Dissertations / Theses on the topic 'Cardiac hypertrophy'
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Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.
Full textClarke, Samantha Jayne. "Biochemical adaptations in cardiac hypertrophy." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395503.
Full textSchans, 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.
Full textFerreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
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Akki, Ashwin. "Lipid overload studies in cardiac hypertrophy." Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441778.
Full textStirparo, G. G. "DEFINITION OF TRANSCRIPTIONAL LANDSCAPE IN CARDIAC MATURATION AND CARDIAC HYPERTROPHY." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/247064.
Full textAro, J. (Jani). "Novel load-inducible factors in cardiac hypertrophy." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212173.
Full textTiivistelmä 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/.
Full textButler, Thomas J. "Impact of dietary manipulation on cardiac hypertrophy." Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:15371.
Full textCrampton, 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.
Full textCrampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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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.
Full textBakgrund: 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.
Braga, Luca. "Identification and characterization of MicroRNAs modulating cardiac hypertrophy." Thesis, Open University, 2017. http://oro.open.ac.uk/51095/.
Full textSayeed, 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.
Full textRichardson, Simon. "Studies of ischaemia and reperfusion in cardiac hypertrophy." Thesis, University of Hull, 2002. http://hydra.hull.ac.uk/resources/hull:13202.
Full textXU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.
Full textPatel, 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.
Full textKelloniemi, A. (Annina). "Novel factors regulating cardiac remodeling in experimental models of cardiac hypertrophy and failure." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526220291.
Full textTiivistelmä Sydämen kuormitus saa aikaan vasemman kammion liikakasvun eli hypertrofian ja sydämen uudelleenmuovautumisen, mikä pitkittyessään johtaa sydämen vajaatoimintaan. Sydämen vajaatoiminta on monimutkainen oireyhtymä, josta länsimaissa kärsii noin 1-2 % aikuisväestöstä, ja esiintyvyys nousee iän myötä. Patologisessa uudelleenmuovautumisessa tapahtuu toiminnallisia ja rakenteellisia muutoksia, joihin liittyy muutoksia geenien ilmentymisessä, sarkomeerin uudelleen järjestäytymistä, sydänlihassolujen koon kasvua, fibroosia, tulehdusta, oksidatiivista stressiä ja aineenvaihdunnan huonontumista. Tämän työn tarkoituksena oli tutkia kolmen uuden tekijän roolia sydämen uudelleenmuovautumisessa erilaisissa kokeellisissa sydämen kuormituksen malleissa. Fosfataasin ja aktiinin säätelijä 1:n (Phactr1) ilmentyminen väheni nopeasti infarktin seurauksena. Adenovirusvälitteinen Phactr1:n ylituotanto muutti luusto- ja sydänlihasaktiinien isomuotojen suhdetta sekä terveessä että infarktisydämessä, samoin viljellyissä sydänlihassoluissa. Phactr1 saattaa säädellä isomuotojen suhdetta seerumiresponsiivisen tekijän (SRF) avulla. Transformoituvan kasvutekijä β1:n stimuloima proteiini 22:n (TSC-22) ilmentyminen nousi nopeasti usean hypertrofisen stimuluksen seurauksena sekä infarktin jälkeen. Lisäksi TSC-22 voisi säädellä kollageeni 3a1:n ilmentymistä sydämessä. Retinan degeneroituvan proteiinin 3 kaltaisen tekijän (Rd3l) ilmentyminen väheni sekä painekuormituksen että infarktin seurauksena. Rd3l-poistogeenisillä hiirillä aortan ahtauman aiheuttama painekuormitus sai aikaan lisääntynyttä sydänlihassolujen hypertrofiaa ja sydämen toimintahäiriöitä. Tämä väitöskirjatutkimus tuo uutta tietoa Phactr1-, TSC-22- ja Rd3l-geeneistä kuormituksen aiheuttamassa sydämen hypertrofiassa ja uudelleenmuovautumisessa. Nämä tulokset auttavat osaltaan ymmärtämään monimutkaisia molekyylitason mekanismeja, jotka johtavat sydämen vaajatoiminnan kehittymiseen
Sharma, Salil. "MicroRNAs as Effectors for Acetyltransferase p300 in Cardiac Hypertrophy." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/684.
Full textGusterson, Rosalind Jane. "The role of CBP and p300 in cardiac hypertrophy." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399576.
Full textTurner, J. E. "Collagen metabolism in normal heart and during cardiac hypertrophy." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47290.
