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Dissertations / Theses on the topic 'Hypertrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Bloem, Liezl Margaretha. "Sarcomeric modifiers of hypertrophy in hypertrophic cardiomyopathy (HCM)." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79795.

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Thesis (PhD)--Stellenbosch University, 2013.<br>ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular morbidity and allcause mortality. Significantly, it is considered a modifiable cardiovascular risk factor as its regression increases overall survival and reduces the frequency of adverse cardiac events. A clear understanding of LVH pathogenesis is thus imperative to facilitate improved risk stratification and therapeutic intervention. Hypertrophic cardiomyopathy (HCM), an inherited cardiac disorder, is a model disease for elucidating the mole

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2

Soana, valentina. "Ornamental Hypertrophy." Thesis, KTH, Arkitektur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-35924.

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The thesis is exploring the potential of the ornament conceived as inhabitable space, exuberant, blissfull in opulence, flamboyant. The coexistence of opposite elements sensations that are overlapping, intertwining and blurring, generates a space that breathes, perspires and froths, exceeding in its blossom.

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3

Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.

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Abstract :Cardiac hypertrophy has been identified as the most important independent risk factor for cardiovascular-related morbidity and mortality and is therefore regarded as a pathological condition. Despite this, beneficial physiological forms also appear to exist, such as in response to exercise, leading to maintained or improved cardiac function. The aim of this thesis was to examine two distinct rodent models, an endurance run-trained rat, and the DOCA-salt hypertensive rat, representing physiological and pathological hypertrophy, respectively, in order to develop a better understanding

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4

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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5

Clarke, Samantha Jayne. "Biochemical adaptations in cardiac hypertrophy." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395503.

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6

Tsang, K. K. "Screening for benign prostatic hypertrophy." Thesis, University of Edinburgh, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663068.

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Benign prostatic hypertrophy (BPH) is a very common disease among men aged 50 and its economic burden on health services continues to grow. The advocation for adopting new screening procedure for BPH begins to emerge. However, a new proposal for screening should be under careful scrutiny and ineffective and inappropriate screening must be avoided. A prospective cohort study has been launched to study the frequency, distribution, and natural history of BPH in two well-defined small communities in Central Scotland. Using the data from the cohort study, the hypothesis that a BPH screening program

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7

Risto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.

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Duchenne Muscular Dystrophy (DMD) is an X-linked disorder, caused by mutations in the DMD gene. This gene encodes dystrophin, a structural protein that links the sarcomere to the extracellular matrix via a trans-membrane protein complex. In the absence of dystrophin the associated glycoprotein complex fails to assemble, leading to sarcolemmal instability, impaired ion handling, skeletal muscle wasting and fibrosis. Patients become non-ambulant in their teens and seldom live past their third decade. Cardiac failure is one of the leading causes of death. The heart initially compensates for reduc

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8

Schans, Veerle Anna Maria van de. "Wnt signaling and cardiac hypertrophy." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=14684.

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9

Stone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4532.

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10

Stone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/4544.

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11

Stone, Michael H. "Development of Skeletal Muscle Hypertrophy." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4579.

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12

RIVERA, NATALIA V. "GENETICS OF LEFT VENTRICULAR HYPERTROPHY." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169564.

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High blood pressure makes the heart work harder and promotes enlargement of the left ventricle, left ventricular hypertrophy (LVH), which is an important risk factor for cardiovascular disease and death. LVH is characterized for the most part by two different sets of observable characteristics (genetic phenotypes): an enlarged left ventricle (1) due to increasing wall thickness and (2) due to increasing wall dilation. The molecular and pathological mechanisms by which either phenotype occurs is unknown. We do know, however, that both phenotypic variations of LVH are determined by quantitat

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13

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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14

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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15

Akki, Ashwin. "Lipid overload studies in cardiac hypertrophy." Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441778.

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16

Wallis, William Richard James. "The cellular pathophysiology of myocardial hypertrophy." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265997.

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17

Howell, Neil John. "Metabolic support in left ventricular hypertrophy." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1492/.

