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Bloem, Liezl Margaretha. "Sarcomeric modifiers of hypertrophy in hypertrophic cardiomyopathy (HCM)". Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79795.
Pełny tekst źródłaENGLISH 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 molecular mechanisms underlying LVH development. LVH, in the absence of increased external loading conditions, is its quintessential clinical feature, resulting from mutations in genes encoding sarcomeric proteins. The LVH phenotype in HCM exhibits marked variability even amongst family members who carry the same disease-causing mutation. Phenotypic expression is thus determined by the causal mutation and additional determinants including the environment, epigenetics and modifier genes. Thus far, factors investigated as potential hypertrophy modifiers in HCM have been relatively removed from the primary stimulus for LVH; and the few studies that have been replicated yielded inconsistent results. We hypothesized that the factors that closely interact with the primary stimulus of faulty sarcomeric functioning, have a greater capacity to modulate it, and ultimately the LVH phenotype in HCM. Plausible candidate modifiers would include factors relating to the structure or function of the sarcomere, including known HCM-causal genes; and the enzymes that function in sarcomere-based energetics. Indeed, the literature highlights the relevance of sarcomeric proteins, Ca2+-handling and myocardial energetics in the development of LVH in HCM. This study, therefore, set out to evaluate the hypertrophy-modifying capacity of such factors by means of family-based genetic association testing in 27 South African HCM families in which one of three unique HCM-causing founder mutations segregates. Moreover, the single and combined effects of 76 variants within 26 candidate genes encoding sarcomeric or sarcomere-associated proteins were investigated. The study identified a modifying role in the development of hypertrophy in HCM for each of the candidate genes investigated with the exception of the metabolic protein-encoding gene, PRKAG1. More specifically, single variant association analyses identified a modifying role for variants within the genes MYH7, TPM1 and MYL2, which encode proteins of the sarcomere, as well as the genes CPT1B, CKM, ALDOA and PRKAB2, which encode metabolic proteins. Haplotype-based association analyses identified combined modifying effects for variants within the genes ACTC, TPM1, MYL2, MYL3 and MYBPC3, which encode proteins of the sarcomere, as well as the genes CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 and PRKAG3, which encode metabolic proteins. Moreover, a number of variants and haplotypes showed statistically significant differences in effect amongst the three HCM founder mutation groups. The HCM-modifier genes identified were prioritised for future studies according to the number of significant results obtained for the four tests of association performed. The genes TPM1 and MYBPC3, which encode sarcomeric proteins, as well as the genes PFKM and PRKAG2, which encode metabolic proteins, were identified as stronger candidates for future studies as they delivered multiple significant results for various statistical tests. This study makes a novel contribution to the field of hypertrophy research as it tested the hypothesis that structural or energy-related factors located within the sarcomere may act as modifiers of cardiac hypertrophy in HCM, and succeeded in identifying a modifying role for many of the candidate genes selected. The significant results include substantial single and within-genecontext variant effects; and identified sizeable variation in the risk of developing LVH owing to the compound effect of the modifier and the individual founder mutations. Collectively, these findings enhance the current understanding of genotype/phenotype correlations and may, as consequence, improve patient risk stratification and choice of treatment. Moreover, these findings emphasize the potential for modulation of disease by further elucidation of some of the avenues identified.
AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) is ‘n onafhanklike voorspeller van kardiovaskulêre morbiditeit en van mortaliteit weens alle oorsake. Van belang is dat dit ‘n wysigbare kardiovaskulêre risiko faktor is, aangesien die afname daarvan algehele oorlewing verhoog en die frekwensie van nadelige kardiale voorvalle verlaag. ‘n Duidelike begrip van LVH patogenese is dus noodsaaklik om verbeterde risiko stratifikasie en terapeutiese intervensie te fasiliteer. Hipertrofiese kardiomiopatie (HKM), ‘n oorerflike hart-siekte, is ‘n model-siekte vir die uitpluis van die molekulêre meganismes onderliggend aan die ontwikkeling van LVH. LVH, in die afwesigheid van verhoogde eksterne lading, is die kern kliniese simptoom van HKM en die gevolg van mutasies in die gene wat kodeer vir sarkomeriese proteïene. Die LVH fenotiepe in HKM toon merkbare veranderlikheid selfs in familie-lede wat dieselfde siekte-veroorsakende mutasie dra. Die fenotiepe word dus bepaal deur die siekte-veroorsakende mutasie asook addisionele determinante insluitend die omgewing, epigenetika en modifiserende gene. Potensiële hipertrofie-modifiseerders wat tot dusver bestudeer is, is betreklik verwyder van die primêre stimulus vir LVH en die paar studies wat gerepliseer is, het teenstrydige resultate gelewer. Ons hipoteseer dat die faktore wat in noue interaksie met die primêre stimulus van foutiewe sarkomeriese funksionering is, ‘n groter kapasitieit het om dit en uiteindelik die LVH fenotiepe in HKM, te moduleer. Aanneemlike kandidaat-modifiseerders sou insluit faktore wat betrekking het tot die struktuur en funksie van die sarkomeer insluitend HKM-oorsaaklike gene en die ensieme wat funksioneer in sarkomeer-gebaseerde energetika. Die literatuur beklemtoon inderdaad die relevansie van sarkomeriese proteïene, Ca2+-hantering en miokardiese energetika in die ontwikkeling van LVM in HKM. Hierdie