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Artykuły w czasopismach na temat "Cardiomyocytes"
Nguyen, Phong D., Sarah T. Hsiao, Priyadharshini Sivakumaran, Shiang Y. Lim i Rodney J. Dilley. "Enrichment of neonatal rat cardiomyocytes in primary culture facilitates long-term maintenance of contractility in vitro". American Journal of Physiology-Cell Physiology 303, nr 12 (15.12.2012): C1220—C1228. http://dx.doi.org/10.1152/ajpcell.00449.2011.
Pełny tekst źródłaDerks, Wouter, i Olaf Bergmann. "Polyploidy in Cardiomyocytes". Circulation Research 126, nr 4 (14.02.2020): 552–65. http://dx.doi.org/10.1161/circresaha.119.315408.
Pełny tekst źródłaZhang, Yidi, Xin Zhao i Yaowei Liu. "A visual detection method of cardiomyocyte relaxation and contraction". AIP Advances 13, nr 2 (1.02.2023): 025028. http://dx.doi.org/10.1063/5.0133456.
Pełny tekst źródłaLieben Louis, Xavier, Pema Raj, Zach Meikle, Liping Yu, Shannel E. Susser, Shayla MacInnis, Todd A. Duhamel, Jeffrey T. Wigle i Thomas Netticadan. "Resveratrol prevents palmitic-acid-induced cardiomyocyte contractile impairment". Canadian Journal of Physiology and Pharmacology 97, nr 12 (grudzień 2019): 1132–40. http://dx.doi.org/10.1139/cjpp-2019-0051.
Pełny tekst źródłaStopp, Sabine, Marco Gründl, Marc Fackler, Jonas Malkmus, Marina Leone, Ronald Naumann, Stefan Frantz i in. "Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development". Proceedings of the National Academy of Sciences 114, nr 30 (11.07.2017): 8029–34. http://dx.doi.org/10.1073/pnas.1703406114.
Pełny tekst źródłaMensah, Isaiah K., i Humaira Gowher. "Signaling Pathways Governing Cardiomyocyte Differentiation". Genes 15, nr 6 (18.06.2024): 798. http://dx.doi.org/10.3390/genes15060798.
Pełny tekst źródłaZhang, Jun, Yuying Gao, Peng Chen, Yu Zhou, Sheng Guo, Li Wang i Jie Chen. "Bone Marrow-Derived Mesenchymal Stem Cells (BMSCs)-Exosome Carrying MiRNA-312 Inhibits Sevoflurane-Induced Cardiomyocyte Apoptosis Through Activation of Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) Pathway". Journal of Biomaterials and Tissue Engineering 12, nr 5 (1.05.2022): 947–52. http://dx.doi.org/10.1166/jbt.2022.2971.
Pełny tekst źródłaChiu, Chiung-Zuan, Bao-Wei Wang, Tun-Hui Chung i Kou-Gi Shyu. "Angiotensin II and the ERK pathway mediate the induction of myocardin by hypoxia in cultured rat neonatal cardiomyocytes". Clinical Science 119, nr 7 (22.06.2010): 273–82. http://dx.doi.org/10.1042/cs20100084.
Pełny tekst źródłaTakaoka, Nanako, Michiko Yamane, Ayami Hasegawa, Koya Obara, Kyoumi Shirai, Ryoichi Aki, Hiroyasu Hatakeyama i in. "Rat hair-follicle-associated pluripotent (HAP) stem cells can differentiate into atrial or ventricular cardiomyocytes in culture controlled by specific supplementation". PLOS ONE 19, nr 1 (26.01.2024): e0297443. http://dx.doi.org/10.1371/journal.pone.0297443.
Pełny tekst źródłaShi, Huairui, Xuehong Zhang, Zekun He, Zhiyong Wu, Liya Rao i Yushu Li. "Metabolites of Hypoxic Cardiomyocytes Induce the Migration of Cardiac Fibroblasts". Cellular Physiology and Biochemistry 41, nr 1 (2017): 413–21. http://dx.doi.org/10.1159/000456531.
