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Dissertations / Theses on the topic 'Heart – Hypertrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.

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2

XU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.

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3

Drawnel, Faye Marie. "Control of myocardial hypertrophic remodelling by integration of calcium signals, kinase cascades and microRNAs." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609969.

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4

Archer, Caroline Rose. "Interactions between GPCR- and growth factor-activated signalling pathways in the induction of cardiac hypertrophy." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648427.

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5

Zhong, Tiecheng. "Ang II-Induced Cardiac Remodeling: Role of PI3-Kinase-Dependent Autophagy." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/28800.

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Heart failure (HF) is a pathological state indicating insufficient blood supply to the peripheral tissues from the heart. The pathophysiology of HF is multifactorial like cardiac remodeling including cardiac hypertrophy, perivascular fibrosis and apoptosis to compensate for the heart?s inability to pump enough blood. Cardiac hypertrophy is initially adaptive to hemodynamic overload; however, it chronically contributes to heart failure and sudden cardiac death. The extracellular regulatory factors and intracellular signaling pathways involved in the cardiac remodeling are not yet fully clear. P

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6

Müller-Brunotte, Richard. "Diastolic heart function in hypertension-induced left ventricular hypertrophy /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-898-3/.

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7

Turner, J. E. "Collagen metabolism in normal heart and during cardiac hypertrophy." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47290.

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8

Loonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.

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p38-mitogen activated protein kinases (p38-MAPKs) are stress activated serine/threonine kinases that are activated during several different cardiac pathologies. Classically, studies have focused solely on p38α signaling in the heart. However, there is also high cardiac expression of the p38γ isoform but little is known about its cardiac function. The aim of this study was to elucidate the signaling pathway of p38γ, with a particular focus on its role in the progression of pathological cardiac hypertrophy. Comparisons of cardiac function and structure of wild type (WT) and p38γ knock out (KO) m

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9

Linehan, Katherine Alison. "Collagen deposition and myocyte hypertrophy in the pressure overloaded heart." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484263.

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10

Benson, Victoria Louise St Vincent's Clinical School UNSW. "The role of calcineurin in high-renin and low-renin animal models of pressure overload left ventricular hypertrophy." Awarded by:University of New South Wales. St Vincent's Clinical School, 2005. http://handle.unsw.edu.au/1959.4/20843.

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Left ventricular hypertrophy (LVH) in response to pressure overload is associated with increased cardiovascular morbidity and mortality, making its prevention an important therapeutic goal. The role of a calcineurin-dependent molecular pathway in the induction of pressure-overload LVH is controversial. The present study tested the hypothesis that, in the setting of LV pressure overload, activation of the systemic renin-angiotensin system was necessary for activation of this calcineurin pathway. Mild LV pressure overload was induced in male Wistar rats by abdominal aortic constriction (AAC) or

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11

Troupes, Constantine. "The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/403786.

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Biomedical Sciences<br>Ph.D.<br>Increases in cardiac afterload caused by disease conditions results in remodeling of heart structure by hypertrophy and alterations in the molecular regulation of contractile performance. These adaptations can be regulated by various Ca2+-dependent signaling processes. STIM1 is an important regulator of Ca2+ signaling in different cell types by sensing endoplasmic reticular Ca2+ levels and coupling to plasma membrane Orai channels. The role of STIM1 in heart is not well understood, given the robust Ca2+ regulatory machinery present within cardiac myocytes. Previ

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12

Long, Meijing, and 龍梅菁. "Prevalence of electrocardiographic abnormalities and the relationship bewtween alcohol use and electrocardiographic-left ventricularhypertrophy in older Chinese people: theGuangzhou biobank cohort study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45789642.

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13

Railson, Julia Elizabeth. "Protective and hypertrophic effects of cardiotrophin-1 in the heart." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341140.

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14

Cloete, Ruben Earl Ashley. "Investigations of Renin-Angiotensin Aldosterone System (RAAS) genes in hypertrophy in hypertrophic cardiomyopathy (HCM) founder families." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/21880.

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Thesis (MScMed)--Stellenbosch University, 2008.<br>ENGLISH ABSTRACT: In hypertrophic cardiomyopathy (HCM), an autosomal dominant disorder, hypertrophy is variable within and between families carrying the same causal mutation, suggesting a role for modifier genes. Associations between left ventricular hypertrophy and left ventricular pressure overload suggested that sequence variants in genes involved in the Renin-Angiotensin Aldosterone System (RAAS) may act as hypertrophy modifiers in HCM, but some of these studies may have been confounded by, amongst other things, lack of adjustment for

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15

Esfandiary, Azadeh [Verfasser]. "Role of uncoupling protein 2 in right heart hypertrophy / Azadeh Esfandiary." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1176965700/34.

