[Estrogen therapy for the climacteric syndrome].
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Biomedical subjects
Publications and source records attributed to O Dapunt.
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This prospective study compares 3 different consecutive treatment protocols of gastroduodenal hemorrhage. Three hundred sixty-one patients underwent emergency endoscopy as the basis for further treatment. Clinical and endoscopic findings, such as site and type of the bleeding source, bleeding activity and intensity, age, and concomitant diseases of the patient were scored between 0 and 6 points, the higher number indicating a higher risk. The mean values of the total score of the 7 risk factors were comparable in the 3 treatment protocols. In period I (n = 77), a total of 16 patients (20.8%) underwent emergency operations because of severe bleeding, 27 (35%) were operated on after cessation of the bleeding, and 34 (44.2%) were treated conservatively. The mortality was 16.9%. In period II (n = 116), patients with actively bleeding lesions (n = 38) underwent endoscopic sclerotherapy, with a primary rate of hemostasis in 95%. As a result, the rate of emergency surgery could be reduced to 12.9% and the mortality for the entire group was reduced to 9.5%. The problem in this protocol was the rate of recurrent bleeding after primary endoscopic hemostasis: 13/116 (11.2%). Eleven of the 13 rebleeders presented with a lesion either on the back wall of the duodenum or with a visible vessel. In period III (n = 168), a total of 83 patients (50%) underwent endoscopic injection therapy with a primary success in 93%. Sixteen patients (9.5%) with lesions of high rebleeding risk (duodenal ulcer on the posterior wall or visible vessel) were scheduled for urgent elective operation after volume resuscitation within 24 hours of emergency endoscopy (mortality, 6.3%).(ABSTRACT TRUNCATED AT 250 WORDS)
In 44 ovarian cancers, CD44 variant (CD44v) expression was investigated immunohistochemically using a variant-specific polyclonal antibody. Patients with CD44v-positive carcinomas had a significantly shorter disease-free survival than patients with CD44v-negative tumors. Overall survival was also significantly reduced for stages III and IV of the International Federation of Gynecology and Obstetrics. Furthermore, a highly significant inverse correlation was observed between CD44v expression and preoperative platelet count. Urinary neopterin concentration, a marker of cell-mediated immunostimulation, did not differ between CD44v-positive and -negative ovarian cancer patients. Moreover, in seven ovarian carcinoma cell lines, modulation of CD44v expression was analyzed by living cell radioimmunoassay. Interferon-alpha, interferon-gamma, tumor necrosis factor, transforming growth factor-beta, all-trans retinoic acid and cisplatin did not affect CD44v expression.
Interferons have a mechanism of action different from chemotherapeutic agents. They modulate many physiologically important cellular functions and are a major building block in the network constructed by the biological response modifiers. Moreover, interferons are known to interact also with anticancer drugs to increase their therapeutic benefit. The aim of the present study was to evaluate the effects of interferon-gamma on cultured ovarian carcinoma cell lines. The growth of 3 out of 4 carcinoma cell lines (OVCAR-3, HTB-77, 2780 vs CRL-1572) was inhibited by interferon-gamma. The same cell lines which were growth inhibited also showed an induction of HLA-DR on their surface. CA-125 was found to be increased in 2 of them (OVCAR-3 and HTB-77) by interferon-gamma, whereas CEA was not detectable even after treatment. For HMFG-I, a shightly increased surface expression was induced on OVCAR-3 cells. HMFG-II expression was not significantly affected by interferon-gamma. The combined treatment with interferon-gamma and cisplatin, retinoic acid, or tumor necrosis factor alpha was studied on the ovarian carcinoma cells. For the combination with cisplatin we observed an additive or synergistic amplification of the antiproliferative activity, whereas tumor necrosis factor alpha resulted in a marked synergism in each case. In contrast to breast cancer cells retinoic acid and interferon-gamma acted synergistically only in one ovarian carcinoma cell line.
In the present study the modulatory effects of inflammatory cytokines, interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), on CA-125 release in established ovarian cancer cell lines and in human peritoneal mesothelial cells (HPMC) both grown as monolayers, were investigated. The purity of mesothelial cell cultures were confirmed by the positivity of the cells for vimentin and cytokeratins 8 and 18, and their negativity for markers CD34 and CD68, thus excluding contamination by endothelial cells and macrophages. The preliminary results of CA-125 measurements in the culture medium clearly indicated differences in the pattern of CA-125 expression and release between normal and malignant cells under the influence of inflammatory cytokines. Furthermore, it seems that normal mesothelial cells play a crucial role as a source of CA-125 found in ascitic fluid or in pleural effusions and possibly even in the serum since secretion of this tumor marker into the culture medium was found to be significantly higher in HPMC than in ovarian cancer cells.