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Kuwahara, 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.
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Egdell, Robin Michael. "Arrhythmogenic phenomena in isolated cardiac myocytes." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322380.
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Iancu, Radu Vlad. "cAMP COMPARTMENTATION IN ADULT CARDIAC MYOCYTES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1220587638.
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Sirna, Josephine Barbara. "Iron regulation in neonatal rat cardiac myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0001/MQ33937.pdf.
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Patel, Trupti. "Mechanisms of Pathogen Sensing in Cardiac Myocytes." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486584.
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Bacterial sepsis and septic shock are major causes ofdeath in the critically ill. The majority ofthese deaths are due to the development ofmyocardial contractile dysfunction. The pathophysiology ofthis phenomenon is incompletely understood,. with previous work focussing on the influence ofcirculating inflammatory mediators ofnon-cardiac origin. Despite the recognised importance ofthese factors in contrit>uting to myocardial dysfunction, how the heart itselfresponds to bacterial pathogens directly has not been fully elucidated. The aims ofthis study were, first, to characterise the functional changes induced in isolated cardiac myocytes by whole bacteria. With the recent identification ofToll-like receptors (TLR)s (pattern recognition receptors (PRR)s) within the cardiac compartment, the second aim was to examine their roles in any changes seen. Finally, the role ofkey inflammatory mediators was examined. A novel method ofevaluating how Gram positive Staphylococcus aureus (S. aureus) or Gram negative Escherichia coli (E. call) directly modified 'populations' ofcardiac rat and mouse myocytes is described. Bacteria not' only decreased the propot:tion ofviable rod-shaped cells, they also decreased the proportion ofcells able to contract to electrical stimulation. S. aureus was found to have more pronounced effects than E. coli. In separate experiments, extracellular oxidants mimicked the effects ofbacteria on cardiac myocytes. The effects ofS. aureus and E. coli were mediated by TLR2ffLR6 and TLR4 respectively. Although no role for nitric oxide was found in bacteria-induced changes in myocyte function, the adverse effects ofS. aureus were partly prevented by specific cyclo-oygenase-2 inhibitors. However, the central hormone mediating the effects of bacteria (and oxidants) was found to be endothelin-l (ET-l), acting on ETA receptors. Caspase activation, without leading to apoptosis, was also implicated in mediating the phenotype changes induced by bacteria. Finally, cardiac myocytes ofthe noncontracting phenotype showed a reduced myofilament sensitivity to calcium, explaining the functional changes seen. Although the data are limited, a similar phenomenon was seen in failing human myocytes.
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Gavino, Belinda Joy E. "Nickel induced rhabdomyosarcoma in cultured cardiac myocytes." Tallahassee, Fla. : Florida State University, 2008. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/341766.
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Thesis (Honors paper)--Florida State University, 2008.Advisor: Dr. P. Bryant Chase, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Includes bibliographical references.
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Vierheller, Janine. "Modelling excitation coupling in ventricular cardiac myocytes." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19158.
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Um die Kontraktion einer Herzmuskelzelle durch den Kalziumeinstrom zu ermöglichen,
ist die Kopplung von Erregung und Kontraktion (ECC) von zentraler Bedeutung.
Durch das elektrische Signal einer Nachbarzelle wird die Depolarisation
des Sarkolemmas verursacht, wodurch sich die L-Typ-Kalziumkanäale (LKK) öffnen
und der Amplifizierungsprozess eingeleitet wird. Letzterer ist bekannt als Kalzium
induzierte Kalzium Freisetzung (CICR). Durch die LKK wird ein Kalziumeinstrom
in die Zelle ermöglicht, welcher zur Öffnung der Ryanodinrezeptoren (RyR) des
Sarkoplasmatischen Retikulums (SR) führt. Durch die Kalziumfreisetzung des SR
wird dieses im Cytoplasma akkumuliert.
Modelle für diese Prozesse werden seit mehreren Jahrzenten entwickelt. Bisher fehlte
jedoch die Kombination aus räumlich aufgelösten Kalziumkonzentrationen der
dyadischen Spalte mit stochastischen Simulationen der einzelnen Kalziumkanäle
und die Kalziumdynamiken in der ganzen Zelle mit einem Elektrophysiologiemodell
einer ganzen Herzmuskelzelle.
In dieser Arbeit entwickleten wir ein neues Modell, in welchem die Konzentrationsgradienten
von einzelnen Kanälen bis zum Ganzzelllevel räumlich aufgelöst
werden. Es wurde der quasistatische Ansatz und die Finite-Elemente-Methode zur
Integration partieller Differentialgleichungen verwendet. Es wurden Simulationen
mit unterschiedlichen RyR Markow-Kette-Modellen, verschiedenen Parametern für
die Bestandteile des SR, verschiedenen Konditionen des Natrium-Kalzium-Austauschers
und unter Einbindung der Mitochondrien durchgeführt. Ziel war es, das physiologische
Verhalten einer Kaninchen-Herzmuskelzelle zu simulieren. In dem neu
entwickelten Multiskalenmodell wurden Hochleistungsrechner verwendet, um detaillierte
Informationen über die Verteilung, die Regulation und die Relevanz von
den im ECC involvierten Komponenten aufzuzeigen. Zukünftig soll das entwickelte
Modell Anwendung bei der Untersuchung von Herzkontraktionen und Herzmuskelversagen
finden.Excitation contraction coupling (ECC) is of central importance to enable the contraction of the cardiac myocyte via calcium in ux. The electrical signal of a neighbouring cell causes the membrane depolarization of the sarcolemma and L-type Ca2+ channels (LCCs) open. The amplifcation process is initiated. This process is known as calcium-induced calcium release (CICR). The calcium in ux through the LCCs activates the ryanodine receptors (RyRs) of the sarcoplasmic reticulum (SR). The Ca2+ release of the SR accumulates calcium in the cytoplasm. For many decades models for these processes were developed. However, previous models have not combined the spatially resolved concentration dynamics of the dyadic cleft including the stochastic simulation of individual calcium channels and the whole cell calcium dynamics with a whole cardiac myocyte electrophysiology model. In this study, we developed a novel approach to resolve concentration gradients from single channel to whole cell level by using quasistatic approximation and finite element method for integrating partial differential equations. We ran a series of simulations with different RyR Markov chain models, different parameters for the SR components, sodium-calcium exchanger conditions, and included mitochondria to approximate physiological behaviour of a rabbit ventricular cardiac myocyte. The new multi-scale simulation tool which we developed makes use of high performance computing to reveal detailed information about the distribution, regulation, and importance of components involved in ECC. This tool will find application in investigation of heart contraction and heart failure.
