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  • CA 19  (1)
  • Congestive, Remodeling, Animal models of human disease, Hypertrophy, Physiological and pathological control of gene expression, Receptor pharmacology  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Stellenwert des Tumormarkers CA 19–9 in der Differentialdiagnose von Raumforderungen im Pankreaskopf (1996)
    Springer
    Der Chirurg 67 (1996), S. 1007-1011 
    Details
    ISSN: 1433-0385
    Keywords: Key words: Pancreatic cancer ; CA 19 ; 9.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Bei 96 Patienten (duktales Pankreascarcinom, n = 34; periampulläres Carcinom, n = 43; chronische Pankreatitis, n = 19) wurde der Stellenwert des Tumormarkers CA 19–9 in der Differentialdiagnose bei Raumforderungen im Pankreaskopf retrospektiv überprüft. Die Sensitivität betrug für das duktale Carcinom 73,5 % und für den periampullären Tumor 48,8 % bei einer Spezifität von 63,2 %. Das carcinoembryonale Antigen war nur bei jedem 5. Patienten erhöht. Durch Kombination beider Tumormarker ließ sich die Sensitivität serologischer Tests nicht steigern. Die schlechte Spezifität von 63 %, die beim Vorliegen eines Verschlußikterus bis auf 33 % sinkt, erlaubt keine zuverlässige präoperative Differenzierung zwischen einem Carcinom und einer chronischen Pankreatitis. Ein postoperativ erhöhter CA-19–9-Serumspiegel weist auf persistierendes Tumorgewebe hin und ist mit einer statistisch signifikant schlechteren Prognose als bei normalen Marker verbunden.
    Abstract: Schlüsselwörter: Pankreascarcinom – CA 19–9.
    Notes: Summary. In 96 patients (ductal pancreatic carcinoma, n = 34; periampullary carcinoma, n = 43; chronic pancreatitis, n = 19) the role of CA 19–9 in the diagnosis of lesions of the head of the pancreas were evaluated. The sensitivity for ductal pancreatic carcinoma was 73.3 %, for periampullary carcinoma 48.8 %, and specificity was 63.2 %. Carcinoembryonic antigen was elevated only in every fifth patient. Even when combining the two tumor markers no increase in sensitivity could be observed. The low specificity of 63 %, which decreased to 33 % in the case of obstructive jaundice, does not allow adequate preoperative differentiation between cancer patients and those with chronic pancreatitis. In cases of postoperatively elevated CA 19–9 level the prognosis is worse than in patients with normal tumor markers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00002512
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    Paper (German National Licenses)
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  • 2
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    G13-Mediated Signaling Pathway Is Required for Pressure Overload-Induced Cardiac Remodeling and Heart Failure [Heart Failure] (2012)
    American Heart Association (AHA)
    Details
    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
    Published by American Heart Association (AHA)
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