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One-Year Outcomes after PCI Strategies in Cardiogenic Shock

Publikováno v: The New England Journal of Medicine, 379, 1699-1710
New England journal of medicine, 379(18), 1699-1710. Massachussetts Medical Society
Thiele, Holger; Akin, Ibrahim; Sandri, Marcus; de Waha-Thiele, Suzanne; Meyer-Saraei, Roza; Fuernau, Georg; Eitel, Ingo; Nordbeck, Peter; Geisler, Tobias; Landmesser, Ulf; Skurk, Carsten; Fach, Andreas; Jobs, Alexander; Lapp, Harald; Piek, Jan J; Noc, Marko; Goslar, Tomaž; Felix, Stephan B; Maier, Lars S; Stepinska, Janina; ... (2018). One-Year Outcomes after PCI Strategies in Cardiogenic Shock. New England journal of medicine NEJM, 379(18), pp. 1699-1710. Massachusetts Medical Society MMS 10.1056/NEJMoa1808788
New England Journal of Medicine
New England Journal of Medicine, Massachusetts Medical Society, 2018, 379 (18), pp.1699-1710. ⟨10.1056/NEJMoa1808788⟩
The New England Journal of Medicine, 379, 18, pp. 1699-1710
The New England journal of medicine

Item does not contain fulltext BACKGROUND: Among patients with acute myocardial infarction, cardiogenic shock, and multivessel coronary artery disease, the risk of a composite of death from any cause or severe renal failure leading to renal-replaceme

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https://hdl.handle.net/2066/200284

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C-terminal phosphorylation of Na(V)1.5 impairs FGF13-dependent regulation of channel inactivation

Autor: Burel, S, Coyan, FC, Lorenzini, M, Meyer, MR, Lichti, CF, Brown, JH, Loussouarn, G, Charpentier, F, Nerbonne, JM, Townsend, RR, Maier, LS, Marionneau, C

Publikováno v: Burel, S; Coyan, FC; Lorenzini, M; Meyer, MR; Lichti, CF; Brown, JH; et al.(2017). C-terminal phosphorylation of Na(V)1.5 impairs FGF13-dependent regulation of channel inactivation. JOURNAL OF BIOLOGICAL CHEMISTRY, 292(42), 17431-17448. doi: 10.1074/jbc.M117.787788. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/2rz48167

Voltage-gated Na+ (NaV) channels are key regulators of myocardial excitability, and Ca2+/calmodulin-dependent protein kinase II (CaMKII)-dependent alterations in NaV1.5 channel inactivation are emerging as a critical determinant of arrhythmias in hea

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http://www.escholarship.org/uc/item/2rz48167

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Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic -Adrenoceptor Blockade in Experimental and Human Heart Failure

Autor: Dewenter, M, Neef, S, Vettel, C, Laemmle, S, Beushausen, C, Zelarayan, LC, Katz, S, von der Lieth, A, Meyer-Roxlau, S, Weber, S, Wieland, T, Sossalla, S, Backs, J, Brown, JH, Maier, LS, El-Armouche, A

Publikováno v: Dewenter, M; Neef, S; Vettel, C; Laemmle, S; Beushausen, C; Zelarayan, LC; et al.(2017). Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic-Adrenoceptor Blockade in Experimental and Human Heart Failure. CIRCULATION-HEART FAILURE, 10(5). doi: 10.1161/CIRCHEARTFAILURE.117.003840. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/46h9g99w

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_______325::689a0c5126cd9f35e71f964f41de78d9
http://www.escholarship.org/uc/item/46h9g99w

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Improvement in Risk Stratification in Transcatheter Aortic Valve Implantation Using a Combination of the Tumor Marker CA125 and the Logistic EuroSCORE

Autor: Husser O, Núñez J, Burgdorf C, Holzamer A, Templin C, Kessler T, Bodi V, Sanchis J, Pellegrini C, Luchner A, Maier LS, Schmid C, Lüscher TF, Schunkert H, Kastrati A, Hilker M, Hengstenberg C

Publikováno v: REVISTA ESPANOLA DE CARDIOLOGIA
r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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https://www.fundanet.incliva.es/publicaciones/ProdCientif/PublicacionFrw.aspx?id=1234

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Exercise training reverses myocardial dysfunction induced by CaMKII delta(C) overexpression by restoring Ca2+ homeostasis

Autor: Hoydal, MA, Stolen, TO, Kettlewell, S, Maier, LS, Brown, JH, Sowa, T, Catalucci, D, Condorelli, G, Kemi, OJ, Smith, GL, Wisloff, U

Publikováno v: Hoydal, MA; Stolen, TO; Kettlewell, S; Maier, LS; Brown, JH; Sowa, T; et al.(2016). Exercise training reverses myocardial dysfunction induced by CaMKII delta(C) overexpression by restoring Ca2+ homeostasis. JOURNAL OF APPLIED PHYSIOLOGY, 121(1), 212-220. doi: 10.1152/japplphysiol.00188.2016. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/25z3x6kx

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http://www.escholarship.org/uc/item/25z3x6kx

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Na+channel function, regulation, structure, trafficking and sequestration

Publikováno v: Chen-Izu, Y; Shaw, RM; Pitt, GS; Yarov-Yarovoy, V; Sack, JT; Abriel, H; et al.(2015). Na+channel function, regulation, structure, trafficking and sequestration. Journal of Physiology, 593(6), 1347-1360. doi: 10.1113/jphysiol.2014.281428. UC Davis: Retrieved from: http://www.escholarship.org/uc/item/1n45t1wz

© 2014 The Physiological Society. This paper is the second of a series of three reviews published in this issue resulting from the University of California Davis Cardiovascular Symposium 2014: Systems approach to understanding cardiac excitation-con

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http://www.escholarship.org/uc/item/1n45t1wz

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CaMKIIdelta overexpression in hypertrophy and heart failure: cellular consequences for excitation-contraction coupling

Autor: Maier Ls

Publikováno v: Brazilian Journal of Medical and Biological Research, Vol 38, Iss 9, Pp 1293-1302 (2005)
Brazilian Journal of Medical and Biological Research v.38 n.9 2005
Brazilian Journal of Medical and Biological Research
Associação Brasileira de Divulgação Científica (ABDC)
instacron:ABDC
Brazilian Journal of Medical and Biological Research, Volume: 38, Issue: 9, Pages: 1293-1302, Published: SEP 2005

Ca/calmodulin-dependent protein kinase IIdelta (CaMKIIdelta) is the predominant isoform in the heart. During excitation-contraction coupling (ECC) CaMKII phosphorylates several Ca-handling proteins including ryanodine receptors (RyR), phospholamban,

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http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2005000900002&tlng=en

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