Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende

Klimawandel und Gesundheit: Was Sie in der Hausarztpraxis wissen müssen und tun können

Die Folgen des Klimwandels haben einen direkten Einfluss auf die Primärversorgung in Deutschland: Hitzeschutz insbesondere bei älteren Patienten, die Zunahme von Infektionen und die Verlängerung der Allergiesesaison spielen medizinisch eine bedeutsame Rolle. Aber auch in der Prävention und der Aufklärung der Patienten kommt den Hausärztinnen und -ärzten eine besondere Rolle zu. Direkt aus der Praxis berichtet im Live-Webinar am 13. Mai von 18 bis 19 Uhr unser Experte Dr. med. Robin Maitra.
Erweiterte Suche
Anmelden
nach oben
Journal of Interventional Cardiac Electrophysiology
Erschienen in: Journal of Interventional Cardiac Electrophysiology 2/2009

01.03.2009

Arrhythmia phenotype in mouse models of human long QT

verfasst von: Guy Salama, Linda Baker , Robert Wolk, Jacques Barhanin, Barry London

Erschienen in: Journal of Interventional Cardiac Electrophysiology | Ausgabe 2/2009

Einloggen, um Zugang zu erhalten

Abstract

Enhanced dispersion of repolarization (DR) was proposed as a unifying mechanism, central to arrhythmia genesis in the long QT (LQT) syndrome. In mammalian hearts, K+ channels are heterogeneously expressed across the ventricles resulting in ‘intrinsic’ DR that may worsen in long QT. DR was shown to be central to the arrhythmia phenotype of transgenic mice with LQT caused by loss of function of the dominant mouse K+ currents. Here, we investigated the arrhythmia phenotype of mice with targeted deletions of KCNE1 and KCNH2 genes which encode for minK/IsK and Merg1 (mouse homolog of human ERG) proteins resulting in loss of function of IKs and IKr, respectively. Both currents are important human K+ currents associated with LQT5 and LQT2. Loss of minK, a protein subunit that interacts with KvLQT1, results in a marked reduction of IKs giving rise to the Jervell and Lange–Nielsen syndrome and the reduced KCNH2 gene reduces MERG and IKr.
Hearts were perfused, stained with di-4-ANEPPS and optically mapped to compare action potential durations (APDs) and arrhythmia phenotype in homozygous minK (minK−/−) and heterozygous Merg1 (Merg+/−) deletions and littermate control mice. MinK−/− mice has similar APDs and no arrhythmias (n = 4). Merg+/− mice had prolonged APDs (from 20 ± 6 to 32 ± 9 ms at the base, p < 0.01; from 18 ± 5 to 25 ± 9 ms at the apex, p < 0.01; n = 8), longer refractory periods (RP) (36 ± 14 to 63 ± 27 at the base, p < 0.01 and 34 ± 5 to 53 ± 21 ms at the apex, p < 0.03; n = 8), higher DR 10.4 ± 4.1 vs. 14 ± 2.3 ms, p < 0.02) and similar conduction velocities (n = 8). Programmed stimulation exposed a higher propensity to VT in Merg+/− mice (60% vs. 10%). A comparison of mouse models of LQT based on K+ channel mutations important to human and mouse repolarization emphasizes DR as a major determinant of arrhythmia vulnerability.
Literatur
1.
Schwartz, P., Locati, E., Napolitano, C., & Priore, S. (1995). The long QT syndrome. In D. Zipes, & J. Jalife (Eds.), Cardiac Electrophysiology: From cell to bedside (p. 788−811, 2ndnd ed.). Philadelphia, PA: WB Saunders.
2.
Surawicz, B. (1989). Electrophysiologic substrate of torsade de pointes: dispersion of repolarization or early afterdepolarizations? Journal of the American College of Cardiology, 14(1), 172−184.PubMedCrossRef
3.
Ackerman, M. J. (1998). The long QT syndrome: ion channel diseases of the heart. Mayo Clinic Proceedings, 73(3), 250−269.PubMedCrossRef
4.
Dessertenne, F. (1966). Ventricular tachycardia with 2 variable opposing foci. Archives des Maladies du Coeur et des Vaisseaux, 59(2), 263−272.PubMed
5.