Full textBrenner, jacob Samuel. "Alternate routes of calcium entry mediating pathological cardiac hypertrophy /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Full textPutinski, Charis. "Caspase-dependent Signaling as an Inductive Cue for Cardiac Hypertrophy." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37728.
Full textStiles, Rebecca. "A Novel Non-Apoptotic Role for Caspase Activity during Cardiac Hypertrophy." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19912.
Full textSASANO, Chieko, Mahmud UZZAMAN, Luni EMDAD, Yoshiko TAKAGISHI, Haruo HONJO, Kaichiro KAMIYA, and Itsuo KODAMA. "Dephosphorylation of Connexin43 Associated with Ventricular Hypertrophy." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2800.
Full textLoonat, 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.
Full textRooij, Eva van. "Novel insights into the calcineurin/NFAT pathway in cardiac hypertrophy." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2004. http://arno.unimaas.nl/show.cgi?fid=7585.
Full textHorikawa, Yousuke Takashi. "The role of caveolin-3 in cardiac protection and hypertrophy." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3360159.
Full textTitle from first page of PDF file (viewed July 28, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Booth, Scott. "The role of Telomeres in the development of Cardiac Hypertrophy." Thesis, Federation University Australia, 2017. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/164437.
Full textThe overall aim of this thesis was to determine the role of telomeres in the development of cardiac hypertrophy. It was hypothesised that changes in cardiomyocyte telomere length and/or maintenance cause cardiac hypertrophy.
Queirós, Ana Maria Gomes Capelo Carregal. "Sex- and oestrogen-dependent regulation of miRNAs in cardiac hypertrophy." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17165.
Full textThe present study aimed to identify sex-differently expressed miRNAs in a late stage of hypertrophy (9 weeks) and the possible role of ERs in the regulation of these differences. Our previous studies identified ERbeta as an important determinant factor of the observed sex differences in pressure overload, playing different roles in males and females. This report identified a total of 30 miRNAs with sex and/or sex*surgery interaction effect 9 weeks after TAC in WT mice. The same effects were not observed in ERbeta-/- animals partially due to the higher expression of these miRNAs in ERbeta-/- females than in their WT counterparts. This study reveals a repression of a number of miRNAs by estradiol and its receptors alpha and beta in female cardiomyocytes, confirming the in vivo results and accentuating the important protective role of oestrogen and ERbeta in the female heart. Six of the miRNAs with sex differences in WT but not in ERbeta-/- hypertrophy models were found to be possible fibrosis regulators by putatively targeting common ERK/MAPK pathway inhibitors. MiR-106a, miR-106b, miR-21, miR-24, miR-27a and miR-27b were subjected to a different regulation by estradiol in cardiac fibroblasts in a sex-dependent manner. In conclusion, this study reinforces the oestrogen and ERbeta protective roles in the female hearts. Estradiol and ERs repress many miRNAs’ expression in both female cardiomyocytes and cardiac fibroblasts, as well as in vivo. In male hearts and cardiac fibroblasts, ERalpha is apparently the major player, regulating in particular potential fibrosis –related miRNAs. The different roles of ERs in male and female hearts are a determinant factor of the observed sex differences in cardiac hypertrophy.
Chiarello, Carmelina. "Role of the scaffolding protein Homer 1a in cardiac hypertrophy." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423423.