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16

Jamshidi, Yalda. "Role of PPAR#alpha# in coronary heart disease and cardiac hypertrophy." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252393.

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17

Yang, Hsiang-Yu. "Sex differences in the progression from cardiac hypertrophy towards heart failure." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/54771.

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This thesis aims to investigate differential changes in Ca2+ and Na+ regulation during the development from cardiac hypertrophy to heart failure (HF) between sexes. Clinical evidences show females are more resistant to the development of cardiac hypertrophy and have better survival in HF than males. Oestrogen is postulated to provide cardioprotection although this is still under debate. This work used guinea pigs (GPs), a species with electrophysiology akin to human, that were subjected to aortic constriction (AC) to study the progression from pressure-overload cardiac hypertrophy to HF betwee

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18

Saeedi, Ramesh. "AMP-activated protein kinase and hypertrophic remodeling of heart muscle cells." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/4065.

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Introduction: Cardiac hypertrophy is an adaptive response to increased myocardial workload that becomes maladaptive when hypertrophied hearts are exposed to an acute metabolic stress, such as ischemia/reperfusion. Acceleration of glycolysis occurs as part of the hypertrophic response and may be maladaptive because it enhances glycolytic metabolite accumulation and proton production. Activation of AMP-activated protein kinase (AMPK), a kinase involved in the regulation of energy metabolism, is proposed as a mechanism for the acceleration of glycolysis in hypertrophied hearts. However, this conc

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19

Li, Qiong. "Factors contributing to the development of cardiac hypertrophy : calcineurin dependent pathway /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19384.pdf.

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20

Davies, Elizabeth Louise. "The role of mitogen-activated protein kinase phosphatase-1 in cardiac hypertrophy." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391714.

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21

Kato, Takao. "Analysis of Metabolic Remodeling in Compensated Left Ventricular Hypertrophy and Heart Failure." Kyoto University, 2010. http://hdl.handle.net/2433/120921.

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22

Lee, G. R. "Alterations in endothelin receptor subtypes in the pathogenesis of hypertension induced ventricular cell hypertrophy." Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246339.

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23

Sneddon, Kenneth Paxton. "Dispersion of repolarisation and refractoriness induced by amiodarone, d-sotalol, myocardial ischaemia and hypertrophy." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300739.

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24

Lygate, Craig Alexander. "Comparative studies in experimental hypertension and cardiac failure." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312137.

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25

Rostami, Maryam. "A proposed pathophysiological role for TNFa in obesity induced cardiac hypertrophy." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/70077.

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The a of TNFa in title is the Greek alpha.<br>Thesis (MSc)--University of Stellenbosch, 2002.<br>ENGLISH ABSTRACT: Background: Cardiac hypertrophy is an adaptive process occurring in response to mechanical overload or tissue injury. The stimuli for cardiac hypertrophy are diverse and vary from increased afterload on the heart to cardiac remodeling in response to cytokines. Amongst others, obesity is characterized by excessive body weight resulting in metabolic disorders. This excess body weight necessitates an increased blood and oxygen delivery to the peripheral tissues, which is achiev

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26

Barr, Larry A. "The Role of Calcium in the Regulation of Pathological Hypertrophy." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/254617.

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Physiology<br>Ph.D.<br>Pathological hypertrophy leads to cardiac dysfunction and heart failure. It is not clearly defined how this process occurs in the cardiomyocyte, or how the pathology can be effectively treated. There are numerous processes that lead to pathological hypertrophy. We developed two models to study pathological hypertrophy and the role that Ca2+ plays. In one model, we administered clinical doses of the leukemia therapeutic drug imatinib to neonatal ventricular cardiomyocytes. This drug has recently been found to be cardiotoxic, and we set out to understand if Ca2+ is involve

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27

Bartoli, Fiona. "Le canal calcique Orai1 : nouvel acteur impliqué dans la physiopathologie cardiaque." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS027.

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Alors que l’entrée SOC (store-operated Ca2+ entry) portée par les canaux calciques TRPCs (transient receptor potential canonical) et Orai1 est essentielle dans les cellules non-excitables, son rôle physiologique dans les cardiomyocytes adultes reste à élucider. Néanmoins, il est largement admis qu’une entrée SOC exacerbée dépendante des canaux TRPCs et de la protéine régulatrice STIM1 participe à la pathogenèse de l’hypertrophie et de l’insuffisance cardiaque (IC) par induction de voies pro-hypertrophiques telles que la CaMKII (Ca2+/calmoduline-dépendante kinase II ) et la calcineurine (CaN)/N

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28

Carstens, N. "The role of renin-angiotensin-aldosterone system (RAAS) genes in the development of hypertrophy in hypertrophic cardiomyopathy (HCM)." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/2667.

