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001			76319
003			ES-MaUEC
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007			cr nn 008mamaa
008			100301s2006 gw s 000 0 eng d
020			_a9783540297154
024	7		_a10.1007/3-540-29715-4 _2doi
040			_aES-MaUEC
050		4	_aRC685.A65 _bB37 2006 EB
082	0	4	_a615
245	0	0	_aBasis and Treatment of Cardiac Arrhythmias _cedited by Robert S. Kass, Colleen E. Clancy
260			_aBerlin, Heidelberg _bSpringer International Publishing _c2006
300			_a1 recurso en línea (IX, 361 p.)
336			_aTexto (visual) _btxt _2rdacontent
337			_aelectrónico _bc _2rdamedia
338			_arecurso electrónico _bcr _2rdacarrier
490	1		_aHandbook of Experimental Pharmacology _x0171-2004 _v171
505	0		_aHistory of Arrhythmias -- Pacemaker Current and Automatic Rhythms: Toward a Molecular Understanding -- Proarrhythmia -- Cardiac Na+ Channels as Therapeutic Targets for Antiarrhythmic Agents -- Structural Determinants of Potassium Channel Blockade and Drug-Induced Arrhythmias -- Sodium Calcium Exchange as a Target for Antiarrhythmic Therapy -- A Role for Calcium/Calmodulin-Dependent Protein Kinase II in Cardiac Disease and Arrhythmia -- AKAPs as Antiarrhythmic Targets? -- ?-Blockers as Antiarrhythmic Agents -- Experimental Therapy of Genetic Arrhythmias: Disease-Specific Pharmacology -- Mutation-Specific Pharmacology of the Long QT Syndrome -- Therapy for the Brugada Syndrome -- Molecular Basis of Isolated Cardiac Conduction Disease -- hERG Trafficking and Pharmacological Rescue of LQTS-2 Mutant Channels
520			_aIn the past decade, major progress has been made in understanding mec- nisms of arrhythmias. This progress stems from much-improved experim- tal, genetic, and computational techniques that have helped to clarify the roles of speci?c proteins in the cardiac cycle, including ion channels, pumps, - changer, adaptor proteins, cell-surface receptors, and contractile proteins. The interactions of these components, and their individual potential as therap- tic targets, have also been studied in detail, via an array of new imaging and sophisticated experimental modalities. The past 10 years have also led to the realization that genetics plays a predominant role in the development of lethal arrhythmias. Many of the topics discussed in this text re?ect very recently undertaken research directions including the genetics of arrhythmias, cell signaling mo- cules as potential therapeutic targets, and traf?cking to the membrane. These new approaches and implementations of anti-arrhythmic therapy derive from many decades of research as outlined in the ?rst chapter by the distinguished professors Michael Rosen (Columbia University) and Michiel Janse (University of Amsterdam). The text covers changes in approaches to arrhythmia therapy over time, in multiple cardiac regions, and over many scales, from gene to protein to cell to tissue to organ
942			_2lcc _cLE
988			_aEBOOK, EBSPRINGERrevisando
650		7	_aArritmia _xTratamiento _9178882 _0comprobar BNE19901278413 _2embne
650		7	_aFarmacología _0comprobar BNE19900953030 _2embne _9137893
700	1		_aKass, Robert S. _eeditor literario _0Local _985318
700	1		_aClancy, Colleen E. _eeditor literario _0Local _985319
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://link.springer.com/book/10.1007/3-540-29715-4 _zAcceso a este recurso digital (usuarios Universidad Europea de Madrid)
901			_ai9783540297154
907			_a.b12819372 _b10-10-17 _c01-10-14
998			_am _a_alco _a_vill _b15-07-17 _cm _dz _eu _feng _ggw _h0
945			_a RC685 .A65 B37 2006 EB _g1 _ieBOOK _j0 _lmae _o- _pEUR0.00 _q- _r- _sb _t15 _u0 _v0 _w0 _x0 _y.i11548599 _z06-04-17
999			_c76319 _d76319 _x1