Full textLe proteine Homer sono una famiglia di proteine coinvolte in molte vie di trasduzione del segnale intracellulare, in cellule eccitabili e non eccitabili. Queste proteine partecipano nell’assemblaggio e nella regolazione di complessi funzionali di ‘signalling’, facilitando il ‘cross-talk’ tra recettori della membrana plasmatica e canali posti sulle membrane dei compartimenti intracellulari (Worley PF. et al., 2007). Le proteine Homer sono costitutivamente espresse nel cervello, dove svolgono la funzione di ‘scaffold’ in molti processi neuronali, quali ad esempio l’omeostasi del calcio intracellulare, la plasticità sinaptica associata all’apprendimento ed alla memoria nel cervello maturo, lo sviluppo embrionale del cervello (Xiao B. et al., 1998; Worley PF. et al., 2007; Foa L. et al., 2009). Tra le diverse varianti di splicing alternativo, l’isoforma Homer 1a agisce da dominante negativo disassemblando i complessi di ‘signalling’ formati dalle altre isoforme Homer. Il gene Homer 1a è trascritto come gene immediato precoce, la sua espressione nelle cellule neuronali è bassa in condizioni basali ed aumenta rapidamente in seguito ad attivazione neuronale (Brakeman PR. et al., 1997). Le proteine Homer sono espresse anche nel muscolo cardiaco, ma la loro regolazione e la loro funzione è ancora poco conosciuta. Nonostante l’importanza degli Homer come proteine regolatrici di complessi coinvolti nelle vie di trasduzione del segnale, pochi studi si sono focalizzati sul loro ruolo nel cuore. A tal riguardo, è stato riportato che l’mRNA codificante per Homer 1a aumenta rapidamente e transientemente in colture di cardiomiociti neonatali in seguito a stimolazione con endotelina-1 ed con altri agonisti ipertrofici (Kawamoto T. et al., 2006). Un successivo lavoro ha evidenziato che, in condizioni di ipertrofia indotta da angiotensina II, anche i livelli di espressione della proteina Homer 1a risultano up-regolati in colture di cardiomiociti neonatali (Guo WG. et al., 2010). Un recente studio ha, invece, dimostrato che l’isoforma Homer 1b/c regola positivamente l’ipertrofia dovuta a stimolazione α-adrenergica, mentre l’isoforma Homer 1a antagonizza tale effetto (Grubb DR. et al., 2011). In questo studio abbiamo esaminato il ruolo della proteina Homer 1a nell’ipertrofia cardiaca. La nostra ipotesi di lavoro è che la proteina Homer 1a sia un modulatore molecolare dell’ipertrofia. A tal fine, abbiamo studiato la presenza, la localizzazione sub-cellulare e la funzione di Homer 1a nel muscolo cardiaco. Analizzando l’espressione di Homer1a in condizioni normali è emerso che la proteina Homer 1a è espressa costitutivamente nel muscolo cardiaco di topo e ratto e nelle cellule HL-1 (una specifica linea cellulare cardiaca). Mediante immunofluorescenze su sezioni di cuore di ratto adulto (analizzate utilizzando il microscopio confocale) abbiamo esaminato la localizzazione sub-cellulare di Homer 1a che risulta essere sarcomerica e perinucleare. Successivamente, abbiamo analizzato l’espressione di Homer 1a in condizioni ipertrofiche; per questa analisi sono stati utilizzati cardiomiociti neonatali di ratto stimolati con l’agonista adrenergico norepinefrina (NE). In questo sistema sperimentale, abbiamo riscontrato un aumento significativo sia dell’mRNA che della proteina Homer 1a in seguito alla stimolazione con NE, mentre non abbiamo rilevato nessuna variazione sull’espressione della proteina Homer 1b/c (una diversa isoforma degli Homer). In cardiomiociti in coltura stimolati con NE, sono state, inoltre, analizzate le vie di trasduzione del segnale adrenergico coinvolte nell’up-regolazione di Homer 1a indotta da NE, usando specifici inibitori dei recettori α1- and β- adrenergici (prazosin e propanololo, rispettivamente). I risultati ottenuti hanno evidenziato che il prazosin, ma non il propranololo, drasticamente riduce l’up-regolazione dell’mRNA di Homer 1a indotta da NE, dimostrando che la via di trasduzione del segnale α1-adrenergico è coinvolta. L’effetto della stimolazione ipertrofica sull’espressione di Homer 1a è stato confermato anche su cellule HL-1 stimolata con NE. In questa linea cellulare abbiamo osservato che un’ora dopo la stimolazione con NE la proteina Homer 1a aumenta di un fattore 2,5. Complessivamente, questi risultati confermano la nostra ipotesi di lavoro e dimostrano il coinvolgimento della proteina Homer 1a nella trasduzione del segnale α1-adrenergico che induce ipertrofia cardiaca. Nella seconda parte di questo studio abbiamo esaminato gli effetti dell’over-espressione di Homer 1a monitorando diversi markers ipertrofici, quali la fosforilazione delle proteine MAPK/ERK1/2, la traslocazione nucleare di NFAT, l’attivazione del promotore di ANF e l’aumento delle dimensioni cellulari. I risultati hanno dimostrato che durante la stimolazione con NE Homer 1a modula la maggior parte di questi (eccezion fatta per la traslocazione nucleare di NFAT che non risulta essere variata dall’over-espressione di Homer 1a), al contrario in condizioni basali (senza stimolazione