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Relevant bibliographies by topics / Myosin Myocardium

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Academic literature on the topic 'Myosin Myocardium'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Myosin Myocardium"

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Buttrick, P., C. Perla, A. Malhotra, D. Geenen, M. Lahorra, and J. Scheuer. "Effects of chronic dobutamine on cardiac mechanics and biochemistry after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (1991): H473—H479. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h473.

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After myocardial infarction in rats, muscle performance in the remaining hypertrophied myocardium deteriorates and is associated with a decrease in myosin adenosinetriphosphatase (ATPase) activity and a shift to the V3 myosin heavy-chain isoform. We have previously shown in another model of hypertrophy, secondary to renovascular hypertension, that chronic intermittent adrenergic stimulation with dobutamine (Db) can prevent this biochemical adaptation. The present study was undertaken to assess the effects of chronic Db treatment on cardiac mass, function, metabolism, and myosin biochemistry in

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Larue, Catherine, Charles Calzolari, Jocelyne Léger, Jean Léger, and Bernard Pau. "Immunoradiometric assay of myosin heavy chain fragments in plasma for investigation of myocardial infarction." Clinical Chemistry 37, no. 1 (1991): 78–82. http://dx.doi.org/10.1093/clinchem/37.1.78.

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Abstract Estimation of the extent and location of infarct is important for the prognosis and hence therapeutic strategy in patients with acute myocardial infarction (AMI). Because cardiac myosin is the major structural protein of the myocardium, and may thus reflect the extent of injured tissue, we established a new sensitive immunoradiometric assay, using a pair of monoclonal antibodies (Mabs) that specifically bind the myosin heavy chain fragments liberated from the myocyte into plasma after a heart attack. A first Mab is linked to a magnetic solid phase. A second Mab, radiolabeled with 125I

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Locher, Matthew R., Maria V. Razumova, Julian E. Stelzer, Holly S. Norman та Richard L. Moss. "Effects of low-level α-myosin heavy chain expression on contractile kinetics in porcine myocardium". American Journal of Physiology-Heart and Circulatory Physiology 300, № 3 (2011): H869—H878. http://dx.doi.org/10.1152/ajpheart.00452.2010.

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Myosin heavy chain (MHC) isoforms are principal determinants of work capacity in mammalian ventricular myocardium. The ventricles of large mammals including humans normally express ∼10% α-MHC on a predominantly β-MHC background, while in failing human ventricles α-MHC is virtually eliminated, suggesting that low-level α-MHC expression in normal myocardium can accelerate the kinetics of contraction and augment systolic function. To test this hypothesis in a model similar to human myocardium we determined composite rate constants of cross-bridge attachment ( fapp) and detachment ( gapp) in porci

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Suematsu, Nobuhiro, Shinji Satoh, Shintaro Kinugawa та ін. "α1-Adrenoceptor-Gq-RhoA signaling is upregulated to increase myofibrillar Ca2+ sensitivity in failing hearts". American Journal of Physiology-Heart and Circulatory Physiology 281, № 2 (2001): H637—H646. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h637.

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α1-Adrenergic stimulation, coupled to Gq, has been shown to promote heart failure. However, the role of α1-adrenergic signaling in the regulation of myocardial contractility in failing myocardium is still poorly understood. To investigate this, we observed 1) the effect of phenylephrine on myofibrillar Ca2+ sensitivity in α-toxin-skinned cardiomyocytes, and 2) protein expression of Gq, RhoA, and myosin light chain phosphorylation using tachypacing-induced canine failing hearts. Phenylephrine significantly increased myofibrillar Ca2+ sensitivity in failing but not in normal cardiomyocytes. Wher

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Khalina, Yana, Sergey Udaltsov, and Zoya A. Podlubnaya. "Ischemic myocardium: Behavior of myosin light chains." Journal of Molecular and Cellular Cardiology 34, no. 6 (2002): A84. http://dx.doi.org/10.1016/s0022-2828(02)91028-x.

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Gregorich, Zachery R., Jitandrakumar R. Patel, Wenxuan Cai, et al. "Deletion of Enigma Homologue from the Z-disc slows tension development kinetics in mouse myocardium." Journal of General Physiology 151, no. 5 (2019): 670–79. http://dx.doi.org/10.1085/jgp.201812214.