studie het beoog om die hipertrofie-modifiserende kapasiteit van sulke faktore te evalueer deur middel van familie-gebaseerde genetiese assosiasie toetse in 27 Suid-Afrikaanse HKM families waarin een van drie unieke HKM-stigter mutasies segregeer. Verder was die enkel en gekombineerde effekte van 76 variante binne 26 kandidaat gene wat kodeer vir sarkomeer en sarkomeer-geassosieerde proteïene, ondersoek. Hierdie studie het ‘n modifiserende rol in die ontwikkeling van hipertrofie in HKM geïdentifiseer vir elk van die kandidaat gene wat ondersoek is, met uitsluiting van die PRKAG1, wat kodeer vir ‘n metaboliese proteïen. Meer spesifiek, enkel variant assosiasie analises het ‘n modifiserende rol geïdentifiseer vir variante in die gene MYH7, TPM1 en MYL2, wat kodeer vir sarkomeriese proteïene, asook die gene CPT1B, CKM, ALDOA en PRKAB2, wat kodeer vir metabolise proteïene. Haplotipe-gebaseerde assosiasie-analises het gekombineerde modifiserende effekte geïdentifiseer vir variante in die gene ACTC, TPM1, MYL2, MYL3 en MYBPC3, wat kodeer vir strukturele proteïene van die sarkomeer asook die gene CD36, PDK4, CKM, PFKM, PPARA, PPARG, PGC1A, PRKAA2, PRKAG2 en PRKAG3, wat kodeer vir metabolise proteïene. Verder het ‘n aantal variante en haplotipes statisties betekenisvolle verskille in effek tussen die drie HKM-stigter mutasie groepe getoon. Die HKM-modifiserende gene wat geïdentifiseer is, is verder geprioritiseer vir toekomstige studies volgens die aantal beduidende resultate wat vir die vier assosiasie toetse verkry is. Die gene TPM1 and MYBPC3, wat kodeer vir sarkomeriese proteïene, asook die gene PFKM and PRKAG2, wat kodeer vir metaboliese proteïene, is geïdentifiseer as sterker kandidate vir verdere studies omdat veelvuldige beduidende resultate vir die verskeie statistiese toetse deur hulle gelewer is. Hierdie studie maak ‘n nuwe bydrae tot die veld van hipertrofie navorsing omdat dit die hipotese dat strukturele en energie-verwante faktore, wat binne die sarkomeer geposisioneer is, potensieel as modifiseerders van kardiale hipertropfie in HKM kan optree, ondersoek het. Dit slaag ook daarin om ‘n modifiserende rol vir baie van die geselekteerde kandidaatgene te identifiseer. Die beduidende resultate sluit in aansienlike enkel en binne-geen-konteks variant-effekte en aansienlike variasie in die risiko vir LVH ontwikkeling verskuldig aan die gekombineerde effek van modifiseerder en individuele stigter mutasies. Gesamentlik verbeter hierdie bevindinge die huidige begrip van genotipe/fenotipe korrelasies en dit mag tot gevolg hê verbeterde pasiënt risiko stratifikasie en keuse van behandeling. Verder beklemtoon hierdie bevindinge die potensiaal vir siekte modulering deur verdere uitpluis van sekere van hierdie geïdentifiseerde navorsingsrigtings.
National Research Foundation
Dr. Paul van Helden
Stellenbosch University
Soana, valentina. "Ornamental Hypertrophy". Thesis, KTH, Arkitektur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-35924.
Pełny tekst źródłaFerreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy". Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
Full Text
Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.
Pełny tekst źródłaClarke, Samantha Jayne. "Biochemical adaptations in cardiac hypertrophy". Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395503.
Pełny tekst źródłaTsang, K. K. "Screening for benign prostatic hypertrophy". Thesis, University of Edinburgh, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663068.
Pełny tekst źródłaRisto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.
Pełny tekst źródłaSchans, 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.
Pełny tekst źródłaStone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4532.
Pełny tekst źródłaStone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/4544.
Pełny tekst źródłaStone, Michael H. "Development of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4579.
Pełny tekst źródłaRIVERA, NATALIA V. "GENETICS OF LEFT VENTRICULAR HYPERTROPHY". Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169564.
Pełny tekst źródłaCloete, 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.
Pełny tekst źródłaENGLISH 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 hypertrophy covariates. To investigate this hypothesis, twenty one polymorphic loci spread across six genes (ACE1, AGT, AGTR1, CYP11B2, CMA and ACE2) of the RAAS were genotyped in 353 subjects from 22 South African HCM-families, in which founder mutations segregate. Genotypes were compared to 17 echocardiographically-derived hypertrophic indices of left ventricular wall thickness at 16 segments covering three longitudinal levels. Family-based association was performed by quantitative transmission disequilibrium testing (QTDT), and mixed effects models to analyse the X-linked gene ACE2, with concurrent adjustment for hypertrophy covariates (age, sex, systolic blood pressure (BP), diastolic BP, body surface area, heart rate and mutation status). Strong evidence of linkage in the absence of association was detected between polymorphisms at ACE1 and posterior and anterior wall thickness (PW and AW, respectively) at the papillary muscle level (pap) and apex level (apx). In single-locus analysis, statistically significant associations were generated between the CYP11B2 rs3097 polymorphism and PW at the mitral valve level (mit) and both PWpap and inferior wall thickness (IW)pap. Statistically significant associations were generated at three AGTR1 polymorphisms, namely, between rs2640539 and AWmit, rs 3772627 and anterior interventricular septum thickness at pap and rs5182 and both IWpap and AWapx. Furthermore, mixed effects model detected statistically significant association between the ACE2 rs879922 polymorphism and both posterior interventricular septum thickness and lateral wall thickness at mit in females only. These data indicate a role for RAAS gene variants, independent of hypertrophy covariates, in modifying the phenotypic expression of hypertrophy in HCM-affected individuals.