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Grandi, Eleonora <1978>. "Computational analysis of excitability in cardiac myocytes." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/497/1/TesiEleonoraGrandi.pdf.
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Grandi, Eleonora <1978>. "Computational analysis of excitability in cardiac myocytes." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2007. http://amsdottorato.unibo.it/497/.
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Mathavan, Neashan Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Parameter optimization in simplified models of cardiac myocytes." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2009. http://handle.unsw.edu.au/1959.4/44709.
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Atrial fibrillation (AF) is a complex, multifaceted arrhythmia. Pathogenesis of AF is associated with multiple aetiologies and the mechanisms by which it is sustained and perpetuated are similarly diverse. In particular, regional heterogeneity in the electrophysiological properties of normal and pathological tissue plays a critical role in the occurrence of AF. Understanding AF in the context of electrophysiological heterogeneity requires cell-specific ionic models of electrical activity which can then be incorporated into models on larger temporal and spatial scales. Biophysically-based models have typically dominated the study of cellular excitability providing detailed and precise descriptions in the form of complex mathematical formulations. However, such models have limited applicability in multidimensional simulations as the computational expense is too prohibitive. Simplified mathematical models of cardiac cell electrical activity are an alternative approach to these traditional biophysically-detailed models. Utilizing this approach enables the embodiment of cellular excitation characteristics at minimal computational cost such that simulations of arrhythmogensis in atrial tissue are conceivable. In this thesis, a simplified, generic mathematical model is proposed that characterizes and reproduces the action potential waveforms of individual cardiac myocytes. It incorporates three time-dependent ionic currents and an additional time-independent leakage current. The formulation of the three time-dependent ionic currents is based on 4-state Markov schemes with state transition rates expressed as nonlinear sigmoidal functions of the membrane potential. Parameters of the generic model were optimized to fit the action potential waveforms of the Beeler-Reuter model, and, experimental recordings from atrial and sinoatrial cells of rabbits. A nonlinear least-squares optimization routine was employed for the parameter fits. The model was successfully fitted to the Beeler-Reuter waveform (RMS error: 1.4999 mV) and action potentials recorded from atrial tissue (RMS error: 1.3398 mV) and cells of the peripheral (RMS error: 2.4821 mV) and central (RMS error: 2.3126 mV) sinoatrial node. Thus, the model presented here is a mathematical framework by which a wide variety of cell-specific AP morphologies can be reproduced. Such a model offers the potential for insights into possible mechanisms that contribute to heterogeneity and/or arrhythmia.
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Anderson, Lorraine G. "Regulation of lipoprotein lipase in cultured cardiac myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24523.pdf.
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Jordan, Peter Nicholas. "Mechanism and control of alternans in cardiac myocytes /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1296101431&sid=8&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Smith, Timothy William. "Low temperature and cation transport in cardiac myocytes." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236212.
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Kennedy, Robert Arnold. "The regulation of Mdm2 expression in cardiac myocytes." Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/11791.
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Klomkleaw, Wuthichai. "ATF3 transgenic mice : structural analysis of cardiac myocytes /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486457871785014.
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Saucerman, Jeffrey J. "Systems analysis of beta-adrenergic signaling in cardiac myocytes /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3175273.
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Vallmitjana, Lees Alexander. "Multiscale image analysis of calcium dynamics in cardiac myocytes." Doctoral thesis, Universitat Politècnica de Catalunya, 2017. http://hdl.handle.net/10803/461083.
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Cardiac myocytes constitute a unique physiological system. They are the muscle cells that build up heart tissue and provide the force to pump blood by synchronously contracting at every beat. This contraction is regulated by calcium concentration, among other ions, which exhibits a very complex behaviour, rich in dynamical states at the molecular, cellular and tissue levels. Details of such dynamical patterns are closely related to the mechanisms responsible for cardiac function and also cardiac disease, which is the first cause of death in the modern world. The emerging field of translational cardiology focuses on the study of how such mechanisms connect and influence each other across spatial and temporal scales finally yielding to a certain clinical condition.
In order to study such patterns, we benefit from the recent and very important advances in the field of experimental cell physiology. In particular, fluorescence microscopy allows us to observe the distribution of calcium in the cell with a spatial resolution below the micron and a frame rate around the millisecond, thus providing a very accurate monitoring of calcium fluxes in the cell.
This thesis is the result of over five years' work on biological signal and digital image processing of cardiac cells. During this period of time the aim has been to develop computational techniques for extracting quantitative data of physiological relevance from microscopy images at different scales. The two main subjects covered in the thesis are image segmentation and classification methods applied to fluorescence microscopy imaging of cardiac myocytes. These methods are applied to a variety of problems involving different space and time scales such as the localisation of molecular receptors, the detection and characterisation of spontaneous calcium-release events and the propagation of calcium waves across a culture of cardiac cells.