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Thesis (MScMedSc (Biomedical Sciences. Molecular Biology and Human Genetics))--University of Stellenbosch, 2009.<br>Hypertrophic cardiomyopathy (HCM), an inherited primary cardiac disorder mostly caused by defective sarcomeric proteins, is considered a model for studying left ventricular hypertrophy (LVH) in the absence of increased external loading conditions. The disease manifests extreme variability in the degree and pattern of LVH, even in HCM patients with the same causal mutation. The clinical phenotype of HCM can therefore be viewed as a product of the effect of sarcomere dysfuncti

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29

Egdell, Robin Michael. "Arrhythmogenic phenomena in isolated cardiac myocytes." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322380.

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30

Shook, Paige, Dr Suman Dalal, Dr Mahipal Singh, and Dr Krishna Singh. "Long-Term Cardioprotective Potential of Exogenous Ubiquitin in the Treatment of Post-Myocardial Ischemia/Reperfusion Injury of the Heart." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/12.

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Background: Heart attack or myocardial infarction (MI) is a major cause of death worldwide. MI is generally attributed to the detrimental effects of myocardial ischemia/reperfusion (I/R) injury. I/R injury induces cell death and reduces heart function. To compensate, the heart remodels with an associated increase in cell death, fibrosis, and hypertrophy, which can further compromise heart function. Ubiquitin (UB) is an evolutionarily conserved protein. Our lab has shown that pre-I/R injury treatment with exogenous UB preserves heart function and reduces fibrosis 3-days post-I/R in mice. A majo

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31

Stafford, Nicholas Pierre. "The independent roles of PMCA1 and PMCA4 in the development and progression of left ventricular hypertrophy and failure." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/the-independent-roles-of-pmca1-and-pmca4-in-the-development-and-progression-of-left-ventricular-hypertrophy-and-failure(bd746ae0-8189-433a-8a0e-ecb4506afe62).html.

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Heart failure is responsible for one in twenty deaths in the UK, and as the average age of the general population increases that number is predicted to rise over the coming years. Hypertrophic growth is believed to be an adaptive response to a chronic increase in workload under circumstances such as hypertension, yet it is also known to contribute to the pathological progression into heart failure. Abnormal calcium handling is known to play a critical role in determining disease progression, not only through its function as the driving force behind myocardial contraction and relaxation but als

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32

Cullen, John Patrick. "Receptor subtypes and associated mechanisms in the stimulation of ventricular cell hypertrophy by angiotensin II and endothelin-1." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287435.

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33

Todd, Carol. "Identification of novel sarcomeric modifiers of hypertrophy in hypertrophic cardiomyopathy using the yeast two-hybrid system." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79819.

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Thesis (MScMedSc)--Stellenbosch University, 2013.<br>ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) occurs when the cardiomyocytes in the left ventricle become enlarged by increasing in mass in response to haemodynamic pressure overload. This can either be attributed to a normal physiological response to exercise or can be the result of a maladaptive process or disease state, such as chronic hypertension. Hypertrophic cardiomyopathy (HCM) is the most common form of Mendelian-inherited cardiac disease. A defining characteristic thereof is primary LVH that occurs when there are no other hy

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34

Matrone, Gianfranco. "Role of cyclin-dependent Kinase 9 in the zebrafish embryonic heart." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/11820.

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Cardiac hypertrophy leading to heart failure remains a leading cause of morbidity and mortality in the 21st century despite major therapeutic advances. Improved understanding of novel molecular and cellular processes contributing to cardiac hypertrophy therefore continues to be important. Cyclin-dependent Kinase 9 (CDK9), part of a family of proteins controlling cell cycle and growth, has emerged as one such potential candidate over the last 5 years. CDK9 is the catalytic subunit of the CDK9/CyclinT complex and acts by phosphorylating the carboxy-terminal domain of RNA polymerase II. Hypertrop

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35

Whitcomb, Elizabeth Jamieson. "Identification of GATA4 Regulatory Mechanisms of Heart Development and Disease." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38830.

