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Libros sobre el tema "Cardiomyocytes"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 5 de octubre de 2024

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1

Skuse, Gary R. y Maureen C. Ferran, eds. Cardiomyocytes. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8.

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2

Michael, Piper Hans y Isenberg Gerrit, eds. Isolated adult cardiomyocytes. Boca Raton, Fla: CRC Press, 1989.

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3

Skuse, Gary R. y Maureen C. Ferran. Cardiomyocytes: Methods and Protocols. New York: Humana Press, 2015.

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4

Yoshida, Yoshinori, ed. Pluripotent Stem-Cell Derived Cardiomyocytes. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1484-6.

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5

Kartha, Chandrasekharan C. Cardiomyocytes in Health and Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9.

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6

Schlüter, Klaus-Dieter, ed. Cardiomyocytes – Active Players in Cardiac Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31251-4.

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7

Yee-Ki, Lee y Siu Chung-Wah. Calcium Handling in hiPSC-Derived Cardiomyocytes. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4093-2.

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8

Luiz, Belardinelli, ed. Effects of extracellular adenosine and ATP on cardiomyocytes. Austin: Landes, 1999.

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9

Sowerby, Andrew John. Anoxia, plasma membrane structure and calcium homeostasis: Photobleaching and microflurescence investigations inisolated rat cardiomyocytes. Uxbridge: Brunel University, 1991.

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10

Lai, Laura R. B. Protein oxidation occurs in cardiomyocytes exposed to an in vitro model of hypoxia/reperfusion injury. Ottawa: National Library of Canada, 1996.

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11

Li, Fen. A novel primary cell clulture system for adult cardiomyocytes involving a 3-D extracellular matrix. Ottawa: National Library of Canada, 1996.

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12

Liu, Bohao. Leveraging the potential of human iPSC-derived cardiomyocytes: From modeling congenital heart disease to treating myocardial infarction. [New York, N.Y.?]: [publisher not identified], 2021.

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13

Kohler-Schütz, Michaela. Die Wirkung von Insulin und (-)-Phenylephrin auf pHi, (Na+)i, (Ca2+)i, (K+)i und Plasmamembranpotential von Cardiomyocyten adulter Ratten. [s.l.]: [s.n.], 1997.

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14

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes. Editado por Hans Michael Piper y Gerrit Isenberg. CRC Press, 2019. http://dx.doi.org/10.1201/9780429290541.

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15

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes. Taylor & Francis Group, 2021.

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16

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes. Taylor & Francis Group, 2019.

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17

Skuse, Gary R. y Maureen C. Ferran. Cardiomyocytes: Methods and Protocols. Springer New York, 2016.

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18

Ikonomidis, John Sotirios. Preconditioning human ventricular cardiomyocytes. 1995.

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19

Yoshida, Yoshinori. Pluripotent Stem-Cell Derived Cardiomyocytes. Springer, 2022.

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20

Kartha, Chandrasekharan C. Cardiomyocytes in Health and Disease. Springer International Publishing AG, 2022.

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21

Rothen-Rutishauser, Barbara Maria. Dynamics of myofibrillogenesis in cardiomyocytes. 1996.

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22

Cardiomyocytes in Health and Disease. Springer International Publishing AG, 2022.

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23

Salvatori, Daniela, Harsha D. Devalla y Robert Passier. Cells to repair the infarcted myocardium. Editado por José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso y Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0030.

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The adult mammalian heart has poor regenerative capacity. Loss of functional cardiomyocytes following myocardial infarction leads to the replacement of functional muscle by scar tissue. This has a detrimental effect on cardiac function and may lead to heart failure. Potential regeneration of severe cardiac damage would require replacement of dead and damaged cardiomyocytes by transplantation, recruitment of endogenous progenitor cells, or induction of cardiomyocyte proliferation. For more than a decade, clinical trials to ameliorate the injured heart have been under way. However, after evaluation of the outcome of these trials it is evident that the beneficial effects of these cell-based transplantations are only marginal, and beneficial effects, if any, are not caused by regeneration of cardiomyocytes. In recent years, alternative approaches and various cell sources have been studied and suggested for cardiac repair. Recent advances in these cell-based therapies or strategies to activate endogenous cardiac repair are discussed.
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24

Schlüter, Klaus-Dieter. Cardiomyocytes – Active Players in Cardiac Disease. Springer, 2016.

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25

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes: Structure and Metabolism. Taylor & Francis Group, 2019.

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26

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes: Structure and Metabolism. Taylor & Francis Group, 2019.

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27

Yee-Ki, Lee y Siu Chung-Wah. Calcium Handling in HiPSC-Derived Cardiomyocytes. Springer, 2012.

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28

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes: Structure and Metabolism. Taylor & Francis Group, 2019.

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29

Piper, Hans Michael y Gerrit Isenberg. Isolated Adult Cardiomyocytes: Structure and Metabolism. Taylor & Francis Group, 2019.

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30

Schlüter, Klaus-Dieter. Cardiomyocytes – Active Players in Cardiac Disease. Springer, 2018.

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31

Piper, Hans Michael. Isolated Adult Cardiomyocytes: Structure and Metabolism. CRC Press, 1989.

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32

Yee-Ki, Lee y Siu Chung-Wah. Calcium Handling in hiPSC-Derived Cardiomyocytes. Springer, 2012.

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33

Schlüter, Klaus-Dieter. Cardiomyocytes - Active Players in Cardiac Disease. Springer London, Limited, 2016.