The experimental images and data have been provided by four internationally renowned collaborators in the field. It is thanks to them and their teams that this thesis has been possible. They are Dr. Leif Hove-Madsen from the Institut de Ciències Cardiovasculars de Catalunya in Barcelona, Prof. S. R. Wayne Chen from the Department of Physiology and Pharmacology in the Libin Cardiovascular Institute of Alberta, University of Calgary, Dr. Peter P. Jones from the Department of Physiology in the University of Otago, and Prof. Glen Tibbits from the Department of Biomedical Physiology & Kinesiology at the Simon Fraser University in Vancouver.
The work belongs to the biomedical engineering discipline, focusing on the engineering perspective by applying physics and mathematics to solve biomedical problems. Specifically, we frame our contributions in the field of computational translational cardiology, attempting to connect molecular mechanisms in cardiac cells up to cardiac disease by developing signal and image-processing methods and machine-learning methods that are scalable through the different scales. This computational approach allows for a quantitative, robust and reproducible analysis of the experimental data and allows us to obtain results that otherwise would not be possible by means of traditional manual methods.
The results of the thesis provide specific insight into different cell mechanisms that have a non-negligible impact at the clinical level. In particular, we gain a deeper knowledge of cell mechanisms related to cardiac arrhythmia, fibrillation phenomena, the emergence of alternans and anomalies in calcium handling due to cell ageing.Els cardiomiòcits constitueixen un sistema fisiològic únic. Són les cèl·lules muscular que formen el cor i proporcionen la força per bombar la sang fent una contracció a cada batec. La regulació d'aquesta contracció es fa mitjançant concentració de calci (entre d'altres ions) i presenta una dinàmica molt complexa tant a l'escala molecular, cel·lular i de teixit. Detalls d'aquesta dinàmica estan fortament relacionats amb la funció cardíaca i per sobre de tot amb patologies cardíaques. La disciplina emergent de la cardiologia translacional es centra en l'estudi de com aquests mecanismes es connecten i s'influencien entre sí a través de diferents escales temporals i espacials finalment donant lloc a condicions clíniques. Per estudiar aquests patrons ens beneficiem dels recents avenços en fisiologia i biologia cel·lular. En particular, la microscòpia de fluorescència ens permet observar la distribució de calci dins una cèl·lula amb una resolució espacial per sota de la micra i temporal per sota del mil·lisegon, permetent un monitoratge acurat dels fluxos de calci en la cèl·lula cardíaca. Aquesta tesi és el resultat de més de cinc anys de feina en processament de senyal i imatge de cardiomiòcits humans. Durant aquest període de temps l'objectiu principal ha estat desenvolupar tècniques computacionals per extraure dades d'imatges de microscòpia amb rellevància fisiològica. Els dos temes principals coberts a la tesi són segmentació d'imatges i classificadors, aplicats a imatges de microscòpia de fluorescència de cardiomiòcits. Els mètodes s'apliquen a diferents problemes involucrant diverses escales espacials i temporals, des de determinar la posició de receptors a l’escala molecular passant detectar i caracteritzar alliberament espontani de calci intracel·lular fins a la propagació d'ones de calci en un cultiu de cèl·lules cardíaques. Les dades experimentals han estat proporcionades per quatre col·laboradors de renom internacional. És gràcies a ells i els seus equips que aquesta tesi ha estat possible. Són el Dr. Leif Hove-Madsen de l'Institut de Ciències Cardiovasculars de Catalunya a Barcelona, el Dr. S.R. Wayne Chen del Department of Physiology and Pharmacology al Libin Cardiovascular Institute of Alberta, University of Calgary, el Dr. Peter P. Jones del Department of Physiology a la University of Otago, i el Dr. Glen Tibbits del Department of Biomedical Physiology & Kinesiology de la Simon Fraser University a Vancouver. El treball pertany a la disciplina de la enginyeria biomèdica, fent èmfasi a la perspectiva de l'enginyeria, aplicant física i matemàtiques per solucionar problemes de la biomedicina. Específicament, s'emmarca en la cardiologia translacional computacional, mirant de connectar mecanismes a l’escala molecular amb patologies cardíaques mitjançant tècniques de processament de dades i aprenentatge automàtic que són escalables a les diferents escales d’aplicació. Aquest enfocament computacional permet una anàlisi quantitatiu, robust i reproduïble de les dades experimentals i ens permet d'obtenir resultats que serien impossibles d'assolir mitjançant els tradicionals mètodes manuals. Els resultats que proporciona la tesi han permès aprofundir en l'enteniment de diferents mecanismes fisiològics amb impacte en l'àmbit clínic. Particularment hem permès d’assolir coneixements relacionats amb l'arítmia cardíaca, la fibril·lació, processos d'alternança i anomalies relacionades amb l’envelliment.
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Landeen, Lee K. "Sphingosine-1-phosphate effects on cardiac fibroblasts and myocytes." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3255461.
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Thesis (Ph. D.)--University of California, San Diego, 2007.Title from first page of PDF file (viewed May 8, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Monte, Frederica del. "Cardiac failure and overload : contractile changes in single myocytes." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339182.
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Camelliti, Patrizia. "Structural and functional coupling of cardiac myocytes and fibroblasts." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418973.
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Smyrnias, Ioannis. "Modulation of contractility and calcium signalling in cardiac myocytes." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609227.
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Bayliss, Rebecca Anne. "Actions of NAADP and other agents in cardiac myocytes." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:8463cf89-a405-4880-9aad-6fa6ebac542d.
