Cardiac remodeling after acute myocardial infarction (MI) is an important process that leads to progressive ventricular enlargement and heart failure. Several variables have been identified to predict an increase in left ventricular (LV) volume and a decrease of LV ejection fraction (LVEF) after an acute MI including infarct size, anterior location, cardiac enzyme level, transmurality of the infarct, patency of the infarct-related artery, end systolic volume (ESV) and mitral deceleration time, etc. / Regional disturbances of LV wall motion have long been recognized to occur in patients with cardiac diseases, such as hypertrophic cardiomyopathy, unstable angina, acute ischemia, and MI. Tissue Doppler imaging (TDI) is recently established for detecting regional contractile abnormalities and asynchrony, and can predict reverse remodeling and improved synchronicity after biventricular pacing therapy in heart failure patients. However, it is unclear whether LV asynchrony plays an important role in the evolutionary changes of LV remodeling after an acute infarction and whether it can predict the changes independently. / The identification of transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. TDI-derived strain rate imaging (SRI) quantifies local rate of myocardial deformation and has the potential to differentiate viable from infarcted myocardium. / Therefore, in this study we aimed to investigate: (1) Whether SRI may differentiate transmural from non-transmural MI as assessed by ce-MRI in routine patients post acute infarction, and establish practical cutoff values for identifying transmural scar tissue from non-transmural or subendocardial infarction with viable myocardium. (2) Whether LV systolic and diastolic asynchrony measured by TDI occurs early after acute MI even in the absence of widening of QRS complexes, and determine if this is explained by the site and extent of the infarction measured by ce-MRI. (3) The relationships between serial measurements of infarct size on ce-MRI and LV remodeling process after an acute infarction, and determine whether early assessment of infarct size predicts progressive ventricular enlargement and cardiac dysfunction, and whether it differs with infarct location. (4) The relationships between LV asynchrony, infarct size and LV remodeling, and determine whether early assessment of LV asynchrony by TDI compared with standard clinical correlates of LV remodeling and infarct size predicts progressive ventricular enlargement and cardiac dysfunction. (Abstract shortened by UMI.) / Zhang Yan. / "April 2005." / Adviser: John E. Sanderson. / Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0175. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 161-192). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

Yang Lu, Louise. / "Architecture Department, Chinese University of Hong Kong, Master of Architecture Programme 2009-2010, design report." / "May 2010." / Includes bibliographical references (leaves 55).

Hung Chun, Ted. / Subtitle on added t.p.: Critical review on urban redevelopment and conservation. / "Architecture Department, Chinese University of Hong Kong, Master of Architecture Programme 2009-2010, design report." / "May 2010." / Text in English with some Chinese. / SEMESTER 1 / Thesis Statement / Definition / Research / Market Town in Hong Kong / SWH / Preliminary Design / SEMESTER 2 / Design Strategy / Design Development / Final Design

