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  • Aortoduodenal fistula  (1)
  • Congestive, Remodeling, Animal models of human disease, Hypertrophy, Physiological and pathological control of gene expression, Receptor pharmacology  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Langenbeck's archives of surgery 379 (1994), S. 197-203 
    ISSN: 1435-2451
    Keywords: Aortoduodenal fistula ; Diagnosis ; Treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An der Klinik und Poliklinik für Allgemein-und Abdominalchirurgie der Johannes-Gutenberg-Universität Mainz wurden zwischen 1984 und Februar 1992 6 Patienten wegen einer aortoduodenalen Fistel operiert. Anamnese, Symptome, Diagnostik und operative Behandlung dieser Patienten werden anhand anderer Studienergebnisse analysiert und dargestellt. Bei allen Kranken wurde zwischen einem und 10 Jahren vor Auftreten der aortoduodenalen Fistel eine Aortenprothese implantiert. Führendes Symptom war die gastrointestinale Blutung. Die Angiographie und die Computertomographie waren in unserem Krankengut die Methoden mit der größten Treffsicherheit. Bei 5 Patienten wurde die infizierte Prothese explantiert, 4 dieser 5 Patienten erhiel ten anschließend einen axillobifemoralen Bypass, em Kranker starb vor der Rekonstruktion. Die Direktnaht der Aorta und Verschluß der Darmläsion mit anschlieBender Netzinterposition wurde bei einem weiteren Patienten durchgeführt. Zwei Kranke, unter Notfallbedingungen im Volumenmangelschock operiert, starben innerhalb der ersten 6 postoperativen Tage. Die anderen Patienten überlebten einen Zeitraum von mindestens einem Viertel bis zu einem Jahr.
    Notes: Abstract Six patients were operated on for an aortoduodenal fistula at the Department of General and Abdominal Surgery, Johannes-Gutenberg-University Mainz. All patients had received an aortic graft implant between 1 and 10 years ago. The etiology, symptoms, and diagnostic and surgical treatment of these six cases are presented, and the results are discussed in comparison with the results of other studies. The main symptom of all of our patients was gastrointestinal bleeding. In our patients arteriography and computed tomography were the best diagnostic procedures. At surgery, five patients underwent graft excision and axillobifemoral bypass (only four patients, as one died before implantation). In the other patient a local repair, with closure of the graft defect and bowel defect, followed by interposition of an omental pedicle, was performed. Two patients died within 6 days of operation due to multiple organ failure.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2012-10-16
    Description: Background— Cardiac remodeling in response to pressure or volume overload plays an important role in the pathogenesis of heart failure. Various mechanisms have been suggested to translate mechanical stress into structural changes, one of them being the release of humoral factors such as angiotensin II and endothelin-1, which in turn promote cardiac hypertrophy and fibrosis. A large body of evidence suggests that the prohypertrophic effects of these factors are mediated by receptors coupled to the G q/11 family of heterotrimeric G proteins. Most G q/11 -coupled receptors, however, can also activate G proteins of the G 12/13 family, but the role of G 12/13 in cardiac remodeling is not understood. Methods and Results— We use siRNA-mediated knockdown in vitro and conditional gene inactivation in vivo to study the role of the G 12/13 family in pressure overload–induced cardiac remodeling. We show in detail that inducible cardiomyocyte-specific inactivation of the α subunit of G 13 , Gα 13 , does not affect basal heart function but protects mice from pressure overload–induced hypertrophy and fibrosis as efficiently as inactivation of Gα q/11 . Furthermore, inactivation of Gα 13 prevents the development of heart failure up to 1 year after overloading. On the molecular level, we show that Gα 13 , but not Gα q/11 , controls agonist-induced expression of hypertrophy-specific genes through activation of the small GTPase RhoA and consecutive activation of myocardin-related transcription factors. Conclusion— Our data show that the G 12/13 family of heterotrimeric G proteins is centrally involved in pressure overload–induced cardiac remodeling and plays a central role in the transition to heart failure.
    Keywords: Congestive, Remodeling, Animal models of human disease, Hypertrophy, Physiological and pathological control of gene expression, Receptor pharmacology
    Electronic ISSN: 1524-4539
    Topics: Medicine
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