Pełny tekst źródłaRozprawy doktorskie na temat "Cardiomyocytes"
Maggiorani, Damien. "Caractérisation de la sénescence des cardiomyocytes et identification de marqueurs associés". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30320/document.
Pełny tekst źródłaAgeing of the organism is associated with several chronic pathologies such as heart failure (HF). Recent studies have demonstrated the link between the accumulation of senescent cells during ageing and age-associated diseases. Cellular senescence, originally defined as a stable cell cycle arrest, acts as a tumorigenic repressor by limiting the proliferation of DNA damaged cells. Despite this protective effect, senescence is characterized by deep remodeling of cell biology which drives functional disorders, such as the acquisition of a senescence-associated secretory phenotype (SASP). Senescence can be induced by telomeric attrition and by exposition to cellular stress signals such as oxidative stress or irradiation, which induce telomeric damage, activation of the DNA Damage Response (DDR) and increased expression of antitumoral genes (p16INK4a, p21CIP1, p53). These genes are classically used as markers of senescence because their expression increases in several tissues during ageing but they are not tissue-specific. Therefore, At the cardiac level, ageing is characterized by cardiomyocytes hypertrophy, increased sensitivity to stress and highest risk of developing HF. Cardiomyocytes are post- mitotic cells and the senescence inductor mechanisms, specifics markers and their role in HF remains poorly understood. This thesis project is articulated around two aims, 1/ studying the role of telomeric damages and mitochondrial dysfunction in triggering cardiomyocyte senescence and 2/ identification of specifics markers. Fisrtly, we shown that aged cardiomyocytes overexpress classic markers of senescence such as p16INK4a, p53 et p21CIP1. Concerning the inductors mechanisms, we studied the implication of telomeric damages (telomere associated foci, TAF). During ageing, we found an increased number of TAFs per cardiomyocytes and their association with hypertrophy. Moreover, TAF- induction in cardiac H9c2 in vitro activated the p53/p21 pathway and induced senescence. These data confirmed the role of TAFs in cardiomyocyte senescence induction. Furthermore, aged cardiomyocytes exhibit a global alteration of genes involved in mitochondrial biology, oxidative stress and metabolism in aged cardiomyocytes that could play a prominent role in TAF accumulation with ageing. In a second part of the study, by using a next generation sequencing method (RNA-seq) we identified 6 new genes highly expressed in senescent cardiomyocytes (Prom2, Kcnk1, Pah, Edn3, Gdf15 and Tgfb2). Expression comparison with other senescent organs and cardiac stromal cells confirmed these new genes as cardiomyocyte specific. Thanks to an in vitro approach, we validate this signature by using different models of stress-induced senescence in cardiac H9c2 cells and demonstrated the implication of the p53 in the regulation of some of these genes. Moreover, Prom2 expression is associated with cardiomyocytes hypertrophy. In conclusion, we demonstrated that, with ageing, cardiomyocytes display a senescence phenotype associated with mitochondrial dysfunction and TAFs. This process is characterized by classic markers (p16INK4, p53/p21CIP1), hypertrophy and new identified signature. These new markers offer innovative perspectives in the understanding and the identification of the cardiac senescence and their potential deleterious role in heart failure
Nelson, Brandon John. "MicroRNA analysis of human embryonic stem cell derived cardiomyocytes and neonatal rat ventricular cardiomyocytes". 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?p1447322.
Pełny tekst źródłaTitle from first page of PDF file (viewed January 15, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 45-48).
Bond, Richard. "Cellular electrophysiology of rat pulmonary vein cardiomyocytes : a comparative study with left atrial cardiomyocytes". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685358.
Pełny tekst źródłaFijnvandraat, Arnoldus Cornelis. "Embryonic stem cell-derived cardiomyocytes". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/68354.