AFRIKAANSE OPSOMMING: Hipertrofiese kardiomiopatie (HCM), ‘n autosomale dominante afwyking, toon hoogs variërende hipertrofie binne en tussen families wat dieselfde siekte-veroorsakende mutasie het, hierdie dui op die moontlike betrokkenheid van geassosieerde modifiserende gene. Assosiasies tussen linker ventrikulêre hipertrofie en linker ventrikulêre druk-oorlading stel voor dat volgorde variasies in gene betrokke in die Renin-Angiotensin Aldosteroon Sisteem (RAAS) mag optree as hipertrofie modifiseerders in HCM. Sommige van hierdie soort studies is egter beperk omdat hulle nie gekompenseer het vir kovariante van hipertrofie nie. Om hierdie hipotese te ondersoek, is die genotipe bepaal by een-en-twintig polimorfiese lokusse, verspreid regoor ses RAAS gene (ACE1, AGT, AGTR1, CYP11B2, CMA and ACE2), in 353 kandidate vanuit 22 Suid-Afrikaanse HCM-families in wie stigter mutasies segregeer. Genotipes was vergelyk met 17 eggokardiografies afgeleide hipertrofiese indekse van linker ventrikulêre wanddikte by 16 segmente wat oor drie longitudinale vlakke strek. Familie-gebaseerde assosiasies was bestudeer deur kwantitatiewe transmissie disequilibrium toetsing (QTDT) en gemengde effek modelle om die X-gekoppelde geen ACE2 te analiseer, met gelyktydige kompensasie vir hipertrofie kovariate (ouderdom, geslag, sistoliese bloed druk (BP), diastoliese BP, liggaamsoppervlak area, hartritme en mutasie-status). Sterk indikasies van koppeling in die afwesigheid van assosiasie is waargeneem tussen ACE1 lokusse en posterior wanddikte (PW) asook anterior wanddikte (AW) by die papillêre spier vlak (pap) en die apeks vlak (apx). In enkel-lokus analises is statisties-betekenisvolle assosiasies gevind tussen die CYP11B2 rs3097 polimorfisme en PW by die mitraalklep vlak (mit) en beide die PWpap en inferior wanddikte (IW)pap. Statisties-betekenisvolle assosiasies was verder gevind by drie AGTR1 polimorfismes, naamlik, tussen rs2640539 polimorfisme en AWmit, rs3772627 en die anterior interventrikulêre septumdikte (aIVS) by die pap en rs5182 by beide die IWpap en AWapx. Gemengde-effek modelle het verder assosiasies aangetoon tussen die ACE2 rs879922 polimorfisme en die posterior interventrikulêre septumdikte en die laterale wanddikte by die mit, slegs in vrouens. Hierdie data dui op ‘n kovariaat-onafhanklike rol vir RAAS genetiese variante in die modifisering van die fenotipiese uitdrukking van hipertrofie in HCM-geaffekteerde individue.
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.
Pełny tekst źródłaENGLISH 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 hypertrophy-predisposing conditions present. Therefore, HCM provides a unique opportunity to study the molecular determinants of LVH in the context of a Mendelian disorder, instead of in more complex disorders such as hypertension. Over 1000 HCM-causing mutations in 19 genes have been identified thus far, most of them encoding sarcomeric proteins residing in the sarcomeric C-zone. However, for many HCM patients no disease-causing genes have been identified. Moreover, studies have shown phenotypic variation in presentation of disease in, as well as between, families in which the same HCM-causing mutation segregates. This has led many investigators to conclude that genetic modifiers of hypertrophy exist. The aim of the study was to identify novel plausible HCM-causing or modifier genes by searching for interactors of a known HCM-causing protein, namely titin. The hypothesis was that genes encoding proteins, which interact with proteins that are encoded by known HCM-causative genes, may also be considered HCM-causing or may modify the HCM phenotype. To this end, the aim was to identify novel interactors of the 11-domain super-repeat region of titin, which resides within the sarcomeric C-zone, using yeast two-hybrid analysis. Five putative interactors of the 11-domain super-repeat region of titin were identified in this study. These interactions were subsequently verified by colocalisation in H9C2 rat cardiomyocytes, providing further evidence for possible interactions between titin and these proteins. The putative interactor proteins of titin determined from the Y2H library screen were: filamin C (FLNC), phosphatidylethanolamine-binding protein 4 (PEBP4), heart-type fatty acid binding protein 3 (H-FABP3), myomesin 2 (MYOM2) and myomesin 1 (MYOM1). The FLNC gene could be a candidate for cardiac diseases, especially cardiomyopathies that are associated with hypertrophy or developmental defects. The putative interaction of titin and PEBP4 is speculated to be indicative of the formation of the interstitial fibrosis and myocyte disarray seen in HCM. Heart-type fatty acid-binding protein 3 has prognostic value to predict recurrent cardiac events. Its suggested interaction with titin is speculated to play a role in inhibiting its functional abilities. Myomesin 2 is jointly responsible, with MYOM1, for the formation of a head structure on one end of the titin string that connects the Z and M bands of the sarcomere. This is speculated to be linked to a developmental error with the result being a defect in sarcomeric structure formation, which could result in pathologies such as HCM. Therefore, these identified proteins could likely play a functional role in HCM due to their interactions with titin. This research could thus help with new insights into the further understanding of HCM patho-aetiology.
AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) ontstaan wanneer die kardiomyosiete in die linkerventrikel vergroot as gevolg van 'n verhoging in massa in reaksie op hemodinamiese drukoorlading. Dit kan toegeskryf word aan 'n normale fisiologiese respons op oefening of kan die gevolg wees van 'n wanaangepaste of siektetoestand, soos chroniese hipertensie. Hipertrofiese kardiomiopatie (HKM) is die mees algemene vorm van Mendeliese oorerflike hartsiekte. 'n Bepalende eienskap daarvan is primêre LVH, wat plaasvind wanneer daar geen ander hipertrofie-predisponerende voorwaardes teenwoordig is nie. Gevolglik bied HKM 'n unieke geleentheid om die molekulêre derterminante van LVH te bestudeer, in die konteks van 'n Mendeliese oorerflike siekte, in plaas van om dit in die meer komplekse siektes soos hoë bloeddruk te bestudeer. Meer as 1000 HKM-veroorsakende mutasies is tot dusver in 19 gene geïdentifiseer. Die meeste van hulle kodeer vir sarkomeriese proteïene wat in die C-sone voorkom. Egter, vir baie HKM-pasiënte is geen siekte-veroorsakende gene al geïdentifiseer nie. Daarbenewens het studies getoon dat variasie in fenotipiese aanbieding van die siekte in, sowel as tussen, families voorkom wat dieselfde HKM-veroorsakende mutasie het. Dit het daartoe gelei dat baie navorsers tot die gevolgtrekking gekom het dat genetiese wysigers van hipertrofie wel bestaan. Die doel van die studie was om nuwe moontlike HKM-veroorsakende of wysiger-gene te identifiseer deur te soek vir interaktors van 'n bekende HKM-veroorsakende proteïen, naamlik titin. Die hipotese was dat gene wat vir proteïene kodeer, wat in wisselwerking is met proteïene wat geïnkripteer word deur bekende HKM-veroorsakende gene, ook oorweeg kan word om HKM te veroorsaak. Dit kan ook die HKM fenotipe verander. Dus was die doel om nuwe interaktors van die 11-domein super-herhaalstreek van titin, soos gevind binne die sarkomeriese C-sone, te identifiseer deur middel van gis-twee-hibried-analise. Vyf vermeende interaktors van die 11-domein super-herhaalstreek van titin is in hierdie studie geïdentifiseer. Hierdie interaksies is later geverifieer met behulp van ko-lokalisering in H9C2-rotkardiomyosiete, wat verdere bewyse vir moontlike interaksies tussen titin en hierdie proteïene verskaf. Die vermeende interaktor-proteïene van titin wat bepaal is vanaf die gis-twee-hibried-biblioteeksifting was as volg: filamin C (FLNC), phosphatidylethanolamine-bindingsproteïen 4 (PEBP4), hart-tipe-vetsuur bindingsproteïen 3 (H-FABP3), myomesin 2 (MYOM2) en myomesin 1 (MYOM1). Die FLNC-geen kan 'n kandidaat vir kardiale siektes, veral kardiomiopatieë, wees wat geassosieer word met hipertrofie of ontwikkelingsafwykings. Die vermeende interaksie van titin en PEBP4 dui daarop om 'n aanduiding te wees vir die vorming van die interstisiële fibrose en miokardiale wanorde, soos gesien in HKM. Hart-tipe-vetsuur bindingsproteïen 3 het prognostiese waarde om herhalende kardiale gebeure te voorspel. Verder dui sy voorgestelde interaksie met titin moontlik daarop dat dit 'n rol kan speel in die inhibering van sy funksionele vermoëns. Myomesin 2 tesame met MYOM1 is verantwoordelik vir die vorming van 'n kopstruktuur aan die een kant van die titinstring wat dan die Z- en M-bande van die sarkomeer verbind. Daar word vermoed dat dit gekoppel is aan 'n ontwikkelingsfout, met die gevolg dat daar 'n defek is in sarkomeriese struktuurvorming, wat weer kan lei tot patologieë soos HKM.
Mrs Wendy Ackerman
Prof Paul van Helden
National Research Foundation (NRF)
Stellenbosch University
Akki, Ashwin. "Lipid overload studies in cardiac hypertrophy". Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441778.
Pełny tekst źródłaWallis, 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.
Pełny tekst źródłaHowell, Neil John. "Metabolic support in left ventricular hypertrophy". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1492/.
Pełny tekst źródłaPhilipot, 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.
Pełny tekst źródłaOsteoarthritis (OA) is an age-related disease whose prevalence increases with late life. In osteoarthritic cartilage, chondrocytes presents age-specific changes such as a decrease in synthesis properties, a decrease in their response to growth and anabolic factors and an increase of cellular senescence. Senescent chondrocytes are characterized by an irreversible cell cycle arrest, DNA damage response activation (ATM/p53/p21), p16INK4a/pRb signaling pathway activation and the establishment of SAPS triggering to hypertrophy. The aim of my PhD project consisting to identify microRNAs involved in chondrocyte premature aging. microRNAs are small endogenous RNAs controlling several biological processes such as proliferation, differentiation and senescence. Two studies show that microRNAs have a preventive role in senescence and hypertrophy. During my PhD, we perform a cellular model based on OA chondrocytes placed in 3D and treated with IL-1β. We identified two miRs: miR-24 and miR-199a-5p. Repression of miR-24 leads to the induction of p16INK4a and MMP1, associated with chondrocyte hypertrophy. Moreover, preliminary datas suggests that miR-199a-5p is a potential regulator of anti-aging hormone Klotho which is deregulated in our model
Crampton, Matthew S., i 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.
Pełny tekst źródłaCrampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
Evaristi, Maria Franscesca. "New biomarkers and therapeutic targets in left ventricular hypertrophy". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30047.
