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  • 1
    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
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  • 2
    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.
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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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