Pełny tekst źródłaRisto, Morten. "Modelling hypertrophy in dystrophic cardiomyocytes". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3402.
Pełny tekst źródłaDe, Marco Margot. "BAG3 role in cardiomyocytes physiopathology". Doctoral thesis, Universita degli studi di Salerno, 2013. http://hdl.handle.net/10556/896.
Pełny tekst źródłaThe anti-apoptotic protein BAG3 is expressed at high levels in skeletal and cardiac muscle in vivo. Our group recently focused its interest on BAG3 role in myocardiocyte proliferation, survival and response to stressful stimuli. We found that BAG3 is upregulated during the differentiation of cardiomyoblasts. Our results prompted us to verify whether bag3 silencing could affect the differentiation state of cardiocytes and we found that bag3 silencing resulted in highly reducing the levels of myogenin. Furthermore, we analyzed BAG3 expression and localization following cell exposure to oxidative stress. In particular, we found that epinephrine in vitro increases BAG3 expression in adult human cardiomyocytes. We evaluated whether BAG3 could be involved in the Tako-tsubo cardiomyopathy (or stress cardiomyopathy) pathogenesis that is characterized by left ventricular dysfunction, with symptoms that can mimic an acute coronary syndrome. The absence of significant cardiovascular risk factors in patients affected by stress cardiomyopathy suggested that it might be associated with a possible genetic etiology. Therefore, we sequenced bag3 gene to check for polymorphisms in 29 patients and 1043 healthy donors. Three polymorphism were highly represented among patients (R71Q, C151R, P407L). We also showed for the first time that BAG3 protein is released from stressed cardiomyocytes and is found in chronic heart failure (HF) patients’ sera. Since anti-BAG3 antibodies are also present in patients’ sera, we developed an ELISA test for their specific detection. In serum samples from chronic HF patients, we found significantly higher values of anti-BAG3 antibodies respect to samples from healthy donors. The presence of anti-BAG3 antibodies in chronic HF patients’ sera and the availability of an ELISA test for their detection can contribute a novel tool for diagnostic and prognostic evaluations. [edited by author]
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Driesen, Ronald Bertie Mario Antonio. "Adaptive remodeling of cardiomyocytes under stress". [Maastricht] : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=11068.
Pełny tekst źródłaKemeny, Naomi. "Alendronate affects calcium dynamics in cardiomyocytes". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40684.
Pełny tekst źródłaAlendronate est efficace dans le traitement de l’ostéoporose. Alendronate a récemment été associe avec une risque élevé de fibrillation auriculaire sérieux. On a examine les effets d’Alendronate sur la de calcium cytosolique ([Ca2+]i) dans les cellules musculaires cardiaques. Les cellules musculaires cardiaques HL-1 étaient chargés avec Fura-2 et examinés par microspectrofluorimetrie. Alendronate (10-8, 10-7, 10-6 M) ont provoqués des oscillations de [Ca2+]i fugaces et haute fréquences à 10-8 M Alendronate (61 ± 10 mHz) comparé aux concentrations plus hautes (42 ± 4 mHz). Dans les cellules traits avec 10-6 M ALN, la réponse à l’application de caféine était avec délai, et a manifesté un diminution dans la rythme et amplitude d’augmentation de [Ca2+]i. L’exposition a l’ALN à long terme (48 h) ont provoqué un délai des élévations de calcium transitoires, et un diminution du rythme d’augmentation de [Ca2+]i suites par les oscillations de [Ca2+]i, caractérisés par un augmentation de fréquences avec 10-8 M Alendronate (54 ± 8 mHz) compare aux concentrations plus hautes (35 ± 5 mHz). Le changement des dynamiques de calcium étaient accompagnés par les changements considérables dans l’expression d’ATPase (SERCA2a), calsequestrin et calreticulin du réticulum sarcoendoplasmique.
Bowers, Keith Cyril. "Pathophysiology of ATP in single cardiomyocytes". Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316576.