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The development and function of the heart is governed by a conserved set of transcription factors (TFs) that regulate gene expression in a cell-type, time point and stimulus driven manner. Of these core cardiac TFs, the most ubiquitously expressed is the zinc finger protein GATA4. In cardiomyocytes, GATA4 is central to proliferation, differentiation, hypertrophy and induction of pro-survival pathways. In cardiac endothelial cells, it is required for valve and septal development, although the exact mechanisms remain unclear. To regulate such a wide array of functions in a spatially and temporal

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36

Philips, Alana Sara Clinical School St George Hospital Faculty of Medicine UNSW. "Molecular insights into the biological role / mechanisms of GATA-4 and FOG-2 in normal cardiac function and in cardiac hypertrophy." Awarded by:University of New South Wales, 2007. http://handle.unsw.edu.au/1959.4/36772.

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The regulation of cardiac-specific genes such as GATA-4 and its co-factor FOG-2 is paramount for normal heart development and function. Indeed, those mechanisms that regulate GATA-4 and FOG-2 function, such as nuclear transport and the post-translational modification of SUMOylation, are of critical importance for cardiogenesis. Therefore the aims of this study were to: i) elucidate the nuclear transport mechanisms of GATA-4; ii) determine the function of SUMOylation on the biological activity of both GATA-4 and FOG-2; and iii) examine how these mechanisms impact on the role of GATA-4 and FOG-2

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37

Davey, Patrick Paul. "A clinical and experimental study of myocardial repolarisation in left ventricular hypertrophy and heart failure." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299520.

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38

Omede, Ameh. "Role of alpha-ketoglutarate receptor G-protein coupled receptor 99 (GPR99) in cardiac hypertrophy." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/role-of-alphaketoglutarate-receptor-gprotein-coupled-receptor-99-gpr99-in-cardiac-hypertrophy(83b04dba-5bfe-4623-ade1-12c779133b80).html.

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Cardiac hypertrophy and heart failure (HF) remains one of the major health problems in the UK and worldwide. However, advances in their management are limited because the underlying pathological mechanisms are not completely understood. Therefore, it is important to understand novel signalling pathways leading to HF. Myocardial hypertrophy is a crucial pathophysiological process that can lead to the development of HF. Signalling initiated by members of G-protein-coupled receptors (GPCRs) proteins plays an important role in mediating cardiac hypertrophy. One member of this family, the G-protein

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39

Hautala, N. (Nina). "The mechanisms involved in the activation of transcription factors and BNP gene expression in loaded heart." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514265327.

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Abstract Cardiac hypertrophy is an adaptive response of the heart to a variety of mechanical, hemodynamic, neurohumoral, and pathologic stimuli. Prolonged pathophysiological load leads to development of left ventricular hypertrophy and ultimately to heart failure. The natriuretic peptides including the B-type natriuretic peptide (BNP) provide the physiological feedback mechanism to suppress the load signal. The aim of the present study was to evaluate the cis elements within the BNP promoter that mediate the cardiac load responses in vivo, and to study the involvement of paracrine fac

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40

Badrian, Bahareh. "Evaluation of the consequences of ERK and STAT3 activation in the heart." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0027.

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[Truncated abstract] The enlargement of the heart, also known as myocardial hypertrophy, is thought to be a compensatory process that maintains the mechanical function of the heart in response to stress factors such as pressure or volume overload. Although this process is initially compensatory, it frequently results in heart failure and death. Cardiac hypertrophy is a complex process involving changes in the individual cardiac muscle cells, cardiac myocytes. As well as the morphological changes that result from hypertrophy, there are molecular changes within each cell that regulate the hypert

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41

Dyukova, Elena [Verfasser]. "The calcium-sensing receptor in heart physiology and development of endothelin-1-dependent hypertrophy / Elena Dyukova." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1144148111/34.

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42

Jin, Jiawei. "Signalling regulation of cardiac hypertrophy by the mitogen activated protein kinase (MAPK) pathways." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/signalling-regulation-of-cardiac-hypertrophy-by-the-mitogen-activated-protein-kinase-mapk-pathways(028e5785-b25f-4459-9668-ad13a2885a40).html.

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Heart failure induced by cardiac hypertrophy is a cause of high mortality in the world and has been the fastest growing cardiovascular disease over the past decade. Cardiac hypertrophy is characterised as a reactive increase in cardiac mass growth with a complex of ventricular remodelling. It occurs initially as a compensatory response to an increased workload but eventually leads to cardiac dysfunction. An in-depth understanding of cardiac hypertrophy and the capacity to regulate it has profound clinical implications. The MAPK pathways provide an important connection between external stimuli

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43

Handa, Nobuhiro. "Quantitative myocardial FDG uptake by positron emission tomography in rat heart and its application for longitudinal multiple studies in progressive hypertrophy of heart model." Kyoto University, 2008. http://hdl.handle.net/2433/135924.

