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  • Animal models of human disease  (1)
  • Biochemistry and metabolism, Other heart failure, Cell signalling/signal transduction, Energy metabolism, Growth factors/cytokines, Hypertrophy  (1)
  • Diagnosis  (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: 2014-07-03
    Description: Rationale : Myostatin is a major negative regulator of skeletal muscle mass and initiates multiple metabolic changes, including enhanced insulin sensitivity. However, the function of myostatin in the heart is barely understood, although it is upregulated in the myocardium under several pathological conditions. Objective : Here, we aimed to decipher the role of myostatin and myostatin-dependent signaling pathways for cardiac function and cardiac metabolism in adult mice. To avoid potential counterregulatory mechanisms occurring in constitutive and germ-line–based myostatin mutants, we generated a mouse model that allows myostatin inactivation in adult cardiomyocytes. Methods and Results : Cardiac MRI revealed that genetic inactivation of myostatin signaling in the adult murine heart caused cardiac hypertrophy and heart failure, partially recapitulating effects of the age-dependent decline of the myostatin paralog growth and differentiation factor 11. We found that myostatin represses AMP-activated kinase activation in the heart via transforming growth factor-β–activated kinase 1, thereby preventing a metabolic switch toward glycolysis and glycogen accumulation. Furthermore, myostatin stimulated expression of regulator of G-protein signaling 2, a GTPase-activating protein that restricts Gaq and Gas signaling and thereby protects against cardiac failure. Inhibition of AMP-activated kinase in vivo rescued cardiac hypertrophy and prevented enhanced glycolytic flow and glycogen accumulation after inactivation of myostatin in cardiomyocytes. Conclusions : Our results uncover an important role of myostatin in the heart for maintaining cardiac energy homeostasis and preventing cardiac hypertrophy.
    Keywords: Biochemistry and metabolism, Other heart failure, Cell signalling/signal transduction, Energy metabolism, Growth factors/cytokines, Hypertrophy
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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  • 3
    Publication Date: 2015-06-11
    Description: The gene SLC4A5 encodes the Na + -HCO 3 – cotransporter electrogenic 2, which is located in the distal nephron. Genetically deleting Na + -HCO 3 – cotransporter electrogenic 2 (knockout) causes Na + -retention and hypertension, a phenotype that is diminished with alkali loading. We performed experiments with acid-loaded mice and determined whether overactive epithelial Na + channels (ENaC) or the Na + -Cl – cotransporter causes the Na + retention and hypertension in knockout. In untreated mice, the mean arterial pressure was higher in knockout, compared with wild-type (WT); however, treatment with amiloride, a blocker of ENaC, abolished this difference. In contrast, hydrochlorothiazide, an inhibitor of Na + -Cl – cotransporter, decreased mean arterial pressure in WT, but not knockout. Western blots showed that quantity of plasmalemmal full-length ENaC-α was significantly higher in knockout than in WT. Amiloride treatment caused a 2-fold greater increase in Na + excretion in knockout, compared with WT. In knockout, but not WT, amiloride treatment decreased plasma [Na + ] and urinary K + excretion, but increased hematocrit and plasma [K + ] significantly. Micropuncture with microelectrodes showed that the [K + ] was significantly higher and the transepithelial potential (V te ) was significantly lower in the late distal tubule of the knockout compared with WT. The reduced V te in knockout was amiloride sensitive and therefore revealed an upregulation of electrogenic ENaC-mediated Na + reabsorption in this segment. These results show that, in the absence of Na + -HCO 3 – cotransporter electrogenic 2 in the late distal tubule, acid-loaded mice exhibit disinhibition of ENaC-mediated Na + reabsorption, which results in Na + retention, K + wasting, and hypertension.
    Keywords: Animal models of human disease
    Print ISSN: 0194-911X
    Topics: Medicine
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