Berul (30 risultati)
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Encuadernación de tapa blanda. Condizione: Bien. A341449. RBA - 269pp Rústica. S.
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Encuadernación de tapa blanda. Condizione: Aceptable. M054023. Edaf . Descubra la verdad sobre si mismo. 269 pp. (M) A24272.
Lingua: Inglese
Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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hardcover. Condizione: New. In shrink wrap. Looks like an interesting title.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: preigu, Osnabrück, Germaniapreigu
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Taschenbuch. Condizione: Neu. Molecular Genetics of Cardiac Electrophysiology | C. Berul (u. a.) | Taschenbuch | xiii | Englisch | 2012 | Springer | EAN 9781461370376 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: GreatBookPricesUK, Woodford Green, Regno UnitoGreatBookPricesUK
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Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Books Puddle, New York, NY, U.S.A.Books Puddle
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Condizione: New. pp. xi + 378 1st Edition.
Lingua: Inglese
Editore: Springer US, Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: AHA-BUCH GmbH, Einbeck, GermaniaAHA-BUCH GmbH
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Buch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more common than previous…ly suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation.
Lingua: Inglese
Editore: Springer, Springer US, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: AHA-BUCH GmbH, Einbeck, GermaniaAHA-BUCH GmbH
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Taschenbuch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more common than p…reviously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Books Puddle, New York, NY, U.S.A.Books Puddle
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Condizione: New. pp. 396.
Lingua: Inglese
Editore: Springer, 2013
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Revaluation Books, Exeter, Regno UnitoRevaluation Books
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Paperback. Condizione: Brand New. reprint edition. 392 pages. 9.25x6.10x0.93 inches. In Stock.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Brook Bookstore On Demand, Napoli, NA, ItaliaBrook Bookstore On Demand
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Condizione: new. Questo è un articolo print on demand.
Lingua: Inglese
Editore: Springer US, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: moluna, Greven, Germaniamoluna
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Gebunden. Condizione: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial…atrial fibrillation is more common than previously .
Lingua: Inglese
Editore: Springer US, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: moluna, Greven, Germaniamoluna
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Condizione: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fib…rillation is more common than previously .
Lingua: Inglese
Editore: Springer US Okt 2012, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, GermaniaBuchWeltWeit Ludwig Meier e.K.
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Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is mo…re common than previously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation. 396 pp. Englisch.
Lingua: Inglese
Editore: Springer US Apr 2000, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, GermaniaBuchWeltWeit Ludwig Meier e.K.
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Buch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more comm…on than previously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation. 396 pp. Englisch.
Lingua: Inglese
Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: preigu, Osnabrück, Germaniapreigu
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Buch. Condizione: Neu. Molecular Genetics of Cardiac Electrophysiology | Jeffrey A. Towbin (u. a.) | Buch | xiii | Englisch | 2000 | Springer | EAN 9780792378297 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu Print on Dem…and.
Lingua: Inglese
Editore: Springer, Springer US Okt 2012, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: buchversandmimpf2000, Emtmannsberg, BAYE, Germaniabuchversandmimpf2000
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Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware -The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more c…ommon than previously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation.Springer-Verlag KG, Sachsenplatz 4-6, 1201 Wien 396 pp. Englisch.
Lingua: Inglese
Editore: Springer US, Springer Apr 2000, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: buchversandmimpf2000, Emtmannsberg, BAYE, Germaniabuchversandmimpf2000
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Buch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware -The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more common t…han previously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as 'lone' atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation.Springer-Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 396 pp. Englisch.
Lingua: Inglese
Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Majestic Books, Hounslow, Regno UnitoMajestic Books
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Condizione: New. Print on Demand pp. xi + 378 Illus.
Lingua: Inglese
Editore: Springer, 2000
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Biblios, frankfurt am main, HESSE, GermaniaBiblios
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Condizione: New. PRINT ON DEMAND pp. xi + 378.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Majestic Books, Hounslow, Regno UnitoMajestic Books
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Condizione: New. Print on Demand pp. 396.
Lingua: Inglese
Editore: Springer, 2012
Serie: Developments in Cardiovascular Medicine, Libro 166 di 253. Libro 166 di 253 - Developments in Cardiovascular Medicine
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Da: Biblios, frankfurt am main, HESSE, GermaniaBiblios
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Condizione: New. PRINT ON DEMAND pp. 396.