El-Sherif, N., Chinushi, M., Caref, E. B., & Restivo, M. (1997). Electrophysiological mechanism of the characteristic electrocardiographic morphology of torsade de pointes tachyarrhythmias in the long-QT syndrome: detailed analysis of ventricular tridimensional activation patterns. Circulation, 96(12), 4392–4399.PubMed
6.
El-Sherif, N., Gough, W. B., & Restivo, M. (1991). Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry. Circulation, 83(1), 268–278.PubMed
7.
Frazier, D. W., Wolf, P. D., Wharton, J. M., Tang, A. S., Smith, W. M., & Ideker, R. E. (1989). Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium. The Journal of Clinical Investigation, 83(3), 1039–1052.PubMedCrossRef
8.
Smith, J. M., Clancy, E. A., Valeri, C. R., Ruskin, J. N., & Cohen, R. J. (1988). Electrical alternans and cardiac electrical instability. Circulation, 77(1), 110–121.PubMed
9.
Shimizu, W., & Antzelevitch, C. (1998). Cellular basis for the ECG features of the LQT1 form of the long-QT syndrome: effects of beta-adrenergic agonists and antagonists and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes. Circulation, 98(21), 2314–2322.PubMed
10.
Wit, A. L., Allessie, M. A., Bonke, F. I., Lammers, W., Smeets, J., & Fenoglio Jr., J. J. (1982). Electrophysiologic mapping to determine the mechanism of experimental ventricular tachycardia initiated by premature impulses. Experimental approach and initial results demonstrating reentrant excitation. The American Journal of Cardiology, 49(1), 166–185.PubMedCrossRef
11.
Antzelevitch, C., Sicouri, S., Litovsky, S. H., Lukas, A., Krishnan, S. C., Di Diego, J. M., Gintant, G. A., & Liu, D. W. (1991). Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells. Circulation Research, 69(6), 1427–1449.PubMed
12.
Antzelevitch, C., Sicouri, S., Lukas, A., Nesterenko, V., Liu, D.-W., & Di Diego, J. M. (1994). Regional differences in the ventricular cells: physical implications. In D. P. Zipes, & J. Jalife (Eds.), Cardiac Electrophysiology: From cell to bedside (pp. 228–245). Philadelphia: WB Saunders.
13.
Barry, D. M., & Nerbonne, J. M. (1996). Myocardial potassium channels: electrophysiological and molecular diversity. Annual Review of Physiology, 58, 363–394.PubMedCrossRef
14.
Salama, G., Lombardi, R., & Elson, J. (1987). Maps of optical action potentials and NADH fluorescence in intact working hearts. The American Journal of Physiology, 252(2 Pt 2), H384–H394.PubMed
15.
Efimov, I. R., Ermentrout, B., Huang, D. T., & Salama, G. (1996). Activation and repolarization patterns are governed by different structural characteristics of ventricular myocardium: experimental study with voltage-sensitive dyes and numerical simulations. Journal of Cardiovascular Electrophysiology, 7(6), 512–530.PubMedCrossRef
16.
Choi, B. R., Nho, W., Liu, T., & Salama, G. (2002). Life span of ventricular fibrillation frequencies. Circulation Research, 91(4), 339–345.PubMedCrossRef
17.
Baker, L. C., London, B., Choi, B. R., Koren, G., & Salama, G. (2000). Enhanced dispersion of repolarization and refractoriness in transgenic mouse hearts promotes reentrant ventricular tachycardia. Circulation Research, 86(4), 396–407.PubMed
18.
Szentadrassy, N., Banyasz, T., Biro, T., Szabo, G., Toth, B. I., Magyar, J., et al. (2005). Apico-basal inhomogeneity in distribution of ion channels in canine and human ventricular myocardium. Cardiovascular Research, 65(4), 851–860.PubMedCrossRef
19.
Mantravadi, R., Gabris, B., Liu, T., Choi, B. R., de Groat, W. C., Ng, G. A., et al. (2007). Autonomic nerve stimulation reverses ventricular repolarization sequence in rabbit hearts. Circulation Research, 100(7), e72–e80.PubMedCrossRef
20.