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Modulation of cardiac rate and contraction through calcium-dependent and independent means are of central import to the ability of an organism to adapt to its environment. Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent calcium-releasing second messenger across a broad range of tissues and organisms. In cardiac myocytes, NAADP is thought to stimulate calcium release from acidic stores which then bolsters filling and release during CICR. Questions remain: as to the potential need for amplification to generate the size of responses observed and the physiological role of the NAADP pathway. In contractile myocytes, photorelease of NAADP caused significant increase in calcium transient amplitude and velocity of transient upstroke and decay. Effects were absent during NAADP photorelease in the presence of Ned-19 or CaMKII inhibitors. Cellular calcium transient responses to β-adrenergic stimulation were significantly reduced in the presence of inhibitors of the NAADP pathway. These data support the hypothesis that NAADP-induced calcium release is relevant during adrenergic stimulation and requires amplification through CaMKII. Rate modulation at the sino-atrial node can occur through the hyperpolarisation-activated current I(f). Basal cardiac rate is a major determinant in cardiac mortality and compounds which specifically affect rate have clinical utility. A compound currently used to treat inflammatory conditions was found to have a significant rate-reducing effect in sino-atrial node preparations mediated by inhibition of I(f). Apelin, an endogenous peptide, has been reported to potently generate improved contractility without development of hypertrophy. Study of its effects in single cells have provided conflicting information, at least in part because of the difficulty in working with the compound. A method for the consistent observation of apelin-mediated contractile responses is presented, focusing on the timecourse of cell contraction. These observations suggest a role for apelin in both inotropy and lusitropy and will enable further research.
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Goodstadt, Leo J. "G-protein modulation of ionic currents in cardiac myocytes." Thesis, University of Oxford, 2000. http://ora.ox.ac.uk/objects/uuid:95df1add-328f-4045-a357-5e5875502812.
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The modulation of L-type calcium current (ICa) and the catecholamine-induced chloride current (ICl,cAMP) by G-protein coupled regulatory pathways were studied in isolated guinea pig cardiac ventricular myocytes using the whole cell patch clamp and flash photolysis techniques. A number of novel findings are reported in this thesis. The rapid release of GTP, the natural ligand of G-proteins, from its inert caged precursor produced a large enhancement of ICa which could be detected within 20 ms of the photolysing light pulse. A fast component of this response persisted under conditions of current rundown and inhibition of cAMP-dependent phosphorylation. This suggests the involvement of a membrane-delimited pathway not dependent on soluble second messengers. The photorelease of the non-hydrolysable GTPγS caused a biphasic increase in ICa in the majority of myocytes and a sustained response in the others. Pipette dialysis with GTPγS had a three-fold effect: pertussis toxin-sensitive inhibition of the ICa responses to isoprenaline, forskolin and photoreleased GTP; competitive inhibition of the enhancement of ICa by further photoreleased GTPγS; and modulation of the kinetics of cAMP-dependent activation of ICl,cAMP and ICa without any significant changes in their magnitudes. The flash photolysis of caged cAMP produced large increases in both ICl,cAMP and ICa but the latter was more than twice as sensitive to cAMP (EC50 = ~ 1.1 μM and ~ 0.47 μM). Urotensin has recently been identified as the ligand for a previously orphaned G-protein coupled receptor, and has been shown to be a potent chronic vasoconstrictor. This thesis reports an additional modulatory effect on ICl,cAMP. μM urotensin had no effect on its own but potentiated responses to sub-maximal sympathetic stimulation. Estrogen reduces forskolin- and isoprenaline-stimulated cAMP accumulation in the rat heart and inhibits cardiac ICa via a G-protein. However, the application of μM ß-estradiol to guinea pig myocytes in the presence of low doses of either forskolin (0.5 μM) or isoprenaline (20 nM) produced large increases in ICl,cAMP. This effect was mediated by a cell surface receptor. The involvement of nitric oxide synthase (NOS) was not required, unlike in acute estrogenic responses in vascular endothelia. Raloxifene, a selective estrogen receptor modulator (SERM), was similarly able to potentiate the results of sympathetic stimulation but with a much slower time course.
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Kirby, Mark Stephen. "The isolation, characterization and pathophysiology of mammalian cardiac myocytes." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47516.
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Bertaso, Federica. "The voltage-gated outward currents of human atrial myocytes." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314146.
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Bhardwaj, Ratan D. "Cytoarcheology: understanding cellular turnover in the human brain and heart /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-130-2/.
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Adams, Wendy A. "The effects of 2,3-butanedione monoxime on calcium regulation in rat ventricular myocytes." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367201.
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Rinne, Andreas. "Gene silencing using adenoviral RNAi vectors in adult cardiac myocytes." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=979850819.
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Iribe, Gentaro. "Effects of mechanical load on calcium handling in cardiac myocytes." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487260.