Chan Chi Kan. / "Architecture Department, Chinese University of Hong Kong, Master of Architecture Programme 2007-2008, design report." / Includes bibliographical references (leaves 52). / Abstracts in English and Chinese. / Chapter 1.0 --- Synopsis --- p.5 / Chapter 2.0 --- Research studies - City scale --- p.6 / Chapter 2.1 --- Review of industrial development in Hong Kong / Chapter 2.2 --- Location of current industrial fabric / Chapter 3.0 --- Research studies - Building scale --- p.8 / Chapter 3.1 --- Typology of industrial buildings in Hong Kong / Chapter 4.0 --- Research studies - Industry in Hong Kong --- p.9 / Chapter 4.1 --- Traditional industry / Chapter 4.2 --- OBM and ODM industry / Chapter 5.0 --- Importance of flatted factory --- p.11 / Chapter 5.1 --- Introduction of flatted factory / Chapter 5.2 --- Occurrcncc of flatted factory / Chapter 5.3 --- Comparison of flatted factory and Mark / Chapter 5.4 --- Architectural quality of flatted factory / Chapter 6.0 --- Case Study - Adaptive reuse of industrial buildings --- p.17 / Chapter 6.1 --- Lingotto Factory / Chapter 6.2 --- Tate Modern / Chapter 6.3 --- Apartment building gasometer / Chapter 6.4 --- "Beijing, Factory 798" / Chapter 7.0 --- Establishment of thesis statement --- p.21 / Chapter 7.1 --- Political point of view / Chapter 7.2 --- Conservation point of view / Chapter 7.3 --- Summary of thesis statement / Chapter 8.0 --- Experimental site --- p.24 / Chapter 8.1 --- Introduction of San Po Kong as experimental site / Chapter 8.2 --- History of site / Chapter 8.3 --- Current situation of site / Chapter 8.4 --- Current condition of site / Chapter 8.5 --- Current condition of existing building / Chapter 9.0 --- Derivation of program --- p.31 / Chapter 9.1 --- New program in San Po Kong / Chapter 9.2 --- Case study of Fontanian / Chapter 9.3 --- Case study of Hong Kong Jockcy Club Creative art centre / Chapter 10.0 --- Key issues of design --- p.34 / Chapter 10.1 --- Vision for future / Chapter 10.2 --- Idea of publicncss / Chapter 10.3 --- Conccpt of New + Old / Chapter 11.0 --- Design development process --- p.36 / Chapter 11.1 --- Programmatic arrangement / Chapter 11.2 --- Rcconnccting six obscure flatted factory / Chapter 11.3 --- Principle of adding new element / Chapter 12.0 --- Architectural design - City level --- p.38 / Chapter 12.1 --- Hypothesis in the future of San Po Kong / Chapter 12.2 --- Development in relationship with Kai Tak / Chapter 13.0 --- Architectural design - Building level --- p.41 / Chapter 13.1 --- Preservation of existing building but with different use / Chapter 13.2 --- Community zone / Chapter 13.3 --- Transformation Zone / Chapter 13.4 --- Public loop / Chapter 14.0 --- Architectural design - Unit leve --- p.49 / Chapter 14.1 --- Variation on the working units in the building / Chapter 14.2 --- Three-dimensional relationship between public visitor and private unit / Chapter 15.0 --- Bilography --- p.52

Poon Ching Pong, Adrian. / "Architecture Department, Chinese University of Hong Kong, Master of Architecture Programme 2009-2010, design report." / "May 2010." / Includes bibliographical references (p. 123). / RESEARCH / Observation --- p.6-7 / Play --- p.8 / Resort? --- p.9 / Images --- p.10 / Modernism & Post-modernism --- p.11-13 / Theme City --- p.14 / Need A Pause? --- p.15 / We Are Hamster --- p.16-17 / World --- p.18-19 / Coney --- p.20 / Play Forms --- p.21-23 / Play Forms & Programs --- p.24-27 / Concept Flow --- p.28-31 / Playgrounds & Play Forms --- p.32-33 / Hotel Concepts --- p.34-35 / W-Hotel --- p.36-37 / Hotel Morphology --- p.38-39 / Generic Hotel Settings --- p.40-41 / Hotel Programs --- p.42-49 / Comparison --- p.50-51 / Hotel-like Living --- p.52 / Argument --- p.53 / Concept --- p.54 / Statement --- p.55 / Murray Building --- p.56 / Conservation --- p.57 / Site Strategy --- p.58-59 / Players --- p.60-61 / Programs --- p.62-63 / Absorption --- p.64-65 / Posters --- p.66-67 / DESIGN / Maze Concept --- p.70 / Transitional Device --- p.71 / Murray Tube --- p.72-73 / Operation --- p.74 / Variations --- p.75 / Facade --- p.76 / Public-access --- p.77 / Structure --- p.78-79 / Game Rules --- p.80 / Guestrooms --- p.81 / Design Programs --- p.82-85 / Perspective Views --- p.86-89 / Section --- p.90-91 / Site Model --- p.92-93 / Maze Concept --- p.94-97 / Concept Model --- p.98-99 / Conceptual Schemes --- p.100-103 / Working Models --- p.104-107 / Final Model --- p.108-111 / Panels --- p.112-117 / APPENDIX / Reference --- p.120-121 / Abstract --- p.122 / Bibliography --- p.123

This thesis examines the adaptive use of historic churches in Indianapolis and Zionsville. It looks at the decline and revitalization of urban neighborhoods which led to the adaptive use of historic churches. It examines seven case studies in Indianapolis and Zionsville, Indiana representing the new use by different congregations, use of historic churches by a not-for-profit organizations, and for-profit uses of historic churches. These case studies typify a national trend toward adaptively using historic churches and retaining them as anchors for the neighborhoods in which they exist. This thesis also makes conclusions about which of the adaptive uses is most desirable and which is lest desirable. / Department of Architecture

