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  • 2000-2004  (2)
  • 1955-1959
  • Color pattern  (1)
  • Key words Molecular genetics – DNA polymorphisms –¶angiotensinogen –¶angiotensin converting enzyme –¶genetic animal models  (1)
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Years
  • 2000-2004  (2)
  • 1955-1959
Year
  • 1
    ISSN: 1432-041X
    Keywords: Key words Butterfly ; Color pattern ; Pigments ; Melanism ; Mimicry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  Butterfly wings are colored late in development, when pigments are synthesized in specialized wing scale cells in a fixed developmental succession. In this succession, colored pigments are deposited first and the remaining areas are later melanized black or brown. Here we studied the developmental changes underlying two wing pattern mutants, firstly melanic mutants of the swallowtail Papilio glaucus, in which the yellow background is turned black, and secondly a Spotty mutant of the satyrid Bicyclus anynana, which carries two additional eyespots. Despite the very different pattern changes in these two mutants, they are both associated with changes in rates of scale development and correspondingly, the final color pattern. In the melanic swallowtail, background scales originally destined to become yellow (normally developing early and synthesizing papiliochrome) show delayed development, fail to make papiliochrome, and subsequently melanize at the same time as scales in the wild-type black pattern. In the B. anynana eyespot, scale maturation begins with the central white focus, then progresses to the surrounding gold ring and later finishes with melanization of the black center. Mutants showing additional eyespots display accelerated rates of scale development (corresponding to new eyespots) in wing cells not normally occupied by eyespots. Thus by either delaying or accelerating rates of scale development, the final color, or position, of a wing pattern element can be changed. We propose that this heterochrony of scale development is a basic mechanism of color pattern formation on which developmental mutants act to change lepidopteran color patterns.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Zeitschrift für Kardiologie 89 (2000), S. 264-268 
    ISSN: 1435-1285
    Keywords: Key words Molecular genetics – DNA polymorphisms –¶angiotensinogen –¶angiotensin converting enzyme –¶genetic animal models ; Schlüsselwörter Molekulargenetik – DNA-Polymorphismen –¶Angiotensinogen – Angiotensin-Converting Enzym –¶Genetische Tiermodelle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Seit der Entdeckung des Renins durch Tigerstedt und Bergmann ist das Renin-Angiotensin-System (RAS) als wichtiger Modulator von Blutdruck und Volumenhomöostase bekannt. Aufgrund dieser Wirkungen wurde dem RAS schon frühzeitig eine pathophysiologische Rolle bei Hypertonie und anderen kardiovaskulären Erkrankungen zugeschrieben. Der therapeutische Stellenwert der Hemmung des RAS durch den Einsatz von Angiotensin Converting-Enzym-(ACE)-Inhibitoren und AngiotensinII (AT1)-Rezeptorantagonisten ist unbestritten. Unklar ist allerdings, inwieweit die mit kardiovaskulären Erkrankungen einhergehenden Veränderungen in der Aktivität des RAS sekundäre und primäre Faktoren darstellen. Es ist bekannt, dass genetische Faktoren wesentlich zur Pathogenese der Hypertonie und ihrer Folgeerkrankungen beitragen. So wurden Genpolymorphismen für nahezu alle Komponenten des RAS beschrieben und in klinischen Studien untersucht. Offen ist jedoch vielfach die funktionelle Relevanz dieser Befunde. Im Folgenden soll daher versucht werden, insbesondere die genetischen Grundlagen einer kausalen Verknüpfung zwischen RAS und Pathogenese der kardiovaskulären Erkrankungen anhand aktueller Befunde zu diskutieren. Hierbei wird beispielhaft auf die Rolle von Angiotensinogen für die Hypertonie und Angiotensin Converting Enzym für Hypertonie, koronare Herzkrankheit und andere kardiovaskuläre Erkrankungen eingegangen.
    Notes: Summary Since the discovery of renin by Tigerstedt and Bergmann, the renin angiotensin system (RAS) has been recognized as an important modulator of blood pressure and volume homeostasis. Based on these functions a pathophysiological role of the RAS in the pathogenesis of hypertension and other cardiovascular disorders has been postulated. The therapeutic benefit of RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensinII (ANGII) antagonists in these conditions has been shown. It remains unclear, however, whether the changes in RAS activity associated with cardiovascular disease are primary or secondary factors. It is well known that hypertension and hypertensive end-organ disease is influenced by genetic factors. Gene polymorphisms for virtually all components of the RAS have been described and investigated in clinical studies. It remains to be determined, however, how relevant these findings are for disease etiology. This review, therefore, will attempt to discuss the causal implications of these genetic studies for cardiovascular disease. The role of angiotensinogen and ACE for hypertension, coronary artery disease and other cardiovascular disorders is discussed in this context in an exemplary fashion.
    Type of Medium: Electronic Resource
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