Niwa, N., Wang, W., Sha, Q., Marionneau, C., & Nerbonne, J. M. (2008). Kv4.3 is not required for the generation of functional Ito,f channels in adult mouse ventricles. Journal of Molecular and Cellular Cardiology, 44(1), 95–104.PubMedCrossRef
21.
Nerbonne, J. M. (2000). Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. The Journal of Physiology, 525(Pt 2), 285–298. In Process Citation.PubMedCrossRef
22.
Xu, H., Guo, W., & Nerbonne, J. M. (1999). Four kinetically distinct depolarization-activated K+ currents in adult mouse ventricular myocytes. The Journal of General Physiology, 113(5), 661–678.PubMedCrossRef
23.
London, B., Wang, D. W., Hill, J. A., & Bennett, P. B. (1998). The transient outward current in mice lacking the potassium channel gene Kv1.4. The Journal of Physiology, 509(Pt 1), 171–182.PubMedCrossRef
24.
Guo, W., Li, H., London, B., & Nerbonne, J. M. (2000). Functional consequences of elimination of i(to,f) and i(to,s): early afterdepolarizations, atrioventricular block, and ventricular arrhythmias in mice lacking Kv1.4 and expressing a dominant-negative Kv4 alpha subunit. Circulation Research, 87(1), 73–79.PubMed
25.
Brunet, S., Aimond, F., Li, H., Guo, W., Eldstrom, J., Fedida, D., Yamada, K. A., & Nerbonne, J. M. (2004). Heterogeneous expression of repolarizing, voltage-gated K+ currents in adult mouse ventricles. The Journal of Physiology, 559(Pt 1), 103–120.PubMedCrossRef
26.
Barry, D. M., Xu, H., Schuessler, R. B., & Nerbonne, J. M. (1998). Functional knockout of the transient outward current, long-QT syndrome, and cardiac remodeling in mice expressing a dominant-negative Kv4 alpha subunit. Circulation Research, 83(5), 560–567.PubMed
27.
London, B., Baker, L. C., Petkova-Kirova, P., Nerbonne, J. M., Choi, B. R., & Salama, G. (2007). Dispersion of repolarization and refractoriness are determinants of arrhythmia phenotype in transgenic mice with long QT. The Journal of Physiology, 578(Pt 1), 115–129.PubMed
28.
Salama, G., & London, B. (2007). Mouse models of long QT syndrome. The Journal of Physiology, 578(Pt 1), 43–53.PubMed
29.
Choi, B. R., Burton, F., & Salama, G. (2002). Cytosolic Ca2+ triggers early afterdepolarizations and Torsade de Pointes in rabbit hearts with type 2 long QT syndrome. The Journal of Physiology, 543(Pt 2), 615–631.PubMedCrossRef
30.
Killeen, M. J., & Sabir, I. N. (2007). Repolarization gradients and arrhythmogenicity in the murine heart. The Journal of Physiology, 583(Pt 2), 419–420.PubMedCrossRef
31.
Pond, A. L., Scheve, B. K., Benedict, A. T., Petrecca, K., Van Wagoner, D. R., Shrier, A., et al. (2000). Expression of distinct ERG proteins in rat, mouse, and human heart. Relation to functional I(Kr) channels. The Journal of Biological Chemistry, 275(8), 5997−6006.PubMedCrossRef
32.
Babij, P., Askew, G. R., Nieuwenhuijsen, B., Su, C. M., Bridal, T. R., Jow, B., et al. (1998). Inhibition of cardiac delayed rectifier K+ current by overexpression of the long-QT syndrome HERG G628S mutation in transgenic mice. Circulation Research, 83(6), 668–678.PubMed
33.
Lees-Miller, J. P., Guo, J., Somers, J. R., Roach, D. E., Sheldon, R. S., Rancourt, D. E., et al. (2003). Selective knockout of mouse ERG1 B potassium channel eliminates I(Kr) in adult ventricular myocytes and elicits episodes of abrupt sinus bradycardia. Molecular and Cellular Biology, 23(6), 1856–1862.PubMedCrossRef
34.
Kupershmidt, S., Yang, T., Anderson, M. E., Wessels, A., Niswender, K. D., Magnuson, M. A., et al. (1999). Replacement by homologous recombination of the minK gene with lacZ reveals restriction of minK expression to the mouse cardiac conduction system. Circulation Research, 84(2), 146–152.PubMed
35.