Pełny tekst źródłaBowman, Peter Ronald Thomas. "Regulation of glucose transport in cardiomyocytes". Thesis, University of Glasgow, 2019. http://theses.gla.ac.uk/41002/.
Pełny tekst źródłaKsiążki na temat "Cardiomyocytes"
Skuse, Gary R., i Maureen C. Ferran, red. Cardiomyocytes. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8.
Pełny tekst źródłaMichael, Piper Hans, i Isenberg Gerrit, red. Isolated adult cardiomyocytes. Boca Raton, Fla: CRC Press, 1989.
Znajdź pełny tekst źródłaSkuse, Gary R., i Maureen C. Ferran. Cardiomyocytes: Methods and Protocols. New York: Humana Press, 2015.
Znajdź pełny tekst źródłaYoshida, Yoshinori, red. Pluripotent Stem-Cell Derived Cardiomyocytes. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1484-6.
Pełny tekst źródłaKartha, Chandrasekharan C. Cardiomyocytes in Health and Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9.
Pełny tekst źródłaSchlüter, Klaus-Dieter, red. Cardiomyocytes – Active Players in Cardiac Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31251-4.
Pełny tekst źródłaYee-Ki, Lee, i 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.
Pełny tekst źródłaLuiz, Belardinelli, red. Effects of extracellular adenosine and ATP on cardiomyocytes. Austin: Landes, 1999.
Znajdź pełny tekst źródłaSowerby, Andrew John. Anoxia, plasma membrane structure and calcium homeostasis: Photobleaching and microflurescence investigations inisolated rat cardiomyocytes. Uxbridge: Brunel University, 1991.
Znajdź pełny tekst źródłaLai, Laura R. B. Protein oxidation occurs in cardiomyocytes exposed to an in vitro model of hypoxia/reperfusion injury. Ottawa: National Library of Canada, 1996.
Znajdź pełny tekst źródłaCzęści książek na temat "Cardiomyocytes"
Bonci, Dèsirèe, Michael V. G. Latronico i Gianluigi Condorelli. "Cardiomyocytes". W Lentivirus Gene Engineering Protocols, 169–79. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1-59259-393-3:169.
Pełny tekst źródłaThiriet, Marc. "Cardiomyocytes". W Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems, 189–269. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5966-8_5.
Pełny tekst źródłaSmart, F. W., W. Claycomb, J. Delcarpio i C. Van Meter. "Cultured Cardiomyocytes". W The Transplantation and Replacement of Thoracic Organs, 775–84. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-0-585-34287-0_87.
Pełny tekst źródłaKartha, Chandrasekharan C. "Cardiomyocytes in Heart Failure". W Cardiomyocytes in Health and Disease, 245–55. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_15.
Pełny tekst źródłaMoore, Jennifer C., Teun P. de Boer, Marcel A. G. van der Heyden, Leon G. J. Tertoolen i Christine L. Mummery. "Stem Cells and Cardiomyocytes". W Cardiovascular Research, 133–55. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-23329-6_8.
Pełny tekst źródłaSzibor, Marten. "Cardiomyocytes: Function and Regeneration". W Cardiomyocytes – Active Players in Cardiac Disease, 25–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31251-4_2.
Pełny tekst źródłaVandergriff, Adam C., M. Taylor Hensley i Ke Cheng. "Cryopreservation of Neonatal Cardiomyocytes". W Methods in Molecular Biology, 153–60. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2572-8_12.
Pełny tekst źródłaSmits, Anke M., Angelique A. van Oorschot i Marie-José Goumans. "Isolation and Differentiation of Human Cardiomyocyte Progenitor Cells into Cardiomyocytes". W Somatic Stem Cells, 339–49. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-815-3_20.
Pełny tekst źródłaKartha, Chandrasekharan C. "Cell Cycle Regulation in Cardiomyocytes". W Cardiomyocytes in Health and Disease, 25–39. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_3.