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In the 'in sitrl heart, electrical excitation of cardiac myocytes induces Ca2+ influx into the cytosolic space, which initiates muscle contraction (excitation contraction coupling) against a background of dynamically changing pre- and afterload conditions. On the other hand, mechanical load affects Ca2+ handling, either directly, or indirectly via modulation of electrical activity (mechano-electric feedback). The aim of this Thesis is to investigate and quantitatively describe the interactions between mechanical activity and Ca2+ handling, using experimental and mathematical modelling tools. Although there are a number of mathematical cardiac cell models available, few are aimed at reproducing beat-by-beat behaviour of Ca2+ handling. Therefore, we developed an original cell model which allows one to reproduce beat-by-beat changes in Ca2+ handling and resultant force production, which formed the basis for mathematical integration of the experimental findings of our Ca2+ handling study in this thesis. For e};perimental research, we developed a novel single cell force-length clamp (MyoStretcher), which uses piezo-control of carbon fibres (CF) to dynamically restrain the mechanical environment of isolated intact cardiomyocytes.Using the M):oStretcher, we subjected single isolated myocardial cells to dynamic contractions with work-loop style force-length (FL) relation, similar to those experienced by the cell 'in sittl. Single cell mechanics studies revealed that the end-systolic FL relation (ESFLR) IS load-independent In ventricular cardiomyoeytes of small mammals (Guinea pig). Modelling-based simulation studies suggest that the load-independent behaviour of ESFLR is the result of the combined effects ofload-dependent Ca2+ and crossbridge kinetics. Furthermore, the impact of diastolic stretch on sarcoplasmic reticulum (SR) Ca2+ handling was investigated. Axial cell stretch increased SR Ca2+ leak, but also and re-uptake of Ca2+ into the previously depleted SR of ventricular cardiomyocytes isolated from Guinea pig. The results were reproduced in model simulations. Axial stretch furthermore caused an acute increase in the Ca2+ spark rate of rat myoeytes. The mechanisms underlying this stretch-induced increase in spark rate act locally, are independent of nitric oxide and stretch-activated ion channels, and require an intact cytoskeleton. In conclusion, this thesis revealed that the interaction between cellular mechanics and Ca2+ handling is an important factor for integrative function of the heart, established several hitherto unknown mechanisms, and provided a novel set of experimental and theoretical tools for further research.
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MacQuaide, Niall. "Spontaneous Ca2+ waves in rabbit cardiac myocytes: a modelling study." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484888.
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Propagating intr~cellular Ca2+ waves in cardiac myocytes occur as a consequence of the overloaded state of the sarcoplasmic reticulum (SR). To examine these events in detail, ventricular cardiomyocytes were isolated from rabbit hearts and permeabilised with p-escin. Cytosolic Ca2+ signals were monitored using Fluo-5F (10J.lM) in combination with laser:scanning confocal microscopy. Through careful calibration ofthe intracellular Ca2+ signals and construction of analysis programs, the fluxes which underlie the Ca2+ wave were derived and subsequently incorporated into a mathematical model. The decline in cytosolic Ca2+ subsequent to rapid application ofcaffeine was used to quantify cellular Ca2+ diffusional loss (diffusional constant = 31.2+/-0.9 S-I). Ca2+ binding to cellular proteins was then calculated and the sum ofthe free Ca2+, bound Ca2+ and Ca2+ lost by diffusion was used as the integral ofthe Ca2+ flux across the SR. The first derivative ofthis was taken as the trans-SR flux rate. From the analysis ofthese signals it was apparent that the Ca2+ released from the SR during a wave was not significantly different from that released on application of lOmM caffeine (0.149 +/-0.10 roM vs. 0.154+/-0.10 mM)). This information, coupled with values ofintra-SR buffering allowed calculation ofintra-SR [Ca2l. This in tum allowed the trans SR [Ca2l gradient to be estimated and the subsequent calculation ofRyR and SERCA mediated Ca2+ flux. These measurements were used to derive parameters for construction of a 3- compartment model of Ca2+ flux using existing models ofCa2+ buffering, SERCA activity and leak. Three experimental interventions were used to study changes in Ca2+ wave properties and assess the effectiveness ofthe model in predicting wave frequency, minimum and maximum [Ca2l. These were: (i) changing extracellular Ca2+, (ii) inhibiting the RyR using tetracaine and (iii) inhibiting SERCA using 2',5'-di(tertbutyl)- I,4-benzohydroquinone (TBQ). As cytosolic Ca2+ was increased from 300 to 900nM, so frequency and systolic Ca2+were shown to 'increase nonlinearly, whilst diastolic [Ca2+] increased linearly. Calculated SR release threshold was found not to change. SERCA Vmax and KD both increased, with Vmax rising from 160 to 380 J.lMs·1 and KD rising from 239±48 to 354±18nM as extracellular [Ca2i was increased from 300nM to ~OOnM. The calculated peak permeability ofRyR mediated flux also increased from 41.1±6.5 to 61.2±3.6 S·l over this range. These changes, when included in the model, subsequently provided acceptable predictions of experimental results. Tetracaine caused frequency ofthe Ca2+ waves to decrease from 0.59±0.03 Hz to 0.35±0.02 Hz, systolic [Ca2l to increase from 2.06±0.11 J.lM to 3..16±0.24 J.lM and diastolic [Ca2l to decrease from 185±9 nM to157±10 nM. Flux analysis indicated that these changes were associated with an increase in the SR release threshold from 1.Ip±0.04 mM to 1.58±0.08 mM (n=6). Implementation ofthis threshold change in the computational model predicted a decrease in Ca2+ wave frequency to a simil~ value to that observed experimentally. The increased systolic [Ca2i was comparable to but greater than that observed experimentally. In contrast, the model predicted diastolic [Ca2l to increase while a decrease diastolic was observed experimentally. Application of the SERCA inhibitor TBQ (lJ.lM) decreased SR Ca2 + content, the amplitude and frequency of Ca2+ waves. Analysis ofthe underlying fluxes suggested that TBQ caused a 43% reduction in SERCA Vmax, with no significant ~hange in KD. Analysis also suggested that this reduction in Vmax was accompanied by a 25% reduction in SR release threshold. While the reduced SERCA Vmax is consistent with TBQ's known action on SERCA, the effect on Ca2+ wave amplitude was unexpected and cannot be easily explained with the current ci+ wave model.
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Ch'en, Frederick Fei-Te. "Regulation of sodium-bicarbonate co-transport in cardiac ventricular myocytes." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393335.
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Zoumpoulidou, Georgia. "Expression of p21superCip1/Wafl in cardiac myocytes under oxidative stress." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498504.