Drici, M. D., Arrighi, I., Chouabe, C., Mann, J. R., Lazdunski, M., Romey, G., et al. (1998). Involvement of IsK-associated K+ channel in heart rate control of repolarization in a murine engineered model of Jervell and Lange-Nielsen syndrome. Circulation Research, 83(1), 95–102.PubMed
36.
Casimiro, M. C., Knollmann, B. C., Ebert, S. N., Vary Jr, J. C., Greene, A. E., Franz, M. R., et al. (2001). Targeted disruption of the Kcnq1 gene produces a mouse model of Jervell and Lange-Nielsen syndrome. Proceedings of the National Academy of Sciences of the United States of America, 98(5), 2526–2531.PubMedCrossRef
37.
Lee, M. P., Ravenel, J. D., Hu, R. J., Lustig, L. R., Tomaselli, G., Berger, R. D., et al. (2000). Targeted disruption of the Kvlqt1 gene causes deafness and gastric hyperplasia in mice. The Journal of Clinical Investigation, 106(12), 1447–1455.PubMedCrossRef
38.
London, B., Trudeau, M. C., Newton, K. P., Beyer, A. K., Copeland, N. G., Gilbert, D. J., et al. (1997). Two isoforms of the mouse ether-a-go-go-related gene coassemble to form channels with properties similar to the rapidly activating component of the cardiac delayed rectifier K+ current. Circulation Research, 81(5), 870–878.PubMed
39.
Marx, S. O., Kurokawa, J., Reiken, S., Motoike, H., D'Armiento, J., Marks, A. R., et al. (2002). Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel. Science, 295(5554), 496–499.PubMedCrossRef
40.
Sanguinetti, M. C. (2000). Long QT syndrome: ionic basis and arrhythmia mechanism in long QT syndrome type 1. Journal of Cardiovascular Electrophysiology, 11(6), 710–712. In Process Citation.PubMedCrossRef
41.
London, B., Newton, K. P., Vesely, M., Wong, J., Ginsberg, G., & Slater, C. (1995). Cloning the mouse homolog of the long QT syndrome gene HERG. Circulation, 92, I–223.
42.
Barhanin, J., Lesage, F., Guillemare, E., Fink, M., Lazdunski, M., & Romey, G. K. (1996). (V)LQT1 and lsK (minK) proteins associate to form the I(Ks) cardiac potassium current. Nature, 384(6604), 78–80.PubMedCrossRef
43.
Vetter, D. E., Mann, J. R., Wangemann, P., Liu, J., McLaughlin, K. J., Lesage, F., et al. (1996). Inner ear defects induced by null mutation of the isk gene. Neuron, 17(6), 1251–1264.PubMedCrossRef
44.
Baker, L. C., Wolk, R., Choi, B. R., Watkins, S., Plan, P., Shah, A., et al. (2004). Effects of mechanical uncouplers, diacetyl monoxime, and cytochalasin-D on the electrophysiology of perfused mouse hearts. American Journal of Physiology. Heart and Circulatory Physiology, 287(4), H1771–H1779.PubMedCrossRef
45.
London, B., Baker, L. C., Lee, J. S., Shusterman, V., Choi, B. R., Kubota, T., et al. (2003). Calcium-dependent arrhythmias in transgenic mice with heart failure. American Journal of Physiology. Heart and Circulatory Physiology, 284(2), H431–H441.PubMed
46.
Trepanier-Boulay, V., St-Michel, C., Tremblay, A., & Fiset, C. (2001). Gender-based differences in cardiac repolarization in mouse ventricle. Circulation Research, 89(5), 437–444.PubMedCrossRef
47.
Drici, M. D., Baker, L., Plan, P., Barhanin, J., Romey, G., & Salama, G. (2002). Mice display sex differences in halothane-induced polymorphic ventricular tachycardia. Circulation, 106(4), 497–503.PubMedCrossRef
48.
Brouillette, J., Rivard, K., Lizotte, E., & Fiset, C. (2005). Sex and strain differences in adult mouse cardiac repolarization: importance of androgens. Cardiovascular Research, 65(1), 148–157.PubMedCrossRef
49.
Choi, B. R., & Salama, G. (2000). Simultaneous maps of optical action potentials and calcium transients in guinea-pig hearts: mechanisms underlying concordant alternans. The Journal of Physiology, 529(Pt 1), 171–188. In Process Citation.PubMedCrossRef
50.
Kanai, A., & Salama, G. (1995). Optical mapping reveals that repolarization spreads anisotropically and is guided by fiber orientation in guinea pig hearts. Circulation Research, 77(4), 784–802.PubMed
