The terminal glycoproteins of fetal, cultivated (7-12 days), and adult nondiabetic and diabetic pancreatic tissues (Balb c, C3h mice) were investigated by lectin histology (peanut-, phytohemagglutinin, wheat germ agglutinin, Ulex europeus I, concanavalin A and Ricinus communis agglutinin, PaP method +/- neuraminidase). Anti-insulin and -glucagon were used to identify islet cells. S-100 antibody showed dendritic reticulum cells, anti-IAK proved MHC II antigens (C3h). Cultured tissue was partly incubated with anti-IAK and complement for lysis of MHC II antigens. On the 19th gestational day fetal pancreatic tissue did not bind peanut agglutinin, Phytohemagglutinin, or wheat germ agglutinin, whereas concanavalin A and Ricinus communis were weakly bound. Terminal fucose residues were not expressed by C3h fetal islet cells in contrast to Balb c. Following neuraminidase digestion peanut agglutinin and phytohemagglutinin were strongly bound, indicating sialic acid-substituted terminal glycoproteins. Cultivated tissue (Day 7) bound all investigated lectins (except Ulex europeus I in C3h mice), indicating maturation of islet cells. In spite of the peak of insulin concentration in the medium we observed a faint binding of anti-insulin and investigated lectins following 12 days of cultivation. This indicates a disorder of terminal glycoprotein synthesis at this point. There was no difference in lectin binding patterns of adult nondiabetic islet cells compared to the cultivated tissue (7 days), but no Ulex europaeus I binding of the adult Balb c mice was observed. S-100 binding decreased during the cultivation period as dendritic reticulum cells became destroyed by cultivation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

[Serum gastrin level in patients with colorectal adenoma or carcinoma].

During the last years interest has focused on the trophic effect of gastrin in colorectal carcinomas. Some reports indicated an increased serum level of gastrin in patients with colorectal adenomas or carcinomas. In a prospective study in 261 patients submitted to colonoscopy fasting serum gastrin concentrations were determined. 91 patients served as control, 89 patients had one or more adenomas, 55 patients suffered from a colorectal carcinoma, 17 had a benign, postoperative stenosis of the colon, and 9 had a chronic inflammatory bowel disease. All patients fulfilled the following criteria: No regular drug intake, no previous gastric or small bowel operation, no known ulcer disease, no abnormalities in serum calcium, creatinine, triglycerides, cholesterol and blood urea. Mean gastrin level was 86.63 +/- 23.8 pg/ml in the control, 84.57 +/- 25.1 pg/ml in the adenoma group and 84.6 +/- 24.4 pg/ml in the carcinoma group. No difference of serum gastrin levels were observed regarding sex, age, tumor stage and localisation.

Adolescent↗

PubMed1991

[Diagnosis and management of lower gastrointestinal hemorrhage. Retrospective analysis of 233 cases].

In a retrospective analysis the diagnostic procedure was evaluated in patients with acute lower gastrointestinal bleeding. Bleeding sources were localized distally to the ligament of Treitz in 233 patients (1979-1988). Patients with hemorrhoidal bleeding were not included. Following exclusion of an upper gastrointestinal bleeding the diagnostic procedure was initiated with a recto-/colonoscopy. Lesions were detected in 77% of the treated patients (n = 136). Angiography localized the bleeding in 68%, in combination with colonoscopy the identification of the bleeding source reached 86.5% in the treated patients. Following scintigraphy the bleeding source was determined in 89.7% of these patients. The sensitivity of colonoscopy (0.93) was superior to the angiography (0.78) and to the scintigraphy (0.75). Apart from neoplasms and adenomas angiodysplasia and Meckel's diverticula were the most common sources of the bleeding in patients who underwent operation. In 61 patients endoscopic therapy was performed, however, 6.5% of these patients had to be operated on later because of persistent bleeding. All together 79 patients underwent operation, 31 for bleeding and 48 for other reasons. 12 patients died, 6 of them were operated on for the bleeding, the other for neoplasms.

Adolescent↗

PubMed1991

Influence of gastrin, gastrin receptor blockers, epidermal growth factor, and difluoromethylornithine on the growth and the activity of ornithine decarboxylase of colonic carcinoma cells.

