Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

Thesis (Ph.D.)--University of Missouri-Columbia, 2006. / 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 (May 2, 2007) Vita. Includes bibliographical references.

Thesis (Ph.D.)--University of Missouri-Columbia, 2006. / 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 (May 2, 2007) Vita. Includes bibliographical references.

Thesis (Ph.D.) - University of Queensland, 2006. / Includes bibliography.

Existing Global Data Computation (GDC) protocols for asynchronous systems are designed for fully connected networks. In this paper, we discuss GDC in a dedicated asynchronous chordal ring, a type of un-fully connected networks. The virtual links approach, which constructs t+1 (t<n) process-disjoint paths for each pair of processes without direct connection to tolerate failures (where t is the maximum number of processes that may crash and n is the total number of processes), can be applied to solve the GDC problem in the chordal but the virtual links approach incurs high message complexity. To reduce the high communication cost, we propose a non round-based GDC protocol for the asynchronous chordal ring with perfect failure detectors. The main advantage of our approach is that there is no notion of round, processes only send messages via direct connections and the implementation of failure detectors does not require process-disjoint paths. Analysis and comparison with the virtual links approach shows that our protocol reduces the message complexity significantly. / Singapore-MIT Alliance (SMA)

Thesis (Ph. D.)--University of Sydney, 2008. / Title from title screen (viewed Jan. 28, 2009) Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Public Health, Faculty of Medicine. Includes bibliographical references and list of publications. Also available in print form.

Η μελέτη αυτή είναι από τις πρώτες που ασχολήθηκαν με τη διερεύνηση του ρόλου της ενδοθηλίνης στη νεφρική νόσο, καθώς και με την παραγωγή της στο νεφρικό ιστό. Στο πρώτο μέρος της διατριβής επιλέχθηκαν δύο ομάδες ασθενών στις οποίες προσδιορίστηκαν τα επίπεδα ενδοθηλίνης-1 στο πλάσμα και στα ούρα: α) ασθενείς με νεφρωσικό σύνδρομο και β) ασθενείς με ΧΝΑ, χωρίς πρωτεϊνουρία. Στη συνέχεια εξετάστηκε κατά πόσο υπήρχε συσχετισμός των επιπέδων της ΕΤ-1 με διαφορετικές νεφρικές παραμέτρους μεγέθη όπως η κάθαρση της κρεατινίνης, η πρωτεϊνουρία και η ροή των ούρων. Τα πρώτα αποτελέσματα παρείχαν ενδείξεις για αυξημένη νεφρική παραγωγή ενδοθηλίνης-1 σε ασθενείς με σπειραματική βλάβη και η απεκκρινόμενη ΕΤ-1 είχε θετική συσχέτιση με το βαθμό της πρωτεϊνουρίας. Στη συνέχεια μελετήθηκε η έκφραση της στο νεφρικό ιστό και ακόμα ειδικότερα, στο σπείραμα, στα σωληνάρια και στο διάμεσο ιστό, καθώς και η μεταβολή των επιπέδων της απεκκρινόμενης ΕΤ-1 κατά τη θεραπευτική αντιμετώπιση της πρωτεϊνουρίας. Πιο αναλυτικά τα αποτελέσματα της διατριβής ήταν τα παρακάτω: α) Τα επίπεδα ΕΤ-1 στο πλάσμα ασθενών με νεφρική νόσο είναι αυξημένα και περίπου τριπλάσια από τα φυσιολογικά. Η αύξηση αυτή είναι ανεξάρτητη από την κάθαρση της κρεατινίνης και από το βαθμό ή την ύπαρξη της πρωτεϊνουρίας. β) Η απεκκρινόμενη ΕΤ-1 στα ούρα ασθενών με νεφρική νόσο, είναι αυξημένη στο διπλάσιο σε σύγκριση με τα φυσιολογικά επίπεδα και αντικατοπτρίζει τη νεφρική της παραγωγή. γ) Η ΕΤ-1 εντοπίζεται στο κυτταρόπλασμα των ενδοθηλιακών κυττάρων του σπειράματος και στα αγγεία του διάμεσου ιστού στο φυσιολογικό νεφρικό παρέγχυμα. δ) Στο νεφρικό ιστό των νεφρωσικών ασθενών η ΕΤ-1 εκτός από το σπείραμα και τα αγγεία του διάμεσου ιστού, εντοπίζεται και στο κυτταρόπλασμα των επιθηλιακών κυττάρων των σωληναρίων (εγγύς και άπω). ε) Δεν παρατηρείται καμία διαφορά στην κατανομή της ΕΤ-1 στις διάφορες τομές μεταξύ των ασθενών με νεφρωσικό σύνδρομο. Η κατανομή της ΕΤ-1 είναι ίδια και είναι ανεξάρτητη από τις διάφορες σπειραματικές νόσους στις οποίες οφείλεται η πρωτεϊνουρία. στ) Συνοπτικά, η έκφραση της ΕΤ-1 είναι μεγαλύτερη στο νεφρικό ιστό των ασθενών με πρωτεϊνουρία σε σύγκριση με την ομάδα των τομών από φυσιολογικό νεφρικό ιστό. ζ) Η απεκκρινόμενη ΕΤ-1 στα ούρα είναι ανάλογη του βαθμού της πρωτεϊνουρίας σε ασθενείς με νεφρωσικό σύνδρομο και μειώνεται παράλληλα με την πρωτεϊνουρία μετά από θεραπευτική αγωγή. / This study investigates the role of endothelin-1 (ET-1) and its production in the renal tissue. Endothelin-1 was determined in plasma and urine in two groups of renal patients: a) patients with nephrotic syndrome and b) patients with chronic renal failure without proteinuria. Endothelin levels were correlated with several renal function parameters such as creatinin clearance, proteinuria and urinary flow. Results showed an increased endothelin renal production in patients with glomerular injury and a positive correlation between endothelin renal excretion and proteinuria. The endothelin expression in the renal tissue was studied and particularly in the glomerulus, tubules and interstitial tissue. Further more, changes in endothelin renal excretion were investigated during immunosuppressive treatment of proteinuria. The results of this study are as follow: a) Endothelin-1 plasma levels in patients with renal disease are increased compared to controls. This increase was independent compared to creatinine clearance and the severity of proteinuria. b) The endothelin renal excretion in patients with renal disease is increased compared to controls and represents its renal production. c) ΕΤ-1 is localized in the cytoplasm of glomerular endothelial cells and in the vessel walls in the interstitial tissue in normal renal parenchyma. d) In patients with neprotic syndrome, ET-1 is also localized in the cytoplasm of epithelial cells in proximal and distal tubules. e) No differences in the renal distribution of ET-1 were observed among tissue samples of nephrotic patients with different primary causes of proteinuria. f) The ΕΤ-1 expression was increased in the renal tissue of patients with proteinuria compared to controls. g) The ΕΤ-1 excretion in urine was positive correlated to the degree of proteinuria and decreases with the reduction of proteinuria after immunosuppressive treatment.