Pełny tekst źródłaLeft ventricular hypertrophy (LVH) is a strong predictor of future heart failure and cardiovascular mortality. Arterial hypertension is considered as the main causative agent for LVH as 30% of hypertensive patients develop LVH. These patients have an increased risk for cardiovascular complications and heart failure. Early diagnosis of LVH and prompt treatment are crucial to reduce LVH and stop its progression towards heart failure. Biomarkers could represent a rapid, effective and low-cost tool to discriminate hypertensive patients with LVH from those with normal LV size. Therefore, we aimed to identify plasma metabolomics biomarkers by 1H NMR to provide novel diagnostic tools for rapid detection of LVH in populations of hypertensive individuals. We realized a cross-sectional study including 48 hypertensive patients with LVH matched with 48 hypertensive patients with normal LV size, and 24 healthy controls. Two-dimensional targeted M-mode echocardiography was performed to measure left ventricular mass index. Partial least squares discriminant analysis was used for the multivariate analysis of the 1H NMR spectral data. From the 1H NMR analysis, we found that the methylene/methyl (-CH2-/-CH3) ratio of aliphatic chain from plasma lipids was significantly increased (p<0.001) in hypertensive patients with LVH compared to hypertensive patients without LVH and to control. Receiver operating characteristic curve showed that a cutoff value of 2.34 provided a 52.08% sensitivity and 85.42% specificity for discriminating LVH (AUC=0.703, p-value<0.001). We propose the -CH2/-CH3 ratio from plasma aliphatic lipid chains as a biomarker for the diagnosis of LVH in arterial hypertension. LVH incidence is also increased in patients with metabolic syndrome (MetS). MetS is defined by central obesity plus any two medical conditions such as dyslipidemia, insulin resistance, and hypertension. These factors synergize to cause LV dysfunction and HF. Published data have shown that MetS patients have low plasma insulin-like growth factor binding protein 2 (IGFBP2). IGFBP2 was shown to play a role in diabetes and metabolism, but studies investigating its role in cardiac diseases are lacking. We first aimed to investigate plasma IGFBP2 levels and cardiac IGFBP2 mRNA levels in MetS patients. Both plasma levels and heart expression levels of IGFBP2 were decreased in patients with MetS compared to control patients. Further, in a C57BL/6J mouse model of 60% high fat diet-induced MetS, we measured cardiac mRNA IGFBP2 levels. According to the observed data in human, mice with MetS showed a decreased cardiac IGFBP2 mRNA level. Finally, we investigated whether a gene therapy strategy using adeno-associated virus 9 carrying human IGFBP2 coding sequence (AAV9-hIGFBP2) could prevent from MetS associated left ventricular hypertrophy. Our data showed that AAV9-hIGFBP2 injection restored durably cardiac IGFBP2 levels in mouse heart and prevented from left ventricle wall thickening, hypertrophy and dysfunction. These clinical and animal data suggest that IGFBP2 is a potential new cardiac therapeutic target in MetS
SASANO, Chieko, Mahmud UZZAMAN, Luni EMDAD, Yoshiko TAKAGISHI, Haruo HONJO, Kaichiro KAMIYA i Itsuo KODAMA. "Dephosphorylation of Connexin43 Associated with Ventricular Hypertrophy". Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2800.
Pełny tekst źródłaAro, J. (Jani). "Novel load-inducible factors in cardiac hypertrophy". Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212173.
Pełny tekst źródłaTiivistelmä Sydänlihas mukautuu lisääntyneeseen kuormitukseen lihassolujen koon kasvun eli hypertrofian avulla. Pitkittyessään hypertrofinen kasvu on kuitenkin tärkeä sydämen vajaatoimintaa ja äkkikuolemaa ennakoiva riskitekijä. Hypertrofisessa vasteessa mekaaninen venytys sekä neurohumoraaliset tekijät saavat aikaan solunsisäisten signaalinvälitysreittien aktivoitumisen, mikä johtaa lisääntyneeseen geenien luentaan ja proteiinituotantoon. Väitöskirjassa tutkittiin uusien kuormitusaktivoituvien tekijöiden, melusiinin, trombospondiini (TSP) -1:n ja -4:n sekä dyksiinin ilmentymistä hypertrofisen vasteen aikana. Melusiinia ilmentyy sydämessä sekä kammioissa että eteisissä, mutta painekuormituksen myötä se aktivoituu nopeasti pääasiassa vasemmassa eteisessä. Sydänlihassolujen soluviljelymallissa melusiinin luenta lisääntyy suoraan mekaanisen venytyksen ja hypertrofisten agonistien vaikutuksesta. Painekuormitus aktivoi nopeasti myös TSP-1:n ja -4:n luentaa sydämessä. TSP-1:n ja -4:n geeniluenta lisääntyy myös kokeellisessa sydäninfarktimallissa. Lisäksi sydämessä TSP-4:ää havaittiin olevan ensisijaisesti endoteelisoluissa. Dyksiinin ilmentyminen lisääntyi sekä painekuormituksen että sydäninfarktin aiheuttaman sydänlihaksen uudelleenmuovautumisen aikana. Mekaaninen kuormitus riitti jo yksinään aktivoimaan dyksiinin geeniluentaa sydämessä. Lisäksi mitogeeni-aktivoituvan p38-proteiinikinaasin havaittiin säätelevän dyksiinin ilmentämistä. Väitöskirjatyössä saatiin uutta tietoa sydänlihaksen kuormituksen aikaisista muutoksista geenien luennassa sydänlihaksessa. Työssä osoitettiin, että painekuormitus aktivoi sydämessä aiemmin vähän tutkittujen geenien, melusiinin, TSP-1:n ja -4:n sekä dyksiinin, ilmentymistä. Näiden tekijöiden aktivoituminen hypertrofisen vasteen alkuvaiheessa antaa viitettä siitä, että tekijät osallistuvat kuormittuneen sydänlihaskudoksen uudelleenmuovautumiseen. Melusiini voi toimia erityisesti eteiskudosta kuormitukselta suojaavissa mekanismeissa, kun taas TSP-4 osoittautui aktivoituvan painekuormituksessa nimenomaan endoteelisoluissa
Sin, Yuan Yan. "The roles of HSP20 in cardiac hypertrophy". Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3581/.
Pełny tekst źródłaButler, Thomas J. "Impact of dietary manipulation on cardiac hypertrophy". Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:15371.
Pełny tekst źródłaLozar, Olivia Mae. "Does Proteasome Activity Impact Skeletal Muscle Hypertrophy?" University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1576264202406223.