51.
London, B., Jeron, A., Zhou, J., Buckett, P., Han, X., Mitchell, G. F., & Koren, G. (1998). Long QT and ventricular arrhythmias in transgenic mice expressing the N terminus and first transmembrane segment of a voltage-gated potassium channel. Proceedings of the National Academy of Sciences of the United States of America, 95(6), 2926–2931.PubMedCrossRef
52.
Zhou, J., Jeron, A., London, B., Han, X., & Koren, G. (1998). Characterization of a slowly inactivating outward current in adult mouse ventricular myocytes. Circulation Research, 83(8), 806–814.PubMed
53.
Shimizu, W., & Antzelevitch, C. (1998). Cellular basis for the ECG features of the LQT1 form of the long-QT syndrome: effects of beta-adrenergic agonists and antagonists and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes. Circulation, 98(21), 2314–2322.PubMed
54.
Han, W., Wang, Z., & Nattel, S. (2001). Slow delayed rectifier current and repolarization in canine cardiac Purkinje cells. American Journal of Physiology. Heart and Circulatory Physiology, 280(3), H1075–H1080.PubMed
55.
Balasubramaniam, R., Grace, A. A., Saumarez, R. C., Vandenberg, J. I., & Huang, C. L. (2003). Electrogram prolongation and nifedipine-suppressible ventricular arrhythmias in mice following targeted disruption of KCNE1. The Journal of Physiology, 552(Pt 2), 535–546.PubMedCrossRef
56.
Thomas, G., Gurung, I. S., Killeen, M. J., Hakim, P., Goddard, C. A., Mahaut-Smith, M. P., et al. (2007). Effects of L-type Ca2+ channel antagonism on ventricular arrhythmogenesis in murine hearts containing a modification in the Scn5a gene modelling human long QT syndrome 3. The Journal of Physiology, 578(Pt 1), 85–97.PubMed
57.
Thomas, G., Killeen, M. J., Gurung, I. S., Hakim, P., Balasubramaniam, R., Goddard, C. A., et al. (2007). Mechanisms of ventricular arrhythmogenesis in mice following targeted disruption of KCNE1 modelling long QT syndrome 5. The Journal of Physiology, 578(Pt 1), 99–114.PubMed
58.
Jost, N., Virag, L., Bitay, M., Takacs, J., Lengyel, C., Biliczki, P., et al. (2005). Restricting excessive cardiac action potential and QT prolongation: a vital role for IKs in human ventricular muscle. Circulation, 112(10), 1392–1399.PubMedCrossRef
59.
Royer, A., Demolombe, S., El Harchi, A., Le Quang, K., Piron, J., Toumaniantz, G., et al. (2005). Expression of human ERG K+ channels in the mouse heart exerts anti-arrhythmic activity. Cardiovascular Research, 65(1), 128–137.PubMedCrossRef
60.
Liu, G. X., Zhou, J., Nattel, S., & Koren, G. (2004). Single-channel recordings of a rapid delayed rectifier current in adult mouse ventricular myocytes: basic properties and effects of divalent cations. The Journal of Physiology, 556(Pt 2), 401–413.PubMedCrossRef
61.
Kuo, H. C., Cheng, C. F., Clark, R. B., Lin, J. J., Lin, J. L., Hoshijima, M., et al. (2001). A defect in the Kv channel-interacting protein 2 (KChIP2) gene leads to a complete loss of I(to) and confers susceptibility to ventricular tachycardia. Cell, 107(6), 801–813.PubMedCrossRef
62.
Hondeghem, L. M. (1992). Development of class III antiarrhythmic agents. J Cardiovasc Pharmacol, 20(Suppl 2(2), S17–22.PubMedCrossRef
63.
64.
Surawicz, B. (1987). Contributions of cellular electrophysiology to the understanding of the electrocardiogram. Experientia, 43(10), 1061–1068.PubMedCrossRef
Metadaten
Titel
Arrhythmia phenotype in mouse models of human long QT
verfasst von
Guy Salama
Linda Baker
Robert Wolk
Jacques Barhanin
Barry London
Publikationsdatum
01.03.2009
Verlag
Springer US
Erschienen in
Journal of Interventional Cardiac Electrophysiology / Ausgabe 2/2009
Print ISSN: 1383-875X
Elektronische ISSN: 1572-8595
DOI
https://doi.org/10.1007/s10840-008-9339-6