con NE) l’over-espressione di Homer 1a di per sé non ha alcun effetto. Nello specifico, i risultati ottenuti hanno rilevato che in cellule HL-1 stimolate con NE la proteina Homer 1a over-espressa significativamente riduce i livelli di fosforilazione delle proteine ERK1/2 di circa il 40%, modulando negativamente la via di trasduzione del segnale MAPK/ERK1/2. Per quanto concerne l’attività promotoriale di ANF, questa attività è significativamente ridotta di circa il 20% nelle cellule HL-1 over-esprimenti Homer 1a e stimolate con NE. Al fine di verificare la specificità di questo effetto sul promotore ANF, abbiamo condotto lo stesso esperimento over-esprimendo l’isoforma Homer 1c ed abbiamo riscontrato che, diversamente da Homer 1a, la proteina Homer 1c non ha alcun effetto sull’attività del promotore ANF in cellule HL-1 stimolate con NE. Successivamente, abbiamo analizzato l’effetto dell’over-espressione di Homer 1a sull’aumento delle dimensioni cellulari durante stimolazione con NE. I risultati ottenuti hanno dimostrato che la proteina Homer 1a è in grado di bloccare significativamente l’aumento delle dimensioni delle cellule HL-1 stimolate con NE. Nell’ultima parte di questo lavoro, abbiamo condotto un’analisi preliminare, in vivo, dell’espressione della proteina Homer 1a in tre modelli di ipertrofia, quali topi con costrizione trasversale dell’aorta, topi transgenici over-esprimenti Gαq e ratti trattati con monocrotalina. Diversamente da quanto ottenuto nel modello cellulare in vitro, in questi modelli l’espressione della proteina Homer 1a non risulta alterata dalle condizioni ipertrofiche, almeno nell’intervallo di tempo considerato. Tuttavia, per quanto riguarda questo approccio in vivo, sarà necessario analizzare l’espressione della proteina Homer 1a in un intervallo di tempo più ampio e, di conseguenza, ulteriori analisi sono richieste. In sintesi, dai nostri risultati relativi alla presenza ed alla localizzazione sub-cellulare di Homer 1a nel tessuto cardiaco è emerso che la proteina Homer 1a è costitutivamente espressa e mostra una localizzazione sarcomerica e peri-nucleare. Nei nostri modelli cellulari in vitro, l’up-regolazione di Homer 1a è un evento precoce dell’ipertrofia indotta da NE e, come dimostrato dagli studi di gain-of fuction, la proteina Homer 1a è in grado di antagonizzare l’avvio e lo sviluppo degli eventi che portano all’ipertrofia α1- adrenergica dipendente. Concludendo, i nostri dati in vitro indicano che Homer 1a è inserito in un meccanismo di feedback negativo in cui agisce come modulatore negativo, bloccando gli steps precoci dell’ipertrofia cardiaca. Tuttavia, ulteriori studi sono necessari per definire il meccanismo alla base di questo processo.
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.
Full textEgdell, Robin Michael. "Arrhythmogenic phenomena in isolated cardiac myocytes." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322380.
Full textLygate, 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.
Full textFinn, Stephen Garret. "The role of Gαâ‚₃ in hypertrophy." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325686.
Full textTroupes, 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.
Full textPh.D.
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. Previous reports indicate that STIM1 may play a role in regulation of cardiac hypertrophy. The goal of this work is to understand how STIM1 can affect contractile Ca2+ regulation in normal and diseased myocytes. We induced cardiac hypertrophy by slow progressive pressure overload in adult cats. Isolated adult feline ventricular myocytes (AFMs) exhibited increased STIM1 expression and activity, which correlated with altered Ca2+ handling. Use of BTP2 to block Orai channels resulted in a reduction of action potential (AP) duration and diastolic spark rate of hypertrophied myocytes, without affecting myocytes from sham-operated animals. Overexpressed STIM1 in cultured AFMs caused persistent Ca2+ influx that resulted in increased diastolic spark rates and prolonged APs, similar to myocytes from banded animals. STIM1 mediated Ca2+ influx could load the sarcoplasmic reticulum and activated CaMKII, which increased spark rates and lead to spontaneous APs. Importantly, STIM1 operated by associating with Orai channels because these effects could be blocked with either BTP2 or with a dominant negative Orai construct. Prolonged Ca2+ entry through this pathway eventually causes cell death. In conclusion, the work presented in this thesis establishes a role for STIM1-Orai in contractile Ca2+ regulation.
Temple University--Theses
Govindaraj, Vijayakumar. "Improved Cardiac Glucose Uptake: A Potential Mechanism for Estrogens to Prevent the Development of Cardiac Hypertrophy." kostenfrei, 2009. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/3591/.
Full textKuwahara, Koichiro. "Involvment of cardiotrophin-1 cardiac myocyte-nonmyocyte interactions during hypertrophy of rat cardiac myocytes in vitro." Kyoto University, 2000. http://hdl.handle.net/2433/180849.