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Punn, Anu. "The molecular basis of adaptation to ischaemia in cardiac myocytes." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418254.
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Clarke, Thomas. "Connexin43 behaviour in cardiac myocytes exposed to ischaemia and hypoxia." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55623/.
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In coronary heart disease, the blood supply to the myocardium is insufficient for its needs and leads to cardiac ischaemia, which is often accompanied by the onset of lethal cardiac arrhythmias. Electrical communication between cardiac myocytes occurs across gap junctions located in intercalated discs. Gap junctions are specialised structures of the plasma membrane which facilitate direct and rapid communication between adjacent cells. Connexin 43 (Cx43) is the most widely expressed of the connexin family and is the main connexin in the heart. A cardiac ischaemia model system was developed to study the various aspects of cardiac myocyte biology. Simulated ischaemia caused neonatal cardiac myocytes to cease synchronous contractions after 3-4 hours and was accompanied by the reversible dephosphorylation of Cx43 after 5 hours. Cx43 dephosphorylation was then reversed by reoxygenating the cells for 30 minutes. In hypoxia the myocytes continued to beat and Cx43 remained phosphorylated. Rotigaptide, an antiairhythmic peptide with protracted action, increased intercellular dye transfer in cardiac myocytes, atrial HL-1 cells and HeLa cells expressing Cx43. The communication-modifying effect of rotigaptide was confined to cells expressing Cx43 since the peptide had no effect on dye transfer in HeLa cells expressing Cx32 and Cx26. Rotigaptide had little effect on cell beating rate or Cx43 expression. Phosphorylation of Cx43 in normoxic and ischaemic cells was also unaffected. Simulated ischaemia induced cardiac myocytes to release a peak of ATP after 80 minutes that was blocked by the connexin mimetic peptide GAP 26 and the gap junction inhibitor 18-a glyccyrrhetinic acid. This suggested that the release of ATP occurred through connexin hemichannels (CxHcs). The rotigaptide analogue AAP10 increased the transient peak of ATP release caused by ischaemia. The model developed has provided a platform to study the effects of simulated ischaemia on Cx43 dependent functions in the heart. Rotigaptide and AAP10 emerge as novel peptides with therapeutic potential for treating heart arrhythmias.
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Hardy, Matthew E. L. "Optically recording the cardiac action potential from isolated ventricular myocytes." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29961.
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The application of potentiometric dyes to isolated ventricular myocytes may provide the opportunity to record changes in drug-induced action potential (AP) morphology without the use of more difficult electrophysiological techniques.;Conditions were optimised for recording cardiac APs from isolated guinea pig ventricular myocytes stimulated at 1Hz using the ratiometric fluorescence emission of the dyes, di-4-ANEPPS and di-8-ANEPPS. Using di-8-ANEPPS, APs of steady duration were recorded for up to 28 min, when exposed to excitation light for 30 s in every 3 min, and using di-4-ANEPPS up to 24 min when exposed for 5 s in every 4 min. Using voltage-clamp protocols simultaneously with fluorescent recordings demonstrated a linear relationship between membrane potential and the fluorescence emission of both di-4-ANEPPS and di-8-ANEPPS.;Changes in action potential duration in response to increasing concentrations of cisapride were measured using a patch electrode or the emission of di-8-ANEPPS. Values for IC50 apparent for action potential prolongation were similar between the two assays. However, cells loaded with dye had an increased basal APD90 and a decreased sensitivity compared to patch electrode recordings, suggesting additional actions of the dye.;Screening a number of structurally similar dyes (di-4-ANEPPS, di-8-ANEPPS, di-12-ANEPPS, di-3-ANEPPDHQ and di-4-ANEPPDHQ) or demonstrated a variety of different pharmacological effects.;A double-blinded validation using the fluorescence emission of di-4-ANEPPS (loaded in guinea pig myocytes) was compared to results from standard proarrhythmia screening techniques: sharp electrode recordings from canine Purkinje fibres and M cells. The data suggest that guinea pig myocytes respond to drug-induced changes in AP morphology in a more similar manner to canine M cells from Purkinje fibres and show that di-4-ANEPPS can be used to monitor changes in AP duration and triangulation in isolated ventricular cells.;This method provides a higher throughput method for safety-pharmacology screens than standard microelectrode techniques, whilst still providing an indication of the effects of test compounds in native tissue.
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Warrier, Sunita. "cAMP BIOSENSORS AND SPATIOTEMPORAL cAMP SIGNALING IN ADULT CARDIAC MYOCYTES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1175718415.
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Janota, Danielle Marie. "Alpha1-Adrenergic Receptor Activation Mimics Ischemic Postconditioning in Cardiac Myocytes." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1406562863.
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Mattern, Janet. "Muscarinic Receptor Modulation of the Phospholipid Effect in Cardiac Myocytes." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc500469/.
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The muscarinic agonist carbachol stimulates a rapid increase in ^32Pi incorporation into phosphatidic acid (PA) and phosphatidylinositol (PI) in calcium tolerant myocytes prepared from heart tissue. The density of muscarinic receptors, determined by [^3H]-QNB binding, is greater in the atria than in the ventricles. 250 uM carbachol decreased specific [^3H]-QNB binding to muscarinic receptors on myocyte membranes by fifty percent. Trifluoperazine, also a phospholipase C inhibitor, inhibited the carbachol stimulated increase in ^32Pi incorporation into PA and PI and did not interfere with muscarinic receptor binding. Therefore, isolated canine myocytes provide a suitable model system to further study the muscarinic receptor stimulated phospholipid effect, and its role in mediating biochemical processes and physiological function in the heart.