This research and documentation project of surviving Indianapolis automobile factories examines the importance of Indianapolis, Indiana, as a center of automobile manufacturing in its early days. Automobile factories appeared in the city as early as 1895, and were often an outgrowth of bicycle or carriage-building companies. This followed a national trend. As the industry grew, Indianapolis firms continued to produce low-volume, high-quality cars instead of the more popular, low-cost cars being produced by Ford and other Michigan-based manufacturers. The recession of 1921 and the Great Depression of 1929 decimated the market for expensive cars and by 1937 all Indianapolis-based firms were out of the automobile business. A number of their production facilities remain and are employed in a variety of uses. This project documents these buildings and recommends a range of adaptive re-uses based on successful conversions. / Department of Architecture

Ziel dieser Arbeit war, in einem experimentellen Ansatz der Frage nachzugehen, welche pathophysiologischen Veränderungen in Bezug auf Hypertrophie und Funktionalität der Herzmuskulatur nach einem Myokardinfarkt durch Calsarcin-1 hervorgerufen werden und welchen Einfluss das Z-Scheiben-Protein in-vivo auf den Kalzium-Calmodulin Signalweg besitzt. Für die dafür durchgeführten Untersuchungen konnte auf drei verschiedene Mauslinien zurückgegriffen werden (Calsarcin-1 knockout-Mäuse, Calsarcin-1 transgene Mäuse, Wildtypmäuse). Die vorliegende Arbeit baut auf den in-vitro Ergebnissen von Frey et al. (2004) auf. Insgesamt wurden 278 Mäuse einer Infarkt- oder Scheinoperation unterzogen. Fünf Wochen nach ihrer Operation wurde das Herz jeder Maus mittels Ultraschall vermessen und auf seine Funktionstüchtigkeit untersucht. Anschließend wurden die Tiere getötet. Die entnommenen Herzen wurden gewogen, die entnommenen Unterschenkel vermessen. Insgesamt 60 Herzen wurden nach konventionellen histologischen Verfahren HE-gefärbt. 39 Mäuse wurden 24 Stunden nach ihrer Infarktoperation getötet. Ihre Herzen wurden mit Evans-blue und Tetrazoliumchlorid gefärbt. Insgesamt gingen Gewebeproben von 67 Herzen in die Untersuchungen auf RNA-Ebene (Real-Time PCR, Dot Blot) ein. Die Herzen von 40 Tieren konnten auf Proteinebene (Western Blot) untersucht werden. Die echokardiologische Untersuchung der Mäuse nach fünf Wochen zeigte eine deutliche Dilatation des linken Ventrikels derjenigen Tiere, die einer Infarktoperation unterzogen worden waren. Die größte Dilatation der drei Infarktgruppen wiesen die Mäuse auf, die nicht in der Lage sind, das Z-Scheiben-Protein Calsarcin-1 auszubilden (0,558 cm (ko Mi) vs. 0,494 cm (Wt Mi); p < 0,001). Diese Mäuse zeigten auch gegenüber den anderen beiden Infarktgruppen die ausgeprägteste systolische Dysfunktion (FS von 0,238% (ko Mi) vs. 0,376% (Wt Mi) und 0,353% (tg Mi); jeweils p < 0,001). Keine Unterschiede bestanden zwischen den Gruppen der scheinoperierten Mäuse. Morphometrische Analysen belegten eine deutliche Hypertrophie der Calsarcin-1 defizienten Mäuse, die durch die Infarktoperation einer biomechanischen Stresssituation ausgesetzt wurden. Als Hypertrophiemaß wurde der Quotient aus Herz- und Körpergewicht gewählt, zusätzlich wurde der Quotient aus Herzgewicht und Tibialänge bestimmt. Bei beiden Messungen unterschied sich das Herzgewicht der knockout-Mäuse mit Infarkt signifikant von den anderen beiden Infarktgruppen. Für das Verhältnis von Herz- zu Körpergewicht wurde für die drei Mäusegruppen ermittelt: 7,55 ± 0,6mg/g (ko Mi ), 5,56 ± 0,23mg/g (WtMi) und 5,73 ± 0,4mg/g (tgMi), wobei p < 0,01 bei ko Mi/Wt Mi und p < 0,86 bei tg Mi / Wt Mi. Für das Verhältnis von Herzgewicht zu Tibialänge ergab sich: 12,4mg/mm (ko Mi), 10,11mg/mm (Wt Mi) und 10,02mg/mm (tg Mi) (p < 0,001 koMi / WtMi, p < 0,27 tg Mi / WtMi). Zwischen den Gruppen der scheinoperierten Mäuse wurden keine signifikanten Unterschiede festgestellt. Auch auf zellulärer Ebene wiesen die Calsarcin-1 knockout-Mäuse mit Myokardinfarkt eine deutliche Hypertrophie auf verglichen mit den Wildtyp-Mäusen mit Infarkt und den Calsarcin-1 transgenen Tieren (Zellgrößenzunahme um 43,12% (koMi), 34,85% (WtMi) und 29,12% (tgMi); jeweils p < 0,001). Von allen drei Infarktgruppen zeigten die knockout-Mäuse nach fünf Wochen die ausgeprägteste Narbenbildung (Fläche der Infarktnarbe in % der Fläche des linken Ventrikels: 73,41±7,85% (ko-Mi), 53,71±3,81% (WtMi) und 48,60±6,04% (tgMi)). Übereinstimmend dazu wiesen die knockout-Mäuse mit Myokardinfarkt eine übermäßige Steigerung der ANP Produktion auf mRNA-Ebene auf. Auf Proteinebene konnte eine Steigerung der Produktion von MCIP nachgewiesen werden (ko Mi 4,3 ± 0,5 vs. Wt Mi 2,3 ± 0,3 ; p < 0,01). Zusammenfassend lassen die Ergebnisse auf eine gesteigerte Aktivität von Calcineurin und auf ein pathologisches Remodeling in der Abwesenheit von Calsarcin-1 schließen. Die Überexpression von Calsarcin-1 scheint dagegen eine pathologische Hypertrophie des Herzmuskels abmildern zu können.