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Aims: To examine the metabolic changes associated with LVH secondary to AS, to examine the role of GIK as an adjunct to myocardial protection during AVR, and to examine the mechanism of its action. Methods: 220 patients with LVH secondary to AS were randomised 1:1 to receive an infusion of GIK at the time of AVR. The primary endpoint of the trial was incidence of low cardiac output state. At pre-specified time points, biopsies of the LV anterior wall were taken for analysis of metabolic changes associated with LVH, and changes in the phosphorylation state of proteins identified as key regulato

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18

Philipot, Didier. "Implication du miR-24 et du miR-199a-5p dans le vieillissement prématuré du chondrocyte au cours de l'arthrose." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T015/document.

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L'arthrose tardive est la plus répandue des maladies ostéo-articulaires dont la prévalence augmente avec l'âge. Dans le cartilage arthrosique, des changements spécifiques des chondrocytes s'opèrent. Ils présentent une diminution de leur propriété de synthèse de la matrice extracellulaire, une diminution de leur réponse aux facteurs de croissance anabolisants et une augmentation de la sénescence cellulaire. Elle est caractérisée par un arrêt irréversible du cycle cellulaire, une érosion des télomères, une activation de la voie de dommages à l'ADN (ATM/p53/p21), une activation de la voie p16INK4

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19

Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.

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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Dete

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20

Crampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.

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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Dete

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21

Evaristi, Maria Franscesca. "New biomarkers and therapeutic targets in left ventricular hypertrophy." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30047.

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L'hypertrophie ventriculaire gauche (HVG) est un remodelage prédicteur du développement d'une insuffisance cardiaque et de la mortalité cardiovasculaire. L'hypertension artérielle est une cause majeure de l'HVG, puisque 30% des patients hypertendus développent une HVG. Un dépistage biologique précoce de l'HVG post hypertensive permettrait d'optimiser la prise en charge des patients et d'empêcher que l'HVG évolue vers l'insuffisance cardiaque. L'utilisation de biomarqueurs est un outil rapide, efficace et peu couteux pour le diagnostic de nombreuses pathologies. Dans la pratique clinique il n'e

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22

SASANO, Chieko, Mahmud UZZAMAN, Luni EMDAD, et al. "Dephosphorylation of Connexin43 Associated with Ventricular Hypertrophy." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2800.

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23

Aro, J. (Jani). "Novel load-inducible factors in cardiac hypertrophy." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212173.

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Abstract Cardiac hypertrophy is an adaptive response to increased cardiac workload. It is initially beneficial, since it helps to maintain cardiac output, but ultimately it is considered as an independent predictor for heart failure and sudden cardiac death. The cardiac hypertrophic response is triggered by mechanical and neurohumoral stimuli and is associated with the activation of complex changes in gene programming and intracellular signaling pathways. The purpose of this study was to investigate the expression of some novel load-induced factors i.e. melusin, thrombospondin (TSP)-1 and -4 a

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24

Sin, Yuan Yan. "The roles of HSP20 in cardiac hypertrophy." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3581/.

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Cardiac hypertrophy often develops to compensate for hemodynamic overload and is associated with heart failure. Recent studies have revealed that overexpression and PKA-mediated phosphorylation of heat shock protein 20 (HSP20) at Ser16 can attenuate hypertrophic growth of cardiomyocytes and trigger cardioprotective functions following sustained β-adrenergic stimulation (Fan et al., 2004, 2005, 2006). However, the molecular mechanism of HSP20 induced cardioprotection remains to be fully elucidated. In order to gain insight into the protective mode of action of HSP20, I attempted to (1) investig

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25

Butler, Thomas J. "Impact of dietary manipulation on cardiac hypertrophy." Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:15371.