Full textLi, 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.
Full textKalynych, Sergei. "Exploring the non-death function of caspase activity during cardiac hypertrophy." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28061.
Full textDecock, Juliette Brigitte Joelle. "The role of protein kinases in the development of cardiac hypertrophy." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285384.
Full textJamshidi, 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.
Full textYang, 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.
Full textSenanayake, Eshan Lankapura. "Left ventricular hypertrophy and myocardial protection with perhexiline during cardiac surgery." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5942/.
Full textRostami, Maryam. "A proposed pathophysiological role for TNFa in obesity induced cardiac hypertrophy." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/70077.
Full textThesis (MSc)--University of Stellenbosch, 2002.
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 achieved by an elevated cardiac output. Total blood volume is also increased in the obese due to the increased tissue volume and vascularity. With time, the obesity induced increase in cardiac preload results in left ventricular hypertrophy and dilatation. Obesity is also associated with complications such as hypertension, insulin resistance and impaired glucose metabolism. In addition, adipose tissue has been implicated to contribute to elevated circulating TNFa levels in obesity and may contribute to the pathophysiology of the heart in obese individuals. The heart is a major cytokine-producing organ that generates amongst others tumor necrosis factor a (TNFa). TNFa is a proinflammatory cytokine, which acts to increase its own production, has cytotoxic and cytostatic effects on certain tumor cells and influences growth and differentiation in virtually all cell types including cardiomyocytes. Elevated levels of TNFa are detected peripherally in almost all forms of cardiac injury and in hypertrophic cardiomyopathy. These elevations are proposed to be deleterious to the heart, although an adaptive role for low levels of TNFa has been proposed. Aim: The aim of the study was to determine whether there is a correlation between obesity and serum, myocardial, and adipose tissue TNFa levels and cardiac hypertrophy. We also wished to determine whether the hearts from the obese animals functioned normally under normoxic conditions and whether they responded differently to ischaemia/reperfusion when compared with their concurrent controls. Materials and Methods: Male Sprague-Dawley rats (n=100) were fed a high caloric diet (HCD) containing 33% rat chow, 33% condensed milk, 7% sucrose and 27% water, or standard laboratory rat chow for 6-12 weeks. Food consumption, body weight gain, heart weight and tibia length were measured. Serum glucose, insulin and lipid levels were also determined. Hearts were excised and perfused on the isolated Working Heart perfusion apparatus and cardiac function was monitored and documented. Hearts were then subjected to 15 minutes of total global ischaemia at 370C, and reperfused for 30 minutes. Cardiac function was again documented. A separate series of hearts were freeze-clamped at different time points during the experimental protocol and stored in liquid nitrogen for the determination of myocardial TNFa and cGMP levels. Serum TNFa levels were determined after 12 weeks on the high caloric or normal/control diet. After 12 weeks on the diet myocardial TNFa levels of the HCD fed animals and their concurrent controls were determined before and during ischaemia. Adipose tissue and myocardial tissue TNFa levels were also determined after 6, 9 and 12 weeks on the respective diets. Myocardial cGMP levels were measured in the HCD fed rats and the control rats after 6, 9, and 12 weeks. These data were used as an indirect index to determine whether the myocardial NOcGMP pathway was activated in the normoxic hearts on the respective diets. Results: The body weight of the HCO fed animals was significantly higher compared with their respective controls after 12 weeks on the diet (459.9 ± 173.8 g and 271.5 ± 102.6 g respectively (p<0.05». The HCO fed animals also had heart