Polyamines are essential factors of cell growth and differentiation. Modulation of the cellular polyamine content by 2-difluoromethylornithine (DFMO) inhibiting ornithine decarboxylase (ODC), or by hormones inducing ODC, influences cell growth. Gastrin acts trophically on some colonic carcinomas and their growth is inhibited by gastrin receptor blockers. The mechanism of the trophic action of gastrin on colonic carcinomas is not known. In this study the effect of gastrin, gastrin receptor blockers, epidermal growth factor (EGF) and DFMO on growth and ODC activity of four human colon carcinoma cell lines (SW 403, SW 1116, LS 174 T and Lovo) was investigated. Growth and ODC activity of all cell lines were inhibited by DFMO. Growth of the SW 403 cell line was increased by gastrin and inhibited by the gastrin receptor blocker benzotrypte. The other cell lines did not respond to gastrin and the gastrin receptor blocker. In SW 403 cells ODC activity was increased by gastrin, and was also elevated after treatment with the gastrin receptor blocker. These in vitro results were confirmed by studies on tumours that developed from SW 403 cells in nude mice. Combination of benzotrypte and DFMO did not enhance the antiproliferative effect. EGF increased growth of SW 403 cells, but no induction of ODC activity was measured. LS 174 T cells were not stimulated by EGF. Medium replacement was the strongest stimulus of ODC activity in SW 403 cells already inducing ODC after 3 h. During cell culture ODC activity was high after seeding and decreased continuously with increasing cell density. These data suggest that gastrin induces ODC in gastrin-sensitive colonic carcinoma cells. DFMO appears to be a valuable antiproliferative agent in colonic carcinoma cells.

Animals↗

PubMed1989

Growth of colorectal carcinoma cells: regulation in vitro by gastrin, pentagastrin and the gastrin-receptor antagonist proglumide.

The growth-regulating effects of pentagastrin, gastrin and the gastrin-receptor antagonist proglumide were investigated in three established cell lines derived from human colorectal carcinomas in vitro and after transplantation into nude mice. In vitro a significant increase of cell growth in the SW 403 cell line incubated with pentagastrin or gastrin was observed. In the Lovo cell line this effect was only detected after synchronization of cell growth. Pentagastrin and gastrin had no effect on the growth of the Ls 174 T cell line. Proglumide reduced cell proliferation in all three cell lines as well as in the L929S cell line derived from fibroblasts, which served as control. After transplantation into nude mice all tumor cell lines increased, Lovo and Ls 174 T as undifferentiated tumor, SW 403 as differentiated. Pentagastrin increased and proglumide decreased growth in SW 403 tumors, whereas no effect was observed on Ls 174 T and Lovo tumors. We therefore conclude that growth of some colorectal carcinomas is regulated by gastrin, but that the effect of proglumide is unspecific rather than related to blockage of gastrin receptors. The growth-regulating effect of gastrin could be due to tumor differentiation.

Animals↗

PubMed1988

[Indications for intracavitary afterloading radiotherapy combined with surgical intervention].

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Bile Duct Neoplasms↗

PubMed1986

Morphometric evaluation of post-ischemic capillary perfusion in selectively vulnerable areas of gerbil brain.

In gerbils the hemispheric blood flow was interrupted for 5 min by bilateral carotid artery occlusion to produce delayed selective destruction of the CA 1 sector of hippocampus. The influence of hemodynamic factors was studied by evaluating the microcirculation before and at two times after ischemia (3 min and 7 days), using Evans blue as an intravital vascular tracer. The density of perfused capillaries and the fractional volume of circulating blood were determined by quantitative morphometry and the values for the vulnerable CA 1 sector compared with those for the resistant CA 3 sector and cerebral cortex. In control animals the number of perfused capillaries in the CA 1 sector was about 20% lower, and the volume of circulating blood about 30% lower, than in the CA 3 sector or cerebral cortex. This difference was markedly enhanced after 5-min ischemia. During the early recirculation phase, capillary perfusion improved in the cortex, whereas in the CA 1 sector (and to a lesser degree also in the CA 3 sector) it declined. After 7 days, the density of perfused capillaries and the volume of circulating blood had returned to control levels in the cerebral cortex and CA 3 sector of hippocampus. In the CA 1 sector, in contrast, the microcirculation had further deteriorated. The density of perfused capillaries was less than 30%, and the circulating blood volume even less than 50%, of that in the cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