress forcing for two topographic configurations. A flat bottom and a meridional ridge case are studied. In the flat bottom case, the new wind stress leads to a significant reduction of the sensitivity to the bottom friction parameter, implying that inertial runaway occurs for smaller values of bottom friction coefficient. The ridge case also gives similar results. In the case of the ridge and the new wind stress formulation, no real inertial runaway regime has been found over the range of parameters explored.

The linear response of a two layer ocean model to a periodic wind stress curl in the presence of bottom topography has been investigated. For periods much less than the time taken for the wind generated baroclinic Rossby waves to pass over the topography (i.e. 'short' periods), the ocean response is primarily that for a homogeneous ocean and thus strongly modified by topography. For periods much longer than this time (i.e. 'long' periods), the Rossby waves compensate for the effect of topography and the non-topographic Sverdrup balance holds. For the Atlantic at 25°N, the long period limit is of the order of years to decades, so at annual period the non-topographic Sverdrup balance is not applicable. Variations in transport can be forced by a wind stress over varying topography, and by the passage of a coastal baroclinic Kelvin wave over varying topography. The relative importance of the above dynamical considerations for the Florida Current can only be determined from a model calculation involving realistic winds, topography and geography. Such a model calculation has been done with observed Bunker wind stress over a two layer ocean. The predicted variation has a Summer maximum and a Fall minimum, in agreement with the measurements of Niiler and Richardson [1973] and more recent STACS data. The one layer model has been forced by monthly means of ATOLL wind stress for the years 1981-1984. The predicted variation was found not to be in agreement with concurrent STACS measurements. A comparison was made between the Bunker winds and the ATOLL winds via various diagnostics. It was found that the meridional component of the wind, which is crucial to the overall Bunker Summer maximum, is of much reduced importance for the ATOLL winds. This could account for the lack of predicted Summer maxima.

Orthostatic vasovagal syncope is the sudden loss of consciousness resulting from a temporary impairment of cerebral blood flow, within approximately an hour of standing. Patients who suffer from this problem have "vasovagal syndrome". The purpose of this thesis was to devise a method to detect the syndrome following the assumption of upright position. Data from 106 syncopal patients undergoing head-up tilt table testing (HUT) were acquired, including electrical activity of the heart (electrocardiogram), blood pressure, oxygen saturation, and cerebral perfusion parameters from near-infrared spectroscopy (NIRS). The data set was examined with the aim of generating automatic diagnoses. Comparison of the rate-pressure product (blood pressure multiplied by heart rate) during the time of syncope with a recommended threshold, in addition to comparison with monitoring the fall of systolic blood pressure during prolonged tilt, yielded an 84% accuracy rate for vasovagal syndrome. The thesis reviewed the techniques used on the aforementioned time series by previous researchers, emphasising the concepts underlying "time-frequency analysis", a method for analysing nonstationary signals. Since even healthy patients experience time-varying frequency information in their haemodynamics, a transform known as the Smoothed Pseudo-Wigner Ville Distribution (SPWVD) is well suited to their analysis. This distribution was applied to RR tachograms, plots of heart period against time. After the smoothing parameters of the SPWVD were chosen based on artificial data, the optimised transform was then applied to a second artificial tachogram to calculate the LF/HF (low- to high-frequency) ratio, an indicator of heart rate variability. The computed LF/HF ratio tracked the expected value within an error margin of 3.6%. Finally, by applying the same transform to clinical data, it was proved to offer better resolution than an alternative known as the Lomb periodogram. Classical techniques from the literature predicting vasovagal syncope were found to fail on the current data set: out of 29 tests, only two yielded statistically significant differences between the two patient groups. These were compared with the author's time-frequency analysis of RR tachograms, linear regression of heart rate, and examination of NIRS oscillations and changes on tilt. Of these, the ICFV during time period P3 was found to perform best (negative predictive value: 0.86). A linear classifier was used to combine the best four predictors; it achieved an overall accuracy of 0.88. Following the data-driven approach, an analytical modelling approach was undertaken. In order to define an appropriate model that traded off simplicity with comprehensiveness, the mechanisms of vasovagal syncope were reviewed. A model of orthostasis was developed, validated, and used toward parameter estimation from patient data. Three parameters (baroreceptor operating point, cardiac effectiveness, and baroreflex gain) were gleaned from the supine baseline recording to "normalise" the model for a given patient, before four new parameters (sympathetic and parasympathetic gains at the sino-atrial node, peripheral vasoconstriction gain, and total blood volume) were estimated from the data collected in the upright position. The expectation was that this approach would improve feature extraction (and hence prediction accuracy) as well as the clinical interpretation of the results. However, the modelling approach was found to offer no significant improvement upon the data-driven signal processing results: a linear classifier on the four post-tilt parameters yielded a negative predictive value of just 0.69. This result may have been due to inaccuracies in the time series data owing to instrumentation error. It is also possible that the modelling approach was not able to provide the quality of feature extraction necessary for predicting vasovagal syncope in the elderly. Finally, methods to predict syncope during mid- to late HUT were examined. Using information derived from heart rate and baroreflex sensitivity, a technique was developed to ease patient comfort by terminating the test approximately 2 minutes before syncope was expected to occur.