weight to body weight ratios that were significantly greater compared with the controls (4.2 ± 0.1 mglg and 3.7 ± 0.1 mglg respectively (p<0.05». The plasma glucose levels of the HCO fed animals were higher than their respective controls (9.2 ± 0.3 mmoiII and 7.8 ± 0.3 mmoiII respectively (p<0.05)), but their insulin levels were similar (12.87 ± 1.02 IlIUlml and 12.42 ± 5.06 IlIU/ml). Plasma lipid profiles (plasma cholesterol, high density lipoprotein (HOL) cholesterol and plasma triacylglyceride (TAG)) were abnormal in the HCO fed animals compared with the control rats. Plasma TAG levels in the HCO fed animals were significantly higher compared with the control rats (0.664 ± 0.062 mmoiII and 0.503 ± 0.043 (p<0.05», while plasma cholesterol levels (1.794 ± 0.058 mmoIII and 2.082 ± 0.062 mmoiII (p<0.05» and HOL cholesterol levels were significantly lower (1.207 ± 0.031 mmoiII and 1.451 ± 0.050 mmoiII (p<0.05». Cardiac mechanical function was similar for both groups before ischaemia, but the percentage aortic output recovery was lower for the hearts from the HCO fed animals when compared with their controls (47.86 ± 7.87% and 66.67 ± 3.76 % respectively (p<0.05». Serum TNFa levels of the HCO fed animals were higher compared with the control animals (51.04 ± 5.14 AU and 31.46 ± 3.72 AU respectively (p<0.05», but myocardial TNFa levels remained lower in these animals (312.0 ± 44.7 pglgram ww and 571.4 ± 132.9 pg/gram ww respectively (p<0.05)). During ischaemia these myocardial TNFa levels increased above those of the controls (442.9 ± 12.4 pg/gram ww and 410.0 ± 12.5 pg/gram ww respectively (p<0.05)). The adipose tissue TNFa levels were significantly increased after 12 weeks on the high caloric diet compared with the control animals (4.4 ± 0.4 pg/gram ww and 2.5 ± 0.3 pg/gram ww respectively (p<0.05)). There was no significant difference in the myocardial cGMP levels of the HCD rats compared with the conrol rats after 6, 9 and 12 weeks. Conclusion: 1) The high caloric diet induced obesity, which lead to cardiac hypertrophy in this study. 2) There was a strong correlation between elevated adipose tissue and serum TNFa levels, and cardiac hypertrophy. 3) Elevated serum TNFa levels did not lead to activation of the myocardial NO-cGMP pathway in the normoxic hearts in this model. 4) The hypertrophied hearts from the HCD fed animals had poorer post-ischaemie myocardial functions than their concurrent controls.
AFRIKAANSE OPSOMMING: Agtergrond: Miokardiale hipertrofie is In aanpassing wat gebeur as In gevolg van meganiese oorbelading of weefsel beskadiging. Verskillende stimuli kan tot miokardiale hipertrofie aanleiding gee soos byvoorbeeld In verhoging in nalading, of miokardiale hermodellering in respons op sitokiene. Verhoging van voorbelading in vetsug mag ook tot hipertrofie aanleiding gee. Vetsug word gekenmerk deur In oormatige liggaamsmassa wat tot metaboliese versteurings lei. Die oormatige liggaamsmassa vereis In verhoging in bloed- en suurstofverskaffing aan die perifere weefsel wat deur In verhoging in die kardiale uitset vermag kan word. Die bloed volume van In vetsugtige individu word ook verhoog as gevolg van In verhoging in weefselvolume en vaskulariteit en met verloop van tyd induseer die verhoogde kardiale voorbelading linker ventrikulêre hipertrofie en dilatasie. Vetsug word ook met verskeie ander siekte toestande soos hipertensie, insulien weerstandigheid en versteurde glukose metabolisme, geassosieer. Vetweefsel dra ook by tot verhoging van tumor nekrose faktor alfa (TNFa) vlakke in die bloed, wat op sy beurt tot miokardiale hipertrofie mag bydra. TNFa is In proinflammatoriese sitokien wat sy eie produksie kan stimuleer. Dit het ook sitotoksiese en sitostatiese effekte op sekere tumor selle en kan groei en differensiasie in bykans alle seltipes, insluitende kardiomiosiete, stimuleer. Die hart kan ook TNFa produseer en verhoogde TNFa vlakke word feitlik in alle vorms van miokardiale besering en hipertrofiese kardiomiopatie waargeneem. Daar word voorgestel dat verhoogde TNFa vlakke vir die hart nadelig is, ten spyte van die vermoeding dat die sitokien In potensiële aanpassings rol by laer vlakke het. Doelstelling: Die doel van hierdie studie was om vas te stelof daar 'n verband