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34

Piper, Hans Michael. Isolated Adult Cardiomyocytes: Electrophysiology and Contractile Function. CRC Press, 1989.

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35

Effects of Extracellular Adenosine and Atp on Cardiomyocytes. International Thomson Publishing Services, 1998.

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36

Calcium Handling in HipscDerived Cardiomyocytes Springerbriefs in Stem Cells. Springer, 2012.

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37

Mumford, David Arthur. Modelling cardiac function using strands of cultured neonatal rat cardiomyocytes. 1985.

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38

Bauwens, Celine L. A scalable bioprocess for generating embyronic stem cell derived cardiomyocytes. 2004.

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39

Musso, Gabriel A. Effects of PP2a inhibition during ischemia/reperfusion on apoptosis in cardiomyocytes. 2005.

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40

Musso, Gabriel A. Effects of PP2a inhibition during ischemia/reperfusion on apoptosis in cardiomyocytes. 2005.

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41

David, Peter Guido. On the role of the tumor suppressor protein p53 in cultured rat cardiomyocytes. 1998.

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42

Elbel, Jörg Andreas. Sol-gel derived titania as culture substrate for long term culturing of differentiated cardiomyocytes. 2001.

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43

Polontchouk, Lioudmila Olegovna. Cell-cell and cell-substratum interactions in the long-term culture of adult cardiomyocytes. 1999.

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44

Harder, Beatrice Andrea. Remodeling of cytoskeletal and contractile structures by growth factors and thyroid hormone in clutured cardiomyocytes. 1997.

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45

Miquerol, Lucile. Origin and development of the cardiac conduction system. Editado por José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso y Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0015.

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The cardiac conduction system represents the ‘wiring’ of the heart and orchestrates the propagation of the electrical activity to synchronize heartbeats. It is built from specialized cardiomyocytes expressing a subset of ion channels and gap junctions indispensable for their electrophysiological properties. Although representing only a very small volume of the heart, the conduction system plays a crucial role in the appearance of cardiac arrhythmias. The cells forming the conduction system are derived from the same cardiac progenitors as the working cardiomyocytes, and the choice between these two fates is acquired during embryonic development. The components of the conduction system are progressively established during cardiac morphogenesis and converge to form an integrated electrical system in the definitive heart. This chapter will discuss recent advances using mouse genetic approaches which have improved understanding of the cellular origin and the transcriptional regulatory networks involved in the development of the conduction system.
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46

Cohen, Gideon. Studies on the role of K+-ATP channels in the preconditioning of cultured human ventricular cardiomyocytes. 2001.

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47

Yilmaz, Ali y Anca Florian. Myocarditis: imaging techniques. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0367.

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The clinical presentation of myocarditis is multifaceted and electrocardiogram (ECG) changes as well as biomarkers tend to be non-specific. Therefore, the diagnosis of myocarditis can be challenging and should be based on an integrated approach including patient history, physical examination, non-invasive tests such as ECG and serum biomarkers, and non-invasive cardiac imaging. As myocarditis may lead to global ventricular dysfunction, regional wall motion abnormalities, and/or diastolic dysfunction, echocardiography should be routinely performed. However, hallmarks of acute myocarditis comprise structural changes such as cardiomyocyte swelling, an increase in extracellular space and water content, accumulation of inflammatory cells, potential necrosis or apoptosis of cardiomyocytes, and myocardial remodelling with fibrotic tissue replacement that can be depicted by cardiovascular magnetic resonance. Nuclear techniques are still not routinely recommended for the work-up of myocarditis—with the possible exception of suspected sarcoidosis—due to limited data, limited diagnostic specificity, limited availability, and risk from radiation exposure. This chapter focuses on those non-invasive cardiac imaging techniques that are used in daily clinical practice for work-up of suspected myocarditis. However, as research continues and novel imaging techniques become available, it is hoped that even more accurate and timely diagnosis of myocarditis will be possible in the near future.
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48

Elliott, Perry, Kristina H. Haugaa, Pio Caso y Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.
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49

Menasché, Philippe. Stem Cell Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0010.

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• Experimental studies suggest that bone marrow-derived stem cells can improve function of infarcted myocardium• This benefit seems to involve paracrine signalling and limitation of left ventricular remodelling rather than true regeneration of cardiomyocytes from donor cells• These experimental findings have been translated in the clinical setting into significant, although moderate, improvements in cardiac function and LV remodelling but the extent to which these benefits impact on event-free long term survival remains to be determined• Optimisation of this therapeutic strategy will require a more comprehensive characterisation of cell functionality and an improvement in the methods used in cell transfer, engraftment, survival and integration.
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50

Meilhac, Sigolène M. Cardiac growth I: Cardiomyocyte proliferation. Editado por José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso y Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0009.

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Efficient contraction of the heart depends on the size and oriented architecture of the myocardium. This is severely compromised by myocardial infarction or in cardiomyopathies. Deciphering the mechanisms underlying heart growth has attracted much attention over the past decade, after the demonstration that the mammalian heart has some potential to regenerate, thus raising hopes that heart repair may become a reality. The mechanisms of cardiac growth during development have been well studied in the mouse model, taking advantage of sophisticated genetic engineering and new tools for tracking cell lineages and behaviour. We discuss the current view of the intrinsic regulation of cardiomyocyte behaviour, as well as how it is modulated by interplay with other cardiac cell types or with the environment. Such fundamental knowledge is important for understanding the origin of congenital heart defects and for the development of novel strategies of heart repair.
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