Weitere Artikel der Ausgabe 2/2009

Journal of Interventional Cardiac Electrophysiology 2/2009 Zur Ausgabe

CASE REPORT

Successful catheter ablation of a ventricular tachycardia storm originating from the left ventricular posterior papillary muscle involved with a remote myocardial infarction

CASE REPORT

Human histopathology of substrate based linear radiofrequency catheter ablation to electrical storm in old inferior myocardial infarction

OriginalPaper

Impact of a comprehensive safety program on radiation exposure during catheter ablation of atrial fibrillation: a prospective study

OriginalPaper

Incidence and predictive factors of atrial fibrillation after ablation of typical atrial flutter

CASE REPORT

Electrophysiologic and histopathologic findings of the ablation sites for ventricular fibrillation in a patient with ischemic cardiomyopathy

CASE REPORT

Demonstration of left ventricular dyssynchrony and resynchrony by ECG-gated SPECT with cardioGRAF in a patient with advanced heart failure and narrow QRS complex

Neu im Fachgebiet Kardiologie

Vorsicht, erhöhte Blutungsgefahr nach PCI!

10.05.2024 Koronare Herzerkrankung Nachrichten

Nach PCI besteht ein erhöhtes Blutungsrisiko, wenn die Behandelten eine verminderte linksventrikuläre Ejektionsfraktion aufweisen. Das Risiko ist umso höher, je stärker die Pumpfunktion eingeschränkt ist.

Triglyzeridsenker schützt nicht nur Hochrisikopatienten

10.05.2024 Hypercholesterinämie Nachrichten

Patienten mit Arteriosklerose-bedingten kardiovaskulären Erkrankungen, die trotz Statineinnahme zu hohe Triglyzeridspiegel haben, profitieren von einer Behandlung mit Icosapent-Ethyl, und zwar unabhängig vom individuellen Risikoprofil.

Gibt es eine Wende bei den bioresorbierbaren Gefäßstützen?

10.05.2024 Periphere arterielle Verschlusskrankheit Nachrichten

In den USA ist erstmals eine bioresorbierbare Gefäßstütze – auch Scaffold genannt – zur Rekanalisation infrapoplitealer Arterien bei schwerer PAVK zugelassen worden. Das markiert einen Wendepunkt in der Geschichte dieser speziellen Gefäßstützen.

Darf man die Behandlung eines Neonazis ablehnen?

08.05.2024 Gesellschaft Nachrichten

In einer Leseranfrage in der Zeitschrift Journal of the American Academy of Dermatology möchte ein anonymer Dermatologe bzw. eine anonyme Dermatologin wissen, ob er oder sie einen Patienten behandeln muss, der eine rassistische Tätowierung trägt.

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen
Bildnachweise