Pełny tekst źródłaShirazi, Farshad 1963. "Metabolic aspects of neonatal rat cardiomyocyte hypertrophy". Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282447.
Pełny tekst źródłaCarstens, 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.
Pełny tekst źródłaHypertrophic 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 dysfunction and of additional genetic modifiers. Components of the renin-angiotensin-aldosterone system (RAAS) are plausible candidate modifiers because of their effect on blood pressure and their direct hypertrophic effect on cardiomyocytes. The present study investigated genes encoding components of the RAAS for association with cardiac hypertrophy traits, in 353 individuals comprised of genetically and echocardiographically affected and unaffected family members, belonging to 22 HCM families with HCM founder mutations by employing a multi-SNP approach with TaqMan allelic discrimination technology. Gene-gene interaction analysis was also performed to investigate the effect of epistasis on hypertrophy. Candidate genes for analysis included the angiotensin II type 2 receptor (AT2 receptor), renin, renin-binding protein (RnBP), the (pro)renin receptor, the mineralocorticoid receptor as well as genes encoding subunits of the epithelial sodium channels (ENaC) and Na+/K+-ATPase that showed evidence for cardiac expression. The present study demonstrates for the first time that variations in the renin and RnBP genes play a role in modulating hypertrophy in HCM, independent of blood pressure and confirms the involvement of the AT2 receptor in hypertrophy in HCM. Additionally we report an association between Na+/K+-ATPase α1- and β1-subunits as well as the ENaC α- and β-subunits and hypertrophy. Significant evidence for epistasis was found between renin and downstream RAAS effectors, suggesting a complex interplay between these RAAS variants and the hypertrophic phenotype in HCM. The identification of such modifiers for HCM may offer novel targets for hypertrophy research and ultimately antihypertrophic therapy.
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.
Pełny tekst źródłaGondran, 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.
Pełny tekst źródłaMuscle mass is largely regulated by signaling pathways controlling the balance between synthesis and degradation of myofibrillar proteins. Thus, myostatin, a member of the TGFβ superfamily, targets a number of signaling networks involved in the regulation of muscle mass, in particular the Akt / mTOR signaling pathway. Myostatin is one of the major inhibitors of myogenesis by exerting a negativecontrol on the proliferation and differentiation of myoblasts. Today, myostatin is involved in many therapeutic strategies which aim to improve muscle function in cases of atrophy or myopathies.GASP-1 and GASP-2 are two secreted proteins containing several domains associated with protease inhibitors, and described as myostatin antagonists. The Animal Molecular Genetics laboratory has developed in vitro and in vivo strategies to determine the functions of GASPs proteins in a myogenic context. First, we generated a transgenic mouse line TgGasp-1 over-expressing the Gasp-1 gene. This line shows an overall increase in skeletal muscle weight and hypertrophy, a consequence of myostatin inhibition. However, unlike myostatin knockout mice (Mstn -/-), this line shows neither hyperplasia, nor change in the proportion of different types of muscle fibers. Moreover, the global metabolism is not affected. In order to better understand the role of GASPs proteins in musculoskeletal development, two complementary approaches were developed during this thesis :(i) the study of a murine TgGasp-2 line over-expressing Gasp-2 reveals a muscular phenotype similar to the TgGasp-1 mice. At 12 weeks, we observed an overall increase in body and some skeletal muscles weight due to a hypertrophy of the myofibers. As the TgGasp-1 mice, and unlike the Mstn -/- mice, the number of fibers and the metabolism of TgGasp-2 mice did not vary compared to the wildtype mice (ii) In silico analyses allow us to identify different biological processes and regulated pathways controlled by GASP-1
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.
Pełny tekst źródłaMovahed, Mohammad, Deborah Strootman, Sharon Bates i 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.
Pełny tekst źródłaSchnell, Frédéric. "Hypertrophie ventriculaire gauche physiologique ou pathologique : Intérêt d’une approche multiparamétrique". Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B021/document.
Pełny tekst źródłaIntroduction: the diagnosis of hypertrophic cardiomyopathy (HCM) in athlete is difficult. Indeed, intense sports practice induces an electrical and morphological physiological remodeling which can be difficult to differentiate from the changes induced in pathology. However, it is essential to diagnose an athlete with a cardiomyopathy. Indeed, in case of underlying cardiomyopathy the athlete will be at risk of sudden cardiac death, but an excessive over diagnosis has strong professional and social consequences. Methods: (1) we have tried to improve the ECG criteria’s, which enable the differentiation between ECG changes induced by exercise and the ECG changes induced by an underlying cardiomyopathy. (2) We tried to define the best investigation algorithm in case of abnormal ECG changes in athletes. (3) We tried to improve the characterization of the phenotype of athletes with HCM as compared to sedentary HCM. (4) We tried to investigate if the use of new imaging technics, i.e. speckle tracking, might improve the diagnostic accuracy and enable a better prognostic evaluation in HCM. Results: We have proposed a new classification of ECG in athletes enabling to decrease the rate of false positive ECG in athletes without decreasing its diagnostic accuracy in HCM. In case of pathological T wave inversion (PTWI) in athletes, we demonstrated that a CMR is mandatory, as echocardiography missed a diagnosis of pathology in 35% of PTWI athletes. Nevertheless, the diagnosis of HCM with current criteria’s of HCM can be challenging. Indeed, HCM athletes have a different phenotype from HCM sedentary, with a better systolic and diastolic function; they also have a better longitudinal function. The assessment of longitudinal function during exercise and mechanical dispersion are promising tool for the diagnosis of HCM in athletes. Indeed, the alteration of longitudinal strain is related to myocardial fibrosis. Exercise echocardiography, i.e. exercise mitral insufficiency, seems to be a prognostic factor in HCM patients. Conclusions: Ours results enabled to develop tools which might help to better differentiate pathological and physiological left ventricular hypertrophy (LVH); but also to better characterize LVH and the prognosis in HCM patients
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.