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Left ventricular hypertrophy (LVH) is a significant risk factor for the development of heart failure (HF), the incidence of which is increased by obesity. Diets high in fat and sugar have been linked with the development of the metabolic syndrome and obesity, and may expose the heart to a unique environment via the differential actions of dietary macronutrients. The main objectives of this study were to determine the effect of differing dietary regimens upon (i) the progression of LVH and whole organism morphology (ii) function and metabolism in the hypertrophied heart, and (iii) cardiac ceram

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26

Lozar, Olivia Mae. "Does Proteasome Activity Impact Skeletal Muscle Hypertrophy?" University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1576264202406223.

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27

Shirazi, Farshad 1963. "Metabolic aspects of neonatal rat cardiomyocyte hypertrophy." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282447.

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The consensus view is that cardiac hypertrophy is an adaptive response to increased work caused by a variety of stimuli. While hypertrophy can be defined as an increase in cell mass without an increase in cell number, not all increases are equivalent in type and amount of protein accumulated. Our goal in this study was to identify the common steps in the process of cardiac hypertrophy. Our working hypothesis was that in all forms of cardiac hypertrophy glucose utilization increases and that the percentage of energy derived from fatty-acid oxidation decreases. The first part of this study entai

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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

Voigt, Christian [Verfasser]. "Early Segmental Relaxation Abnormalities in Hypertrophic Cardiomyopathy for Differential Diagnostic of Patients with Left Ventricular Hypertrophy / Christian Voigt." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2021. http://d-nb.info/1238231098/34.

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30

Gondran, Tellier Victor. "Étude du rôle des protéines GASP dans le développement musculaire par des approches in vivo et de prédiction in silico." Thesis, Limoges, 2016. http://www.theses.fr/2016LIMO0099/document.

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La masse musculaire est largement régulée par des voies de signalisation contrôlant l'équilibre entre la synthèse et la dégradation des protéines myofibrillaires. Ainsi, la myostatine, membre de la superfamille des TGFβ, cible un certain nombre de réseaux de signalisation impliqués dans la régulation de la masse musculaire, notamment la voie de signalisation Akt/mTOR. La myostatine est un des inhibiteurs majeurs de la myogenèse en exerçant un contrôle négatif sur la prolifération et différenciation des myoblastes. A l’heure actuelle, la myostatine est au centre de nombreuses stratégies thérape

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31

Pearson, David R. "Comparison of isotonic and isokinetic work induced hypertrophy as evaluated by computed tomography." Virtual Press, 1987. http://liblink.bsu.edu/uhtbin/catkey/487144.

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Six male subjects (26.0+3.1 years), performed an exercise regimen of repeated knee extension exercises in an attempt to induce size and strength changes in the quadriceps muscle (thigh). Their left thigh was trained using an isotonic (IST) lifting protocol and the right thigh was trained using an isokinetic (ISK) device. The total amount of torque produced by each protocol was the same and knee extensions were performed at a common velocity (120 deg/sec). Training was performed 3 days per week for a period of 8 weeks. Data were presented as means (±SD) for pre-and post-training values with a l

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32

Movahed, Mohammad, Deborah Strootman, Sharon Bates, and Sudhakar Sattur. "Prevalence of suspected hypertrophic cardiomyopathy or left ventricular hypertrophy based on race and gender in teenagers using screening echocardiography." BioMed Central, 2010. http://hdl.handle.net/10150/610116.

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BACKGROUND:The goal of this study was to evaluate the prevalence of suspected hypertrophic cardiomyopathy (HCM) in a population of teenagers undergoing screening echocardiography for the detection of HCM.METHOD:The Anthony Bates Foundation performs screening echocardiography for the prevention of sudden death. A total of 2,066 students were studied between the ages of 13 to 19 years. Suspected HCM was defined as any wall thickness greater than or equal to] 15 mm. LVH was defined as wall thickness greater than or equal to] 13 mmRESULTS:Prevalence of suspected HCM was 0.7% (14/2066). After adjus

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33

Schnell, Frédéric. "Hypertrophie ventriculaire gauche physiologique ou pathologique : Intérêt d’une approche multiparamétrique." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B021/document.