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Enigma Homologue (ENH) is a component of the Z-disc, a structure that anchors actin filaments in the contractile unit of muscle, the sarcomere. Cardiac-specific ablation of ENH protein expression causes contractile dysfunction that ultimately culminates in dilated cardiomyopathy. However, whether ENH is involved in the regulation of myocardial contractility is unknown. To determine if ENH is required for the mechanical activity of cardiac muscle, we analyze muscle mechanics of isolated trabeculae from the hearts of ENH+/+ and ENH−/− mice. We detected no differences in steady-state mechanical p

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Toepfer, Christopher N., Markus B. Sikkel, Valentina Caorsi, et al. "A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 2 (2016): H465—H475. http://dx.doi.org/10.1152/ajpheart.00899.2015.

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Myocardial remodeling in response to chronic myocardial infarction (CMI) progresses through two phases, hypertrophic “compensation” and congestive “decompensation.” Nothing is known about the ability of uninfarcted myocardium to produce force, velocity, and power during these clinical phases, even though adaptation in these regions likely drives progression of compensation. We hypothesized that enhanced cross-bridge-level contractility underlies mechanical compensation and is controlled in part by changes in the phosphorylation states of myosin regulatory proteins. We induced CMI in rats by le

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Patel, Jitandrakumar R., Daniel P. Fitzsimons, Scott H. Buck, Mariappan Muthuchamy, David F. Wieczorek та Richard L. Moss. "PKA accelerates rate of force development in murine skinned myocardium expressing α- or β-tropomyosin". American Journal of Physiology-Heart and Circulatory Physiology 280, № 6 (2001): H2732—H2739. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2732.

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In myocardium, protein kinase A (PKA) is known to phosphorylate troponin I (TnI) and myosin-binding protein-C (MyBP-C). Here, we used skinned myocardial preparations from nontransgenic (NTG) mouse hearts expressing 100% α-tropomyosin (α-Tm) to examine the effects of phosphorylated TnI and MyBP-C on Ca2+ sensitivity of force and the rate constant of force redevelopment ( k tr). Experiments were also done using transgenic (TG) myocardium expressing ∼60% β-Tm to test the idea that the α-Tm isoform is required to observe the mechanical effects of PKA phosphorylation. Compared with NTG myocardium,

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Ma, Weikang, Marcus Henze, Robert L. Anderson, et al. "The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium." Circulation Research 129, no. 6 (2021): 617–30. http://dx.doi.org/10.1161/circresaha.120.318647.

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Rationale: Myofilament length-dependent activation (LDA) is the key underlying mechanism of cardiac heterometric autoregulation, commonly referred as the Frank-Starling Law of the heart. Although alterations in LDA are common in cardiomyopathic states, the precise structural and biochemical mechanisms underlying LDA remain unknown. Objective: Here, we examine the role of structural changes in the thick filament during diastole, in particular changes in the availability of myosin heads, in determining both calcium sensitivity and maximum contractile force during systole in permeabilized porcine

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Bing, O. H., N. L. Hague, C. L. Perreault, et al. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (1994): H1112—H1121. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h1112.

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To examine the mechanisms by which thyroid hormone modulates the inotropic state of rat myocardium, we studied the effects of thyroid state on isolated rat left ventricular papillary muscle function and intracellular calcium transients in the baseline state and in response to calcium and isoproterenol. Marked differences in contractile state of papillary muscles from hypothyroid and thyroid hormone-treated rats seen under baseline conditions (1.0 mM bath calcium, 30 degrees C, stimulation rate 12/min) do not appear to be due to differences in intracellular calcium concentration ([Ca2+]i) or to

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Dissertations / Theses on the topic "Myosin Myocardium"

1

O'Neill, Stephen Charles. "Myosin and electrophysiological heterogeneity in cardiac muscle." Thesis, Connect to e-thesis, 1987. http://theses.gla.ac.uk/1012/.

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Uys, Gerrida Mathilda. "Investigations of the role of myomegalin in the phosphorylation of cardiac myosin binding protein C." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5460.