No description available.

The time-averaged velocity field in the North Pacific was estimated in two sets of inverse calculations. The planetary geostrophic equations were the basis for dynamical models of the flow in each case. The inverse estimates of the circulation were obtained by minimizing a positive-definite cost function, which measured the inconsistency of the model's predictions against a set of observations comprised of a large, high-quality hydrographic data set, and surface fluxes of heat, fresh water, and momentum. In the first part of this work, four solution methods for the generalized inverse of a linear planetary geostrophic model of the North Pacific are compared. A conjugate gradient solver applied to the equation for the generalized inverse, expressed in terms of a representer expansion, was the most computationally efficient solution method. The other methods, in order of decreasing efficiency, were, a conjugate gradient descent solver (preconditioned with the inverse of the model operators), a direct solver for the representer coefficients, and a second conjugate gradient descent solver (preconditioned so that the diagonal elements of the cost Redacted for Privacy function Hessian were unity). All but the last method were successful at minimizing the penalty function. Inverse estimates of the circulation based on the linear planetary geostrophic model were stable to perturbations in the data, and insensitive to assumptions regarding the model forcing and boundary condition uncertainties. A large calculation, which involved approximately 18,000 observations and 60,000 state variables, indicated that the linear model is remarkably consistent with the observations. The second part of this work describes an attempt to use a nonlinear planetary geostrophic model (which included realistic bottom topography, lateral momentum mixing, out-cropping layers, and air-sea fluxes of heat, freshwater, and momentum) to assimilate the same hydrographic data set as above. Because of the nonlinearity in the model, descent methods (rather than a representer-based method) were used to solve the inverse problem. The nonlinearity of the model and the poor conditioning of the cost function Hessian confounded the minimization process. A solver for the tangent-linearization of the planetary geostrophic system should be used as a preconditioner if calculations of this type are attempted in the future. / Graduation date: 1996

No description available.

Heart disease is attributed as the highest cause of death in the world. Although this could be alleviated by heart transplantation, there is a chronic shortage of donor hearts and so mechanical solutions are being considered. Currently, many Ventricular Assist Devices (VADs) are being developed worldwide in an effort to increase life expectancy and quality of life for end stage heart failure patients. Current pre-clinical testing methods for VADs involve laboratory testing using Mock Circulation Loops (MCLs), and in vivo testing in animal models. The research and development of highly accurate MCLs is vital to the continuous improvement of VAD performance. The first objective of this study was to develop and validate a mathematical model of a MCL. This model could then be used in the design and construction of a variable compliance chamber to improve the performance of an existing MCL as well as form the basis for a new miniaturised MCL. An extensive review of literature was carried out on MCLs and mathematical modelling of their function. A mathematical model of a MCL was then created in the MATLAB/SIMULINK environment. This model included variable features such as resistance, fluid inertia and volumes (resulting from the pipe lengths and diameters); compliance of Windkessel chambers, atria and ventricles; density of both fluid and compressed air applied to the system; gravitational effects on vertical columns of fluid; and accurately modelled actuators controlling the ventricle contraction. This model was then validated using the physical properties and pressure and flow traces produced from a previously developed MCL. A variable compliance chamber was designed to reproduce parameters determined by the mathematical model. The function of the variability was achieved by controlling the transmural pressure across a diaphragm to alter the compliance of the system. An initial prototype was tested in a previously developed MCL, and a variable level of arterial compliance was successfully produced; however, the complete range of compliance values required for accurate physiological representation was not able to be produced with this initial design. The mathematical model was then used to design a smaller physical mock circulation loop, with the tubing sizes adjusted to produce accurate pressure and flow traces whilst having an appropriate frequency response characteristic. The development of the mathematical model greatly assisted the general design of an in vitro cardiovascular device test rig, while the variable compliance chamber allowed simple and real-time manipulation of MCL compliance to allow accurate transition between a variety of physiological conditions. The newly developed MCL produced an accurate design of a mechanical representation of the human circulatory system for in vitro cardiovascular device testing and education purposes. The continued improvement of VAD test rigs is essential if VAD design is to improve, and hence improve quality of life and life expectancy for heart failure patients.