Pełny tekst źródłaLeft 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 syndrome were significantly related to left ventricular relative wall thickness and concentric remodeling, but less to LVH. Left ventricular relative wall thickness was inversely related to insulin sensitivity in skeletal muscle and borderline significantly directly related to insulin sensitivity in the myocardium in a healthy, normotensive sample of the cohort investigated with positron emission tomography, whereas left ventricular mass index was not related to myocardial or skeletal muscle insulin sensitivity. At age 70, echocardiographic LVH was related to a variety of common electrocardiographic diagnoses. In a prospective mortality analysis with baseline at age 70 and a median follow-up time of five years, echocardiographic and electrocardiographic LVH predicted mortality independently of each other and of other cardiovascular risk factors, implying that echocardiographic and electrocardiographic LVH in part carry different prognostic information.
In summary, components of the insulin resistance syndrome predicted LVH twenty years later, but were cross-sectionally more related to increased left ventricular relative wall thickness and concentric remodeling. Echocardiographic and electrocardiographic LVH predicted mortality independently of each other and of components of the insulin resistance syndrome.
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.
Pełny tekst źródłaBakgrund: Syftet med den här avhandlingen var att studera transkriptions-mönster och extracellulär signalering vid hjärthypertrofi för att bättre förstå de mekanismer som startar, styr och underhåller tillväxten. Hjärthypertrofi, onormal tillväxt av hjärtmuskeln, är en riskfaktor för andra hjärt-kärlsjukdomar och dödlighet. Hypertrofi av hjärtmuskeln är ett tillstånd, oberoende av bakomliggande sjukdom, där hjärtmuskeln strävar efter att kompensera för ökad arbetsbelastning. Denna omställning av hjärtat innefattar fysiologiska förändringar orsakade av ett förändrat genuttryck, modifiering av miljön utanför cellen och ändrad cell-till-cell signalering. Mikrovesiklar och exosomer är små membranomslutna bubblor som frisätts från cellmembranet, ut i cellens omgivning. De kan förmedla budskap mellan celler och påverka olika processer i målceller. Metoder och material: Avhandlingen innefattar två olika microarraystudier på olika material. I den första studien användes hjärtbiopsier från 8 patienter med hypertrofisk obstruktiv kardiomyopati (HOCM) och 5 kontroller utan hjärtsjukdom. I det andra projektet användes hjärtvävnad från 6 aortaligerade och 6 skenopererade (kontroller) råttor vid tre olika tidpunkter (1, 6 och 42 dagar efter kirurgiskt ingrepp). För att påvisa skillnader i genuttryck analyserades proverna med Illumina helgenom microarray och multivariat dataanalys. Avhandlingens andra del innehåller två studier om mikrovesiklar och exosomer. Odlade hjärtmuskelceller (HL-1) stimulerades med tillväxt-faktorer (TGF-β2 eller PDGF BB) och ostimulerade celler användes som kontroll. Mikrovesiklar och exosomer renades fram med centrifugeringar och ultracentrifugering av cellodlingsmediet för att sedan karakteriseras med olika metoder för att studera storlek, ytmarkörer och innehåll. Illumina helgenom microarray användes för att studera microvesiklarnas och exosomernas mRNA innehåll. Resultat: I de två olika microarraystudierna hittades gentranskript och grupper av gentranskript som skiljde sig mellan kontroller och den hypertrofa hjärtvävnaden. När HOCM patientproverna jämfördes med kontroller hittades nedreglering av MYH6, EGR1 och FOS samt uppreglering av ACE2, JAK2 och HDAC5. Efter multivariat dataanalys av materialet från råtta, hittades 5 grupper av gentranskript med intressanta mönster som kunde kopplas till den hypertrofiska utvecklingen av hjärtmuskeln: "Ateroskleros", "ECM och adhesionsmolekyler", "Fettsyrametabolism", "Glukosmetabolis-men" och "Mitokondrien". Mikrovesiklarna hade en diameter på 40-300 nm och innehöll kromosomala DNA-sekvenser. När mikrovesiklarna överfördes till en annan celltyp (fibroblaster) resulterade det i ett förändrat genuttryck i fibroblasterna. Exosomer från hjärtmuskelcellerna som odlats med eller utan tillväxtfaktor hade en diameter på 50-80 nm. En stor pool av olika gentranskript var gemensam för alla exosomer oavsett stimulering eller ej. En mindre pool av gentranskript varierade i innehåll mellan de stimulerade och ostimulerade hjärtmuskelcellerna. I den gemensamma gentranskript poolen var ca 14 % ribosomala, ca 14 % var okända och ca 5 % var associerade till mitokondrien och dess funktion. Slutsats: Microarraystudierna visade att transkriptionsreglering i ett stabilt skede av hypertrofiutvecklingen är en balans mellan pro- och anti-hypertrofiska mekanismer och att olika gengrupper var olika reglerade vid olika tidpunkter i hjärtmuskeltillväxten. OPLS-DA är ett mycket användbart och kraftfullt verktyg när man analyserar genexpressionsdata, särskilt för att hitta grupper av gen-transkript som är svåra att upptäcka med traditionell statistik. Microvesikel- och exosomstudierna visade att mikrovesiklar och exosomer som frisätts från hjärtmuskelceller innehåller både DNA och RNA och kan vara inblandade i händelserna i målceller genom att underlätta en rad processer, inklusive ändringar av genuttryck. Olika stimulering av hjärtmuskelcellen kan påverka innehållet i exosomernas som produceras, vilket indikerar att exosomernas signalfunktion kan variera beroende på hjärtmuskelcellens tillstånd.
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/.
Pełny tekst źródłaSilberberg, 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.