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Kawamura, Teruhisa. "Expression of p300 protects cardiac myocytes from apoptosis in vivo." Kyoto University, 2004. http://hdl.handle.net/2433/147539.
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Martinez, Franco Ibeth Andrea. "Mechanism of cell death in cardiac myocytes exposed to doxorubicin." [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0015730.
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LODRINI, ALESSANDRA MARIA. "Cellular senescence and failure in human and animal cardiac myocytes." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/301783.
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Nel corso del mio dottorato sono stata coinvolta principalmente in due progetti con lo scopo di studiare la disfunzione cardiaca indotta da invecchiamento o chemioterapia.
Il primo studio aveva lo scopo di riprodurre e caratterizzare i meccanismi dell’invecchiamento utilizzando cardiomiociti (CMs) da cellule staminali pluripotenti indotte umane (hiPSCs) e inoltre testare terapie cardioprotettive, come gli esosomi (Exo) da cellule progenitrici cardiache (CPCs). L’invecchiamento cardiaco coinvolge rimodellamenti a livello dei singoli CMs che predispongono allo scompenso cardiaco e la cui incidenza aumenta con l’avanzare dell’età. Curiosamente, fino ad ora non è stato ancora sviluppato un modello di invecchiamento cardiaco umano.
Abbiamo riprogrammato CPCs umane ad iPSC e successivamente le abbiamo differenziate in CMs. Un fenotipo simile alla senescenza (SenCMs) è stato indotto con un breve trattamento (3 ore) con doxorubicina (Dox) a concentrazioni sub-letali (0.2 µM). 24 ore dopo il trattamento, alcuni SenCMs sono stati esposti ad Exo (~2·10^3 particelle/cellula) isolati dal medium di coltura delle CPCs. Il trattamento con Dox induce senescenza, come confermato dall’attivazione di p21 e dalla maggiore positività a SA-β-gal in confronto ai controlli (cCMs). Analisi biochimiche hanno rivelato la presenza di stress ossidativo e un potenziale di membrana mitocondriale depolarizzato nei SenCMs, con una ridotta produzione di ATP dai mitocondri. I SenCMs hanno anche difetti nel calcium handling e un QTc prolungato a causa dell’aumento di INaL. Questi effetti sono mitigati dal trattamento con Exo. Complessivamente, i SenCMs ricapitolano il fenotipo dei CMs invecchiati in termini di markers di senescenza e proprietà elettriche e metaboliche. Inoltre, l’esposizione ad Exo prodotti da CPCs limita molte delle anomalie cardiache indotte dall’invecchiamento.
Il secondo studio mirava a valutare la disfunzione cardiaca causata dalla somministrazione in combinazione di Dox e Trastuzumab (Trz) in miociti cardiaci di ratto. Il trattamento combinato con Dox e Trz in pazienti con cancro al seno è limitato a causa della cardiotossicità, che si manifesta con disfunzione contrattile ed aritmie. Il ruolo specifico dei due agenti nella cardiotossicità causata dalla terapia combinata è però non ancora del tutto chiarito.
I ratti hanno ricevuto 6 dosi di Dox, Trz o entrambi in maniera sequenziale. La disfunzione del ventricolo sinistro (LV) mediata da Dox era aggravata dalla somministrazione di Trz. Il trattamento con Dox, ma non con Trz, induceva danno ai tubuli T, prolungamento della durata del potenziale d’azione (APD), aumento dell’incidenza di post-depolarizzazioni tardive (DADs), decadimenti dei transienti di Ca2+ più lenti e la fuoriuscita di Ca2+ dal reticolo in Ca2+ sparks o Ca2+ embers. Il trattamento in combinazione esacerbava queste anomalie. Trz, ma non Dox, riduceva l’ampiezza dei transienti di Ca2+ e il contenuto di Ca2+ nel reticolo sarcoplasmatico (SR). Entrambi gli agenti aumentavano le onde di Ca2+ spontanee e diminuivano l’espressione di SERCA. Questi risultati suggeriscono che Dox, ma non Trz, potrebbe causare danno ai tubuli T in vivo e, inoltre, indurre cambiamenti nei parametri elettrici e nel Ca2+-handling. Mentre Dox induceva cambiamenti reversibili nei parametri elettrofisiologici, la successiva somministrazione di Trz impediva il rescue. Questi risultati illustrano il ruolo specifico di Dox e Trz e il loro ruolo nella cardiotossicità.During my PhD I was involved mainly in two research projects aimed to study myocardial dysfunction induced by aging or chemotherapy. The first study aimed to reproduce and characterize mechanisms involved in aging using cardiomyocytes (CMs) from human induced pluripotent stem cells (hiPSCs), and to test cardioprotective therapies, like cardiac progenitor cell (CPC)-derived exosomes (Exo). Aging of the heart involves adverse remodeling in CMs which results in heart failure with incidence that increases with age. Interestingly, till now we lacked a human model of cardiac aging. We reprogrammed CPCs into hiPSCs and subsequently differentiated in hiPSC-derived CMs. A senescence-like phenotype (SenCMs) was induced by short exposure (3 hours) to doxorubicin (Dox) at sub-lethal concentration (0.2 µM). 24h following DOX treatment, SenCMs were exposed to Exo (~2·103 particles/cell) collected from culture media of CPCs by ultracentrifugation. Dox treatment induced senescence, as confirmed by activation of p21 and increased SA-β-gal positivity compared to control CMs (cCMs). Biochemical analysis revealed presence of oxidative stress and a depolarized mitochondrial membrane potential due to the treatment, which resulted in decreased ATP production by mitochondria. SenCMs also showed impaired calcium handling and prolonged QTc vs. cCMs due to upregulation of INaL. These effects were mitigated by exposure to Exo. Overall, SenCMs recapitulate the phenotype of aged CMs in terms of senescence markers and electrical and metabolic properties. Additionally, exposure to CPC-derived Exo limited age-related cardiac anomalies. The second study aimed to study the cardiac dysfunction dependent on the combined administration of Dox and trastuzumab (Trz) through evaluation of cardiac performance, T-tubule