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Thesis (PhD (Biomedical Sciences))--University of Stellenbosch, 2010.<br>Bibliography<br>ENGLISH ABSTRACT: Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac muscle disorder worldwide. The disease is characterized by extreme variability in the amount of hypertrophy that develops in different patients in response to sarcomeric protein-encoding gene mutations. The underlying defect in HCM is altered contractility of the sarcomere, primarily due to a defective sarcomere. Although numerous disease-causing genes have been identified for HCM, the factors that modify the amount of

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Braz-Ruivo, Luis. "An investigation for latent parvovirus DNA in the myocardium and serum antibodies against myosin and laminin in dogs with dilated cardiomyopathy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0007/NQ43249.pdf.

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Kreutziger, Kareen L. "Investigating the molecular mechanisms of cooperative tension generation in skeletal and cardiac muscle by altering acto-myosin interactions and engineering troponin C calcium binding kinetics /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8060.

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Razvadauskaite, Giedre. "Survival and differentiation of implanted skeletal myoblasts in the native and in the cryoinjured myocardium." Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0106103-155714.

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Thesis (M.S.)--Worcester Polytechnic Institute.<br>Keywords: myoblasts; dexamethasone; infarction; cryoinjury; desmin; myosin heavy chain; differentiation. Includes bibliographical references (p. 54-59).

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Korte, F. Steven. "Thick filament regulation of myocardial contraction." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4383.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.<br>The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "August 2006" Includes bibliographical references.

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Lima, Aline Regina Ruiz [UNESP]. "Estudo do músculo diafragma em ratos com insuficiência cardíaca crônica: composição das miosinas e expressão dos fatores de regulação miogênica." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/92159.

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Made available in DSpace on 2014-06-11T19:25:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-02-25Bitstream added on 2014-06-13T19:32:57Z : No. of bitstreams: 1 lima_arr_me_botfm.pdf: 825853 bytes, checksum: 593e370c7aa688abb20c1b7dda04672a (MD5)<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)<br>Estudos clínicos e experimentais têm sugerido que anormalidades da musculatura esquelética podem colaborar para a ocorrência precoce de dispnéia e fadiga em pacientes com insuficiência cardíaca crônica. Em músculos periféricos e respiratórios, frequentemente observa-

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Cliquet, Florence. "Immunonéphélémétrie à supports microparticulaires : dosages de marqueurs de nécrose myocardique : étude des interactions non spécifiques." Nancy 1, 1992. http://docnum.univ-lorraine.fr/public/SCD_T_1992_0407_CLIQUET.pdf.

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Les progrès récents de la cardiologie permettent une réduction de la mortalité due à l'infarctus du myocarde, grâce à la mise en place d'un traitement fibrinolytique entrepris rapidement destiné à désobstruer l'artère coronaire bouchée. Un des objectifs de notre travail a consisté à mettre au point des dosages de marqueurs sériques par immunonéphélémétrie à supports microparticulaires, technique simple et rapide. La myoglobine constitue la détermination biologique la plus précoce après constitution de la nécrose myocardique. Le dosage de la myosine, libérée plus tard des cellules lésées, perme

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Lima, Aline Regina Ruiz. "Estudo do músculo diafragma em ratos com insuficiência cardíaca crônica : composição das miosinas e expressão dos fatores de regulação miogênica /." Botucatu : [s.n.], 2010. http://hdl.handle.net/11449/92159.

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Resumo: Estudos clínicos e experimentais têm sugerido que anormalidades da musculatura esquelética podem colaborar para a ocorrência precoce de dispnéia e fadiga em pacientes com insuficiência cardíaca crônica. Em músculos periféricos e respiratórios, frequentemente observa-se modificação na composição das cadeias pesadas da miosina (MyHC) na insuficiência cardíaca. Os mecanismos e vias intracelulares de sinalização responsáveis pela alteração das MyHCs ainda não estão completamente definidos. Na insuficiência cardíaca direita induzida por monocrotalina, foi verificado que a expressão dos fato

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Addisu, Anteneh. "Natriuretic peptides as a humoral link between the heart and the gastrointestinal system." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002406.

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Books on the topic "Myosin Myocardium"

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¹¹¹Indium-labeled antimyosin monoclonal antibody. Physicians & Scientists Pub. Co., 1992.

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McCully, James Donald *. Myocardial cell gene regulation during the aging and cardiomyopathic disease processes: characterization of a Syrian hamster myosin heavy chain gene. 1989.