Pełny tekst źródłaBraga, Luca. "Identification and characterization of MicroRNAs modulating cardiac hypertrophy". Thesis, Open University, 2017. http://oro.open.ac.uk/51095/.
Pełny tekst źródłaSayeed, 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.
Pełny tekst źródłaRichardson, Simon. "Studies of ischaemia and reperfusion in cardiac hypertrophy". Thesis, University of Hull, 2002. http://hydra.hull.ac.uk/resources/hull:13202.
Pełny tekst źródłaWoltz, John W. "Cardiovascular Risk and Left Ventricular Hypertrophy in Firefighters". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367940479.
Pełny tekst źródłaXU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE". University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.
Pełny tekst źródłaPatel, Parth Mahendra, i Parth Mahendra Patel. "Deciphering the Role of FXR1 in Cardiac Hypertrophy". Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625115.
Pełny tekst źródłaDavies, Justin Edgar Rees. "Coronary haemodynamics in hypertension and left ventricular hypertrophy". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7793.
Pełny tekst źródłaChang, 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.
Pełny tekst źródłaGerhardt, 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.
Pełny tekst źródłaAl, 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.
Pełny tekst źródłaPostnatal muscle growth in mice mainly occurs by hypertrophy and by anincrease of myofibres length. This increase in myofibres area is controlled by multiple signaling pathways such as Notch signaling, which is involved in activation of satellite cells (SC) at the beginning of postnatal muscle growth in mice. The O-fucosylation of EGF-like repeats within the extracellular domain of NOTCH receptors, mediated by protein O-fucosyltransferase 1 (POFUT1), plays a key role in the modulation of receptor-ligand interactions (R-L), necessary for activation of Notch signaling. Pofut1cax/cax mice are hypomorphic for the Pofut1 gene. In addition to skeletal defects, our results show postnatal muscular hypertrophy, no hyperplasia and a reduced pool of SC. To understand the origin of this hypertrophy, primary cultures of myoblasts derived from SC (SCDM) from skeletal muscles were studied in proliferating and differentiating conditions. Pofut1cax/cax SCDM showed a reduced Notch signaling due to aless efficient R-L interactions provoked by a low O-fucosylation of EGF-like repeats. This results in decreased expression of Pax7, a marker of undifferentiated state, and a change in the expression of myogenic regulatory factors (Myod, Myf5 and Myogenin). Subsequently, the proportion of Pax7+/MyoD- progenitors decreased while the proportion of Pax7-/MyoD+ cells committed in differentiation increased. These findings corroborate early differentiation of Pofut1cax/cax SCDM.Our results indicate that this postnatal muscle hypertrophy in Pofut1cax/caxmice is due to the fact that activated satellite cells are more prone todifferentiate and fuse with pre-existing myofibres that returning toquiescence
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.
Pełny tekst źródłaPremessa: Sino ad ora, nessuna tecnica diagnostica non invasiva appare soddisfacente nel differenziare la Miocardiopatia Ipertrofica (HCM) dalla Cardiopatia ipertensiva (H-LVH). Abbiamo ipotizzato che nella HCM la presenza di peculiari e localizzate alterazioni tessutali causi una significativa riduzione della deformazione sistolica regionale e della riflettività tessutale, nonostante la funzione sistolica globale possa apparire normale. Metodi: Venti pazienti con HCM non ostruttiva, 20 pazienti ipertesi (HTN) e 15 controlli sani (NTN), tutti simili per età e sesso, sono stati sottoposti ad acquisizione ecocardiografica standard e mirata all’acquisizione dei segnali in radiofrequenza e dei segnali doppler tessutali dalle tre camere apicali, seguendo un modello ventricolare sinistro a 16 segmenti. In seguito, per ciascun segmento sono state ottenute curve di deformazione ad elevata risoluzione e curve di Integrated Backscatter. Risultati: I pazienti HCM hanno presentato valori medi di strain sistolico (Ssys), strain rate sistolico (SR) e di variazioni cicliche dell’Integrated Backscatter (CVIB) significativamente ridotti rispetto ai soggetti ipertesi o normotesi, anche se si è evidenziata una rilevante sovrapposizione tra i valori dei segmenti HCM e dei segmenti HTN. Tuttavia, quando si sono identificati segmenti con deformazione quasi assente (segmenti ND con Ssys>-5.68%), si sono riscontrati almeno 2 segmenti ND in ciascun soggetto HCM, eterogeneamente distribuiti nel ventricolo sinistro, mentre nessun HTN o NTN ne possedeva alcuno. Inoltre, nei pazienti HCM, Ssys, SR e CVIB dei segmenti medio-basali del setto interventricolare e della parete posteriore non correlavano con i relativi spessori tele-diastolici rilevati in M-mode dalla parasternale asse-lungo (analisi di regressione lineare), dimostrando che non vi sono differenze nella performance cardiaca tra i pattern asimmetrico e concentrico di HCM. Nel complesso, i pazienti HTN hanno presentato valori di Ssys, SR e CVIB lievemente ma significativamente ridotti rispetto ai controlli, con le riduzioni più importanti a livello del setto basale. Inoltre, la presenza di strain post-sistolico è risultato essere un fenomeno rilevante che può contribuire alla disfunzione sistolica e diastolica nell’ipertrofia ventricolare sinistra patologica. Oltretutto, un’analisi di regressione lineare ha evidenziato la correlazione tra Ssys e CVIB (R=0.54, P<0.0001). Conclusioni: L’analisi della deformazione e delle riflettività tessutale può facilmente discriminare HCM da H-LVH. In particolare, HCM è caratterizzata in modo esclusivo dalla presenza di segmenti con deformazione quasi assente, distribuiti in modo non uniforme nel ventricolo sinistro ed indipendenti dal grado o dal pattern di ipertrofia ventricolare.
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.
Pełny tekst źródłaArcher, 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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