The objective of this thesis is to investigate the pathophysiology of the coronary slow phenomenon (CSFP). The experimental work of this thesis has taken a 'bedside to benchtop' approach with clinical observations made in the second chapter guiding the application of basic research techniques in subsequent chapters. Chapter 1 ; The CSFP is a disorder of the coronary microcirculation ; hence chapter 1 specifically reviews the current understanding of this vascular territory and concludes with a summary of the clinical disorders affecting it, concentrating on the CSFP. Chapter 2 ; investigated the angiographic response of the CSFP to a calcium channel blocking agent with antianginal efficacy in this disorder ( mibefradil ). Mibefradil administration was associated with an acute improvement of coronary flow indices which occurred despite background vasodilator therapy with conventional calcium channel antagonists. Chapter 3 ; investigated the in vitro response of human microvessels to mibefradil in comparison to conventional calcium channel blockers. Mibefradil was found to be a more potent agent both in terms of vasodilatation and the prevention of vasoconstriction. Both findings support the clinical observations and point to its selective action on the calcium T channel subtype as a potential mechanism. Chapter 4 ; examined the expression of T type calcium channels at the level of the microvasculature and compared T channel expression in CSFP patients and controls. T channels were found to be expressed at two or more orders of magnitude greater than the L channels. No difference in T channel expression between patients and controls was found. Chapter 5 ; examined the vasomotor reactivity of isolated subcutaneous arterial microvessels to various vasoactive substances between controls and CSFP patients. CSFP patients were found to have a selective hyper reactivity to endothelin. Chapter 6 ; examined plasma endothelin levels in CSFP patients and controls and the relationship between endothelin levels and angina frequency in the CSFP cohort. A small but statistically significant elevation of endothelin-1 was present in patients with the CSFP. A positive association between plasma endothelin fluctuation and angina frequency was also found in the CSFP cohort but not between absolute endothelin levels and angina symptoms. / Thesis (Ph.D.)-- The University of Adelaide, School of Medical Sciences, 2006.

The relationship between the general circulation of the ocean and, along-isopycnal and vertical mixing is explored. Firstly, advection down isopycnal tracer gradients is related to mixing in specific regions of the ocean. Secondly, a general inverse method is developed for estimating both mixing and the general circulation. Two examples of down gradient advection are explored. Firstly the region of Mediterranean outflow in the North Atlantic. Given a known transport of warm salty water out of the Mediterranean Sea and the mean hydrography of the eastern North Atlantic, the vertical structure of the along-isopycnal mixing coefficient, K, and the vertical mixing coefficient, D, is revealed. Secondly, the Southern Ocean Meridional Overturning Circulation, SMOC, is investigated. There, relatively warm salty water is advected southward, along-isopycnals, toward fresher cooler surface waters. The strength and structure of the SMOC is related to K and D by considering advection down along-isopycnal gradients of temperature and potential vorticity. The ratio of K to D and their magnitudes are identified. A general tool is developed for estimating the ocean circulation and mixing; the \textit{tracer-contour inverse method}. Integrating along contours of constant tracer on isopycnals, differences in a geostrophic streamfunction are related to advection and hence to mixing. This streamfunction is related in the vertical, via an analogous form of the depth integrated thermal wind equation. The tracer-contour inverse method combines aspects of the box, beta spiral and Bernoulli methods. The tracer-contour inverse method is validated against the output of a layered model and against in-situ observations from the eastern North Atlantic. The method accurately reproduces the observed mixing rates and reveals their vertical structure.

The objective of this thesis is to investigate the pathophysiology of the coronary slow phenomenon (CSFP). The experimental work of this thesis has taken a 'bedside to benchtop' approach with clinical observations made in the second chapter guiding the application of basic research techniques in subsequent chapters. Chapter 1 ; The CSFP is a disorder of the coronary microcirculation ; hence chapter 1 specifically reviews the current understanding of this vascular territory and concludes with a summary of the clinical disorders affecting it, concentrating on the CSFP. Chapter 2 ; investigated the angiographic response of the CSFP to a calcium channel blocking agent with antianginal efficacy in this disorder ( mibefradil ). Mibefradil administration was associated with an acute improvement of coronary flow indices which occurred despite background vasodilator therapy with conventional calcium channel antagonists. Chapter 3 ; investigated the in vitro response of human microvessels to mibefradil in comparison to conventional calcium channel blockers. Mibefradil was found to be a more potent agent both in terms of vasodilatation and the prevention of vasoconstriction. Both findings support the clinical observations and point to its selective action on the calcium T channel subtype as a potential mechanism. Chapter 4 ; examined the expression of T type calcium channels at the level of the microvasculature and compared T channel expression in CSFP patients and controls. T channels were found to be expressed at two or more orders of magnitude greater than the L channels. No difference in T channel expression between patients and controls was found. Chapter 5 ; examined the vasomotor reactivity of isolated subcutaneous arterial microvessels to various vasoactive substances between controls and CSFP patients. CSFP patients were found to have a selective hyper reactivity to endothelin. Chapter 6 ; examined plasma endothelin levels in CSFP patients and controls and the relationship between endothelin levels and angina frequency in the CSFP cohort. A small but statistically significant elevation of endothelin-1 was present in patients with the CSFP. A positive association between plasma endothelin fluctuation and angina frequency was also found in the CSFP cohort but not between absolute endothelin levels and angina symptoms. / Thesis (Ph.D.)-- The University of Adelaide, School of Medical Sciences, 2006.