organization, and electrophysiological changes in cardiac myocytes from an in-vivo rat model. Combined treatment with Dox and Trz in patients with HER2-positive cancer is limited by cardiotoxicity, as manifested by contractile dysfunction and arrhythmia. The respective roles of the two agents in the cardiotoxicity of the combined therapy are incompletely understood. Adult rats received 6 doses of either Dox or Trz, or the two agents sequentially. Dox-mediated left ventricular (LV) dysfunction was aggravated by Trz administration. Dox treatment, but not Trz, induced T-tubule disarray. Moreover, Dox, but not Trz monotherapy, induced prolonged action potential duration (APD), increased incidence of delayed afterdepolarizations (DADs) and beat-to-beat variability of repolarization (BVR), and slower Ca2+ transient decay. Although APD, DADs, BVR and Ca2+ transient decay recovered over time after the cessation of Dox treatment, subsequent Trz administration exacerbated these abnormalities. Trz, but not Dox, reduced Ca2+ transient amplitude and SR Ca2+ content. Both agents increased Ca2+ waves and downregulated SERCA. Finally, Dox increased resting Ca2+ waves, Ca2+ spark frequency, spark-mediated sarcoplasmic reticulum (SR) leak, and long-lasting Ca2+ release events (so-called Ca2+ “embers”). These results suggest that Dox, but not Trz, may cause T-tubule disarray in cardiac myocytes in vivo while also inducing overall larger changes in electrical parameters and intracellular Ca2+ handling. While Dox-induced changes in electrical parameters are reversible, subsequent Trz administration prevents their recovery. These findings illustrate the specific roles of Dox and Trz, and their interactions in cardiotoxicity and arrhythmogenicity.
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Miwa, Keiko, Jong-Kook Lee, Kyoko Hidaka, Rong-qian Shi, Gen Itoh, Takayuki Morisaki, and Itsuo Kodama. "Paracrine Factors from Cultured Cardiac Cells Promote Differentiation of Embryonic Stem Cells into Cardiac Myocytes." Research Institute of Environmental Medicine, Nagoya University, 2003. http://hdl.handle.net/2237/7580.
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Terracciano, Cesare Maria Nicola. "Effects of intracellular acidosis on CA²⁺ regulation mechanisms in cardiac myocytes." Thesis, Imperial College London, 1995. http://hdl.handle.net/10044/1/7910.
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Gonzalez, Jara Fabian Rodrigo. "Mechanisms regulating expression of the mkp-1 gene in cardiac myocytes." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428678.
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Peters, Christian G. "SNARE-Mediated Exocytosis of Atrial Natriuretic Peptide from Atrial Cardiac Myocytes." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1179405759.
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Ehara, Natsuhiko. "Activators of PPARγ antagonize protection of cardiac myocytes by endothelin-1." Kyoto University, 2005. http://hdl.handle.net/2433/144738.
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Herron, Todd J. "Molecular regulation of power output in single rat skinned cardiac myocytes." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3052177.
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Jeong, Gloria Young Ju. "Neutrophil-mediated damage to cardiac myocytes: inhibition by 4-methoxy nitroxide." Thesis, The University of Sydney, 2014. https://hdl.handle.net/2123/27283.
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Inflammation following acute myocardial infarction (AMI), leads to the recruitment of neutrophils to affected heart cells and hypochlorous acid (HOCl) produced by neutrophil myeloperoxidase (MPO) can further damage cardiac cells. This process involves activation of MAP kinases via enhanced tyrosine kinase (TK) and decreased protein tyrosine phosphatase (PTP) activities that promote an imbalance in cellular phosphorylation.
Inhibition of neutrophil-MPO by low molecular weight nitroxides may prevent this secondary damage and re-balance intracellular signalling. Cardiac myocyte-like H9c2 cells were coincubated with isolated human neutrophils that were either (i) untreated (control); (ii) activated with chemical stimulants or (iii) pre-treated with 4-Methoxynitroxide (MetT, 25 μM). Cells were co-cultured for 4 h and harvested. These were taken for genetic, biochemical
and molecular analysis. Exposure of H9c2 cells to activated neutrophils resulted in a weak trend to decreased cell viability vs the control. Cells treated with activated neutrophils also showed increased TK activity as judged by enhanced phosphorylation of MAP kinases p38 and ERK1/2 vs the control as assessed by Western blotting and immunofluorescent microscopy. Total PTP activity decreased in parallel with increased MAP kinase activity in the same H9c2 cells exposed to activated neutrophils. By contrast, pre-incubation of cells with MetT ameliorated increases in MAP kinase activity and restored PTP activity to baseline. Levels of mRNA for pro-inflammatory tumour necrosis factor, NFκB and antioxidants superoxide dismutase-1 were up-regulated in the presence of activated neutrophils, and pre-treatment with MetT inhibited these gene responses. Overall, the adverse effects of neutrophil-derived HOCl on cultured cardiac myocytes were ameliorated with a pharmacological dose of MetT suggesting that nitroxides may be beneficial in the setting of AMI.
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Champattanachai, Voraratt. "Effects of hexosamine biosynthesis on an in vitro model of cardiac ischemia." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008d/champattanachai.pdf.
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McArthur, Lisa. "Investigating interactions between rat adult cardiac myocytes and fibroblasts in the heart." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8512/.
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