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The most common cause of death in patients with sepsis/septic shock is deterioration of the function of multiple organs, termed multiple organ dysfunction syndrome. Although our understanding of mechanisms involved in the pathophysiology of sepsis-induced tissue damage has improved substantially, therapy of these syndromes still remains largely supportive. The hallmark of sepsis is an overwhelming systemic production of both pro- and anti-inflammatory mediators leading to generalized endothelial and epithelial damage, microcirculatory-mitochondrial distress, altered endocrine and coagulation homeostasis and cellular immune hyporesponsiveness. Therefore, the hypothesis that modulation of this excessive immunological and biological response to infection might improve patient outcome appears reasonable. Hemoelimination techniques represent biologically plausible way to provide non-specific removal of soluble pro- and anti-inflammatory mediators, although the concept of blood purification in sepsis remains a matter of considerable debate. The aim of this thesis was to elucidate effects of 1) high volume hemofiltration (HVHF) and 2) coupled plasma filtration adsorption (CPFA) in a long-term, hyperdynamic porcine septic shock model, which fulfils the criteria for human sepsis. We hypothesized that both HVHF and...

Applications of theories of interpersonal blame to consumer behavior have largely focused on understanding when consumers blame companies for their misbehavior. The current research moves beyond past work by shedding new light on the processes underlying consumer blame. In Essay 1, a pilot study and five experiments—in contexts of both fictitious and actual high-profile product failures—show that blame may be incorrectly directed toward the victim. The findings show that (1) consumers exaggerate blame for a victim possessing negative (especially immoral) dispositional traits because (2) that individual is seen as deserving of suffering in general and, as a result, (3) consumers are less likely to take punitive action against the company. The experiments support a “moral dominance” effect whereby victim blame is driven more heavily by perceived differences in the victim’s morality than sociability (or competence), because only morality leads consumers to judge the victim as deserving of suffering in general. In Essay 2, a new line of inquiry is proposed pertaining to consumer inferences of company blame and attitudes when the company engages in cause marketing. By engaging in socially responsible behavior, consumers may infer that the company is signaling a (1) negative attitude, (2) moral judgement, and (3) blame judgement toward the perpetrator of that harm. Each predicts the amount of praise the company receives—depending on consumers’ own attitudes, judgments, and blame toward the perpetrator—but blame inferences predict praise most strongly. This is because blame provides a unique signal about the company’s stance on an issue. Two studies support these blame inference predictions.