1 leaf folds out. Photos glued in. / Digitized by Kansas State University Libraries

Thesis (MSc (Physiological Sciences))--University of Stellenbosch, 2009. / Physiological cardiac hypertrophy is characterized by the heart’s ability to increase mass in a reversible fashion without leading to heart failure. In contrast, pathological cardiac hypertrophy leads to the onset of heart failure. For this study, we investigated a model of physiological hypobaric hypoxia-mediated right ventricular (RV) hypertrophy (RVH). Here our hypothesis was that the hypertrophic response and associated changes triggered in the RV in response to chronic hypobaric hypoxia (CHH) (increased RV mass, function and respiratory capacity) are reversible. To test our hypothesis we exposed male Wistar rats to 3 weeks of CHH and thereafter removed the hypoxic stimulus for 3 and 6 weeks, respectively. Adaptation to 3 weeks of CHH increased the RV to left ventricle (LV) plus interventricular septum ratio by increased (223.5 ± 7.03 vs. 397.4 ± 29.8, p<0.001 versus normoxic controls), indicative of RVH. Hematocrit levels, RV systolic pressure and RV developed pressure (RVDP) were increased in parallel. Mitochondrial respiratory capacity was not significantly altered when using both carbohydrate and fatty acid oxidative substrates. After the 3-week normoxia recovery period, the RV to LV ratio was increased but to a lesser extent compared to the 3-week hypoxic time-point, i.e. 244.7 ± 11.2 vs. 349.64 ± 3.8, p<0.001 versus normoxic controls. Moreover, hematocrit levels were completely normalized. However, the RV systolic pressure and the functional adaptations, i.e. increased RVDP induced by CHH exposure still persisted in the 3-week recovery (3HRe) group. Also, pyruvate utilization was increased versus matched controls (p<0.04 vs. matched controls). Interestingly, we found that at the 6-week recovery time point functional parameters were largely normalized. However, the RV to LV ratio was still increased by 269.3 ± 14.03 vs. 333.9 ± 11.7, p<0.0001 vs. matched controls. Furthermore, palmitoylcarnitine utilization was increased (p<0.03 vs. matched controls). In conclusion, we found that exposure to CHH resulted in various adaptive physiological changes, i.e. enhanced hematocrit levels, increased RV mass linked to greater RV contractility and respiratory function. It is important to note that all these changes only occurred in the RV and not in the LV. Furthermore, when a normoxic recovery period (3 and 6 weeks, respectively) were initiated, these physiological parameters largely normalized. Together, the findings of this thesis clearly show the establishment of a reversible model of RV physiological hypertrophy. Our future work will focus on disrupting signaling pathways underlying this process and to thereafter ascertain whether reversibility is abolished. Elucidation of such targets should provide a unique opportunity to develop novel therapeutic agents to treat patients and thereby reduce the burden of heart disease.