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Introduction : Le diagnostic de cardiomyopathie hypertrophique (CMH) est difficile chez l’athlète. En effet, le remodelage physiologique induit par l’entraînement physique intense entraîne des modifications électriques et morphologiques qui peuvent mimer une cardiomyopathie. Or il est indispensable de poser le diagnostic de cardiomyopathie avec certitude chez un athlète. Ne pas contre-indiquer un athlète avec une cardiomyopathie l’expose à un risque de mort subite, mais poser un diagnostic par excès l’expose à de lourdes répercussions tant professionnelles que sociales. Méthodes : (1) Nous avo

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34

Sundström, Johan. "Left ventricular hypertrophy and the insulin resistance syndrome." Doctoral thesis, Uppsala University, Department of Public Health and Caring Sciences, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-580.

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<p>Left ventricular hypertrophy (LVH) and the insulin resistance syndrome are common conditions associated with a markedly increased cardiovascular risk. In a fairly large prospective longitudinal study of men from the general population, we found that an unfavorable serum fatty acid profile and components of the insulin resistance syndrome such as dyslipidemia, obesity and hypertension at age 50 predicted the prevalence of LVH at age 70. In cross-sectional analyses at age 70, several components of the insulin resistance<sup> </sup>syndrome were significantly related to left ventricular relati

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35

Gennebäck, Nina. "Cardiac hypertrophy : transcription patterns, hypertrophicprogression and extracellular signalling." Doctoral thesis, Umeå universitet, Medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-59470.

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Background: The aim of this thesis was to study transcription patterns and extracellular signalling of the hypertrophic heart to better understand the mechanisms initiating, controlling and maintaining cardiac hypertrophy. Cardiac hypertrophy is a risk factor for cardiovascular morbidity and mortality. Hypertrophy of the myocardium is a state, independent of underlying disease, where the myocardium strives to compensate for an increased workload. This remodelling of the heart includes physiological changes induced by a changed gene expression, alteration of the extracellular matrix and diverse

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36

Sundström, Johan. "Left ventricular hypertrophy and the insulin resistance syndrome /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4919-0/.

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37

Silberberg, Jonathan S. "Left ventricular hypertrophy in end-stage renal disease." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61836.

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38

Braga, Luca. "Identification and characterization of MicroRNAs modulating cardiac hypertrophy." Thesis, Open University, 2017. http://oro.open.ac.uk/51095/.

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The adult heart is capable of remodelling in response to different pathological stimuli; in most cases, a phase of compensated hypertrophy evolves into frank dysfunction and heart failure. To identify microRNAs able to prevent cardiac hypertrophy and preserve cardiac function, we performed a high-content microscopy, high-throughput functional screening for human microRNAs able to reduce neonatal cardiomyocyte (CM) cell size using a whole-genome microRNA library. The most effective anti-hypertrophic microRNA was hsa-miR-665. In a model of transverse abdominal aortic constriction (TAC) in 8 week

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39

Sayeed, Rana Ahmed. "Patterns of ion channel expression in cardiac hypertrophy." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616262.

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40

Richardson, Simon. "Studies of ischaemia and reperfusion in cardiac hypertrophy." Thesis, University of Hull, 2002. http://hydra.hull.ac.uk/resources/hull:13202.

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Cardiac hypertrophy may be associated with an enhanced susceptibility to ischaemic/reperfusion injury but the mechanisms remain unresolved. There is evidence for an increased dependence on glucose metabolism in cardiac hypertrophy, which may be beneficial in normoxia but detrimental in ischaemia. The role of glycogen, the major endogenous substrate during ischaemia, to the enhanced susceptibility of the hypertrophied heart to ischaemic/reperfusion injury is unclear. Work in this thesis investigates the role of glycogenolysis to the severity of ischaemia, and assesses oxidative substrate utilis

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41

Woltz, John W. "Cardiovascular Risk and Left Ventricular Hypertrophy in Firefighters." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367940479.

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42

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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Patel, Parth Mahendra, and Parth Mahendra Patel. "Deciphering the Role of FXR1 in Cardiac Hypertrophy." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625115.