Pełny tekst źródłaKartha, Chandrasekharan C. "Cardiomyocyte Senescence". W Cardiomyocytes in Health and Disease, 187–205. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85536-9_12.
Pełny tekst źródłaStreszczenia konferencji na temat "Cardiomyocytes"
Baicu, Catalin F., i Michael R. Zile. "Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells". W ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23158.
Pełny tekst źródłaSargent, Carolyn Y., Luke A. Hiatt, Sandhya Anantharaman, Eric Berson i Todd C. McDevitt. "Cardiogenesis of Embryonic Stem Cells is Modulated by Hydrodynamic Mixing Conditions". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193129.
Pełny tekst źródłaLiu, Honghai, Julie X. Yun, Russel K. Pirlo, Delpine Dean, Hai Yao, Martine Laberge i Bruce Z. Gao. "The Dependence of Mechanical Properties of Adult Rat Myocytes on Cell Alignment". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193024.
Pełny tekst źródłaYoung, Jennifer L., Kyle Kretchmer i Adam J. Engler. "Temporally-Stiffening Hydrogel Regulates Cardiac Differentiation via Mechanosensitive Signaling". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14674.
Pełny tekst źródłaRodriguez, Marita L., Charles E. Murry i Nathan J. Sniadecki. "Assessment of Induced Pluripotent Stem Cell-Derived Cardiomyocyte Contractility Using Micropost Arrays". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14640.
Pełny tekst źródłaGarcia, A., M. T. Nazari-Shafti, A. Kurtz, M. Gossen i C. Stamm. "Inducible Differentiation of iPS-Derived Cardiomyocyte Precursor Cells into Cardiomyocytes Using Biomimetic shRNA Technology". W 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678868.
Pełny tekst źródłaWilliams, Brian, Sandeep Anand, Jagannathan Rajagopalan i Taher Saif. "Artificial Swimmer Powered by Cardiomyocytes". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14854.
Pełny tekst źródłaKim, Jinseok, Sungwook Yang, Jeongeun Baek, Sewan Park, Hyeon Cheol Kim, Eui-Sung Yoon i Kukjin Chun. "Cardiomyocytes Self-Powered Polymer Microrobot". W TRANSDUCERS 2007 - 2007 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2007. http://dx.doi.org/10.1109/sensor.2007.4300406.
Pełny tekst źródłaLiu, Wenhao, Parvin Forghani, Qingyu Chen, Lawrence C. Armand, Chunhui Xu i Shu Jia. "3D imaging of hiPSC-derived cardiomyocytes with light-field microscopy". W Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/fio.2023.fm1e.3.
Pełny tekst źródłaHurley, Jennifer R., i Daria A. Narmoneva. "Fibroblasts Induce Mechanical Changes in the Extracellular Environment and Enhance Capillary-Like Network Formation". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193093.
Pełny tekst źródłaRaporty organizacyjne na temat "Cardiomyocytes"
Pailino, Lia, Lihua Lou, Alberto Sesena Rubfiaro, Jin He i Arvind Agarwal. Nanomechanical Properties of Engineered Cardiomyocytes Under Electrical Stimulation. Florida International University, październik 2021. http://dx.doi.org/10.25148/mmeurs.009775.
Pełny tekst źródłaGabrielson, Kathleen L. Akt Rescue in Cardiomyocytes but not Breast Cancer Cells after Doxorubicin and Anti-erbB2 Treatment. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2005. http://dx.doi.org/10.21236/ada435439.
Pełny tekst źródłaliao, xiaoqian, xingyu fan, ziyi wang, shumin huang i zhixi hu. Prognostic value of heart-type fatty acid binding protein in heart failure: a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2022. http://dx.doi.org/10.37766/inplasy2022.3.0126.
Pełny tekst źródłaEvaluation of the utility of stem-cell derived cardiomyocytes for drug proarrhythmic potential. EMBL-EBI, marzec 2020. http://dx.doi.org/10.6019/chembl4295262.
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