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44

Marck, Pauline. "Rôle de la triadine dans le développement de l'insuffisance cardiaque." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05S018/document.

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L’insuffisance cardiaque (IC) est une cause majeure de mortalité dans les pays industrialisés. Ce syndrome est le résultat de nombreuses maladies cardiaques qui induisent dans un premier temps un remodelage adaptatif du myocarde : l’hypertrophie du ventricule gauche (HVG). Dans le cœur, le calcium libéré à partir du réticulum sarcoplasmique (RS) est à l’origine de la contractilité. Ce mécanisme est contrôlé par un macro-complexe moléculaire, composé du récepteur de la ryanodine (RyR2), et de protéines stabilisatrices associées dont la junctine (JCN), la calséquestrine (CSQ2), et la triadine (T

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45

Lalonde, Julie Kathleen. "TC10, a mammalian Rho GTPase responsible for actin cytoskeleton reorganization and cardiac hypertrophy in the murine heart." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26507.

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Rho guanosine triphosphatases (GTPases) act as molecular switches, cycling between two conformational states: an active, GTP-bound state and an inactive, GDP-bound state to control many complex cellular events in eukaryotic cells. Many Rho GTPases, including RhoA, Cdc42 and Rac1, have been extensively characterized and are involved in actin reorganization, activation of MAPK cascades, cell cycle progression, cellular proliferation, invasion, differentiation and apoptosis. TC10 was identified and classified as a Rho GTPase over ten years ago, however the precise role of this protein, which is h

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46

Löser, Alexandra [Verfasser], and Elke [Akademischer Betreuer] Oetjen. "Epigenetic mechanisms of transcriptional regulation in cardiac hypertrophy using engineered heart tissue / Alexandra Löser ; Betreuer: Elke Oetjen." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1175584738/34.

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47

Mahmod, Masliza. "Multiparametric cardiovascular magnetic resonance for the assessment of cardiac function and metabolism in hypertrophy and heart failure." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:ff24c167-e00d-4c6d-9809-82203979ba7a.

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Both hypertrophied and failing hearts are characterised by pathological left ventricular (LV) remodelling, impaired myocardial energy status and alteration in substrate metabolism. Cardiac magnetic resonance imaging (CMR) and magnetic resonance spectroscopy (MRS) are powerful tools in the characterisation of these disease conditions. More recent techniques have allowed assessment of myocardial steatosis using <sup>1</sup>H-MRS and tissue oxygenation using blood oxygen level dependent (BOLD) CMR. In hypertrophy and heart failure, studies on steatosis and the relationship with other parameters s

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48

Segun, Utomi Victor. "The 'athletic heart' : insights from modern imaging tools in Caucasian and West African athletes." Thesis, Liverpool John Moores University, 2015. http://researchonline.ljmu.ac.uk/4557/.

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A seminal study by Morganroth et al (1975) demonstrated a differential pattern of cardiac adaptation with prolonged exercise training; of eccentric pattern of left ventricular hypertrophy (LVH) in endurance trained athletes (ET) and concentric LVH in resistance trained athletes (RT). Specific inconsistencies related to the nature of any adaptation to RT; the value of new imaging technologies; the relative importance of scaling of cardiac data for differences in body size; the impact of training on the right ventricle (RV) and the fit of differential pattern of adaptation in athletes with Black

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49

Ng, Dominic Chi Hiung. "Characterizing intracellular signaling mechanisms involved in the progression of cardiac hypertrophy and failure : involvement of JAK/STAT and MAPK pathways." University of Western Australia. Biochemistry and Molecular Biology Discipline Group, 2003. http://theses.library.uwa.edu.au/adt-WU2003.0032.

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[Truncated abstract] The innate ability of the heart to compensate for an increase in workload as a result of disease or injury, through an increase in size and mass is known as cardiac hypertrophy. The hypertrophy of the heart compensates for an increase in workload with an increase in cardiac output. However, excessive hypertrophy can result in cardiac dysfunction and substantially increases the risk of cardiac failure and mortality. The molecular mechanisms that regulate the development of cardiac hypertrophy and cardiac failure are not entirely understood. Traditionally, the G-protein Cou

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50

Ashrafian, Houman. "The role of PGC-1a in the transcriptional regulation of energy homeostasis in cardiac hypertrophy and heart failure." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504288.

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