tussen vetsug en serum, miokardiale en vetweefsel TNFa vlakke en miokardiale hipertrofie, bestaan. Ons het ook gepoog om te bepaal of harte van vetsugtige diere normaal funksioneer en of die response van sulke harte op isgemie-herperfusie van die van ooreenstemmende kontroles verskil. Materiaal en tegnieke: Manlike Sprague-Dawley rotte (n=100) is vir 6-12 weke op 'n hoë kalorie dieët (HKD) geplaas. Die HKD het uit 33% rotkos, 33% gekondenseerde melk, 7% sukrose en 27% water bestaan. Kontrole diere het standaard laboratorium rotkos ontvang. Voedselinname, liggaamsmassa toename, serum insulien, glukose en lipied vlakke is ook bepaal. Harte is geïsoleer en geperfuseer volgens die Werk Hart perfusie metode en hart funksie is gemonitor en gedokumenteer. Harte is vervolgens aan 15 minute globale isgemie by 3rC blootgestel en daarna weer vir 30 minute geherperfuseer waartydens hartfunksie weer gedokumenteer is. 'n Aparte groep harte is op spesifieke tydsintervalle gedurende die eksperimentele protokol gevriesklamp en in vloeibare stikstof gestoor vir die bepaling van miokardiale TNFa en sGMP vlakke. Serum TNFa vlakke is bepaal na 12 weke op die dieët. Na die diere 12 weke op die HKD was, is hierdie diere en hulooreenstemmende kontroles se miokardiale TNFa vlakke voor en na isgemie bepaal. Vetweefsel en miokardiale TNFa vlakke is ook onderskeidelik na 6, 9 en 12 weke bepaal. Miokardiale sGMP vlakke is in die HKD diere en in die kontrole diere na 6, 9 en 12 weke bepaal. sGMP vlakke is gebruik as 'n indirekte indeks van aktivering van die miokardiale NO-sGMP boodskapper pad. Resultate: Na 12 weke op die dieët was die liggaamsmassa van die HKD diere beduidend hoër in vergeleke met hulooreenstemmende kontroles (459.9 ± 173.8 g en 271.5 ± 102.6 g (p<0.05)). Die HKD diere se hart massa tot liggaam massa verhouding was ook beduidend hoër in vergelyking met die van kontroles (4.2 ± 0.1 mglg en 3.7 ± 0.1 mglg (p<0.05)). Alhoewel insulien vlakke dieselfde was (12.42 ± 5.06 j.lIU/ml en 12.87 ± 1.02 j.lIU/ml), was serum glukose vlakke van die HKD diere hoër as die van die ooreenstemmende kontroles (9.2 ± 0.3 mmoiii en 7.8 ± 0.3 mmoiii (p<0.05)). Plasma lipied profiele (HOL cholesterol, plasma cholesterol en trigliseriede) was abnormaal in die HKD diere. Plasma TAG vlakke in die HKD diere was beduidend hoër as die van die kontroles (0.664 ± 0.062 mmoiii en 0.503 ± 0.043 (p<0.05)), terwyl plasma cholesterol vlakke (1.794 ± 0.058 mmoiii en 2.082 ± 0.062 mmoiii (p<0.05)) en HOL cholesterol vlakke beduidend laer was (1.207 ± 0.031 mmoiii en 1.451 ± 0.050 mmoiii (p<0.05)). Miokardiale meganiese funksie was dieselfde vir beide groepe voor isgemie, maar die persentasie aorta omset herstel tydens herperfusie was laer in die HKD diere in vergelyking met die van kontrole diere (47.86 ±. 7.87% en 66.67 ± 3.76% (p<0.05)). Serum TNFa vlakke van die HKD diere was beduidend hoër as die van kontrole diere (51.04 ± 5.14 AU en 31.46 ± 3.72 AU (p<0.05)), maar miokardiale TNFa vlakke was laer (312.0 ± 44.7 pglgram nat gewig en 571.4 ± 132.9 pglgram nat gewig (p<0.05)). Die vetweefsel TNFa vlakke was ook beduidend verhoog na 12 weke op "n hoë kalorie dieët wanneer dit vergelyk word met die van kontrole diere (4.4 ± 0.4 pglgram nat gewig en 2.5 ± 0.3 pglgram nat gewig respektiewelik (p<0.05)). Daar was geenbeduidende verskille in die miocardiale vlakke van sGMP in die HKD diere in vergelyking met die kontroles na 6, 9 en 12 weke. Gevolgtrekkings: 1) "n Hoë kalorie dieët het in dié studie vetsug geïnduseer en tot miokardiale hipertrofie gelei. 2) Daar was "n positiewe korrelasie tussen verhoogde vetweefsel en serum TNFa vlakke, en miokardiale hipertrofie. 3) Verhoogde serum TNFa vlakke het nie tot die aktivering van die miokardiale NO-sGMP pad in hierdie model gelei nie. 4) Die hipertrofiese harte het tydens herperfusie ná isgemie swakker as hulooreenstemmende kontroles gefunksioneer.
Wilkins, Benjamin Joseph. "Calcineurin-NFAT Signaling in Cardiac Hypertrophy: In Sickness and In Health?" University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1088446389.
Full textWilkins, Benjamin J. "Calcineurin-NFAT signaling in cardiac hypertrophy in sickness and in health? /." Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1088446389.