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Ebashi, Setsuro, and Iwao Ohtsuki. Regulatory Mechanisms of Striated Muscle Contraction. Springer, 2008.

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1922-, Ebashi Setsurō, and Ohtsuki Iwao, eds. Regulatory mechanisms of striated muscle contraction. Springer, 2007.

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Regulatory mechanisms of striated muscle contraction. Springer, 2007.

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(Editor), Setsuro Ebashi, and Iwao Ohtsuki (Editor), eds. Regulatory Mechanisms of Striated Muscle Contraction (Advances in Experimental Medicine and Biology). Springer, 2007.

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Book chapters on the topic "Myosin Myocardium"

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Gupta, Mahesh P., Madhu Gupta, Evelyn Dizon, and Radovan Zak. "Sympathetic control of cardiac myosin heavy chain gene expression." In Biochemistry of Signal Transduction in Myocardium. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1275-8_15.

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van der Velden, J., Z. Papp, N. M. Boontje, et al. "Myosin Light Chain Composition in Non-Failing Donor and End-Stage Failing Human Ventricular Myocardium." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9029-7_1.

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Bachinsky, Victor, Oleh Ya Vanchulyak, Alexander G. Ushenko, et al. "Diagnosis of Acute Coronary Insufficiency by the Method of Mueller Matrix Analysis of Myosin Myocardium Networks." In Multi-parameter Mueller Matrix Microscopy for the Expert Assessment of Acute Myocardium Ischemia. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1450-7_3.

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Rupp, Heinz, and R. Jacob. "Correlation between total catecholamine content and redistribution of myosin isoenzymes in pressure loaded ventricular myocardium of the spontaneously hypertensive rat." In Controversial issues in cardiac pathophysiology. Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11374-5_15.

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Rupp, H., R. Jacob, and N. S. Dhalla. "Signal Transduction in Myocardial Hypertrophy and Myosin Expression." In Developments in Cardiovascular Medicine. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1513-1_9.

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Zhang, Mei Luo, Samer Elkassem, Allen W. Davidoff, Kaoru Saito, and Henk E. D. J. ter Keurs. "Losartan inhibits myosin isoform shift after myocardial infarction in rats." In Biochemistry of Hypertrophy and Heart Failure. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9238-3_16.

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Ivanov, Georgi, Stylian Stoeff, Radko Pelov, and Milka Metodieva. "Electrophoretic Mobility of Myosin-Treated Lymphocytes from Patients with Myocardial Infarction." In Electromagnetic Fields and Biomembranes. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9507-6_47.

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Dillmann, Wolfgang H. "Diabetes Mellitus and Hypothyroidism Induce Changes in Myosin Isoenzyme Distribution in the Rat Heart — Do Alterations in Fuel Flux Mediate These Changes?" In Myocardial and Skeletal Muscle Bioenergetics. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5107-8_35.

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Kissling, G., and H. Rupp. "The influence of myosin isoenzyme pattern on increase in myocardial oxygen consumption induced by catecholamines." In Controversial issues in cardiac pathophysiology. Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11374-5_11.

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Takeda, N., T. Ohkubo, T. Hatanaka, A. Takeda, I. Nakamura, and M. Nagano. "Myocardial contractility and left ventricular myosin isoenzyme pattern in cardiac hypertrophy due to chronic volume overload." In Cardiac Energetics. Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-11289-2_21.

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Conference papers on the topic "Myosin Myocardium"

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Kaier, Thomas, Carsten Stengaard, Jack Marjot, et al. "148 Cardiac myosin-binding protein C to diagnose acute myocardial infarction in the pre-hospital setting, using multi-factorial nomograms." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.145.

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Ji, SY, ZQ Cheng, and NL Stephens. "The Role of Myocardin and Elk-1 in Regulation of Smooth Muscle Type Myosin Light Chain Kinase Expression in Airway Smooth Muscle." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2058.

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Reports on the topic "Myosin Myocardium"

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Zhang, John Q. Post-Myocardial Infarction and Exercise Training on Myosin Heavy Chain and Cardiac Function. Science Repository, 2019. http://dx.doi.org/10.31487/j.jicoa.2019.01.08.

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