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Rationale: Cardiac hypertrophy is the enlargement of the heart and can be induced by pathological and non-pathological events. The Fragile X family of RNA-binding proteins have been shown to be involved in cardiac structure and development (Mientjes et al, 2004) (Padje et al, 2009). Potential links between FXR1 and hypertrophy have not been significantly studied. Objective: To study the effect that varying expression of FXR1 has upon hypertrophy, and the molecular role FXR1 plays in hypertrophy. Method and Results: Following a voluntary running protocol, FXR1 wild-type mice had significant car

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44

Davies, Justin Edgar Rees. "Coronary haemodynamics in hypertension and left ventricular hypertrophy." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7793.

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The coronary blood flow waveform is unique, being determined by simultaneous changes in pressure originating at either end of the coronary artery. However, by measuring the coronary pressure waveform alone, it is not possible to separate the pressure contributions originating from the coronary microcirculation from those originating in the aorta. In this thesis wave intensity analysis was applied to unobstructed human coronary arteries to separate the contributions originating in the coronary microcirculation from those originating in the aorta, in subjects with and without left ventricular hy

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45

Chang, Ching-Jey George. "Prostate, benign hypertrophy and prostatic carcinoma - a study of cell biology of prostate and chemotherapy for prostatic hypertrophy and prostatic cancer /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487856906256116.

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46

Gerhardt, Florian. "Einfluss einer 24-stündigen Behandlung von ventrikulären neonatalen Kardiomyozyten mit einem Adipozyten-konditionierten Medium auf Hypertrophie-assoziierte Signalwege und Zellproteine." Doctoral thesis, Universitätsbibliothek Leipzig, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-224990.

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Die weltweite Zunahme der Prävalenz von Übergewicht und Adipositas und den damit verbundenen medizinischen und sozioökonomischen Herausforderungen stellt eine der wesentlichen Herausforderungen der modernen medizinischen Versorgung dar. Im Mittelpunkt stehen dabei insbesondere die Auswirkungen von Übergewicht und Adipositas auf das kardiovaskuläre System und den damit verbundenen funktionellen und strukturellen Veränderungen der kardiovaskulären Funktion. Als Mediatoren dieser funktionellen und strukturellen Veränderungen stehen dabei zunehmend Adipozytokine im Interesse wissenschaftlicher Arb

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Al, Jaam Bilal. "Aspects biochimiques et cellulaires de la dérégulation du processus myogénique chez des souris hypomorphes pour le gène Pofut I." Thesis, Limoges, 2016. http://www.theses.fr/2016LIMO0086/document.

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La croissance musculaire postnatale chez la souris s’effectue principalement par une hypertrophie et un allongement des fibresmusculaires. L’augmentation de l’aire des fibres est contrôlée par plusieurs voies de signalisation telle que la voie Notch, qui est impliquée dans l’activation des cellules satellites (CS) en début de croissance musculaire postnatale chez la souris. La O-fucosylation, médiée par la protéine O-fucosyltransférase 1 (POFUT1), des répétitions EGF-like de la partie extracellulaire des récepteurs NOTCH joue un rôle déterminant dans la modulation des interactions récepteur-li

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48

Orlando, Silvia. "DIFFERENTIATION BETWEEN HYPERTROPHIC CARDIOMYOPATHY AND HYPERTENSIVE LEFT VENTRICULAR HYPERTROPHY: THE ROLE OF STRAIN RATE IMAGING STUDY AND INTEGRATED BACKSCATTER ANALYSIS." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3426557.

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Background: To date, any non-invasive technique is satisfactory to differentiate Hypertrophic Cardiomyopathy (HCM) from hypertensive left ventricular hypertrophy (H-LVH). We hypothesized that in HCM the presence of local peculiar tissue abnormalities results in the significant impairment of the regional systolic deformation and myocardial reflectivity, even if global function appears normal. Methods: Twenty non-obstructive HCM patients, 20 age- and gender-matched hypertensive patients (HTN) and 15 healthy volunteers (NTN) underwent grey-scale and tissue Doppler ultrasound imaging from three

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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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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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