Full textHarper, Shavonn Christine. "The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/498061.
Full textPh.D.
Pathological cardiac hypertrophy (PCH) occurs in response to pathological stimuli affecting the heart such as coronary artery disease, myocardial infarction, or hypertension. PCH is also be independent risk factor for cardiac events and/or sudden death. Despite therapeutic advancements in the treatment of cardiovascular diseases (CVD) and heart failure, deaths due to CVD remain the leading cause of mortality worldwide. Furthermore, treatment of these cardiovascular diseases slows their progression, but individuals eventually progress to heart failure, which has a 5-year survival rate of approximately 50 percent. There is a clear need for development of new therapies that can reverse PCH and the associated damage to the heart. As healthcare improves, populations are living longer, and illness due to age increases. One issue that occurs with aging is loss of normal cardiac function leading to heart failure. This functional decline is accompanied by morphological changes in the heart, including hypertrophy. Although it is well documented that myocardial remodeling occurs with aging, the mechanisms underlying these changes are poorly understood. Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor β (TGF-β) superfamily of proteins, which regulate a number of cellular processes. Shared circulation of a young mouse with an old mouse or a single daily intraperitoneal (IP) injection of GDF11 for 30 days was shown to reverse aging-induced pathological cardiac hypertrophy. This molecule is highly homologous with another TGF-β family member, myostatin, which is a known negative growth regulator of skeletal muscle. We began by attempting to validate published data claiming that a single daily intraperitoneal (IP) injection of 0.1 mg/kg/day of GDF11 could reverse aging induced cardiac hypertrophy. We performed a blinded study during which treated 24-month-old C57BL/6 male mice with a single IP injection of 0.1 mg/kg/day of GDF11for 28 days and monitored changes in cardiac function and structure using echocardiography (ECHO). We also looked for differences in fibrosis, myocyte size, markers of pathological hypertrophy and heart weight. We were unable to find any differences between vehicle treated age mice and GDF11 treated aged mice in any of the measured parameters. While we did find an increase in heart weight between 8-week-old mice and the 24-month-old mice, there was no difference in the heart weight to body weight ratios of these groups of animals. From these data we concluded that our aged- mice did not have pathological hypertrophy and the dose of GDF11 used in this study did not have any effect on cardiac structure or function. Hypertensive heart disease results in changes in cardiac structure and function including left ventricular hypertrophy, systolic and/or diastolic dysfunction. It is also a leading cause of heart failure. Members of the TGF-β superfamily of proteins have been shown to be involved in many of the processes that occur in the heart in response to hypertension, such as the fibrotic response. Although it was previously shown that treatment with 0.1 mg/kg of GDF11 did not prevent pressure overload induced cardiac hypertrophy, we found this dose was too low to alter cardiac structure in our aging study. In addition, a single GDF11 dose is insufficient to fully address this issue. We therefore performed a blinded dose-ranging study to investigate the effects of GDF11 on pressure overload induced cardiac hypertrophy using transverse aortic constriction (TAC) which mimics the effects of chronic hypertension on the heart. In this study, animals received TAC surgery and were assigned to treatment groups so that there were no differences in wall thickness, cardiac function, or pressure gradients across the aortic constriction at the start of the treatments 1 week after TAC. Mice were given 0.5 mg/kg/day of GDF11, 1.0 mg/kg/day GDF11, 5.0 mg/kg/day of GDF11, or vehicle via a single daily IP injection for 14 days. Using these higher doses, we found that GDF11 had dose dependent effects on both cardiac structure and function following TAC. Myocyte cross sectional area was dose-dependently decreased compared to vehicle treated mice in both sham and TAC conditions. Cardiac function was preserved in the 1.0 and 5.0 mg/kg groups treatment groups after TAC. Left ventricular internal chamber dimensions were preserved with the 1.0 mg/kg treatment group. Treatment with GDF11 caused a dose dependent decrease on both body weight and heart weight in both normal and TAC mice, but with an effect on heart weight in the TAC mice that was independent of body weight. However, the 5.0 mg/kg dose caused large reductions in body weight (cachexia) and death. Our results show that GDF11 can reduce pathological hypertrophy and cardiac remodeling after pressure overload, but there is a narrow therapeutic range.
Temple University--Theses
Huang, Brandon Pei Han. "The regulation of protein synthesis in adult rat cardiomyocytes." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/976.
Full textSaeedi, Ramesh. "AMP-activated protein kinase and hypertrophic remodeling of heart muscle cells." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/4065.
Full text