Reference

Effects of ulcerogens on gastroduodenal epithelial proliferation

Effects of ulcerogens on gastroduodenal epithelial proliferation. Eastwood, Gregory L. (Med. Sch., Univ. Massachusetts, Worcester, MA 01605, USA). Mech. Mucosal Prot. Upper Gastrointest. Tract, 27-32. Edited by: Allen, Adrian. Raven: New York, N. Y. (English) 1984. 125-04-2 and 53-86-1 which are cas registry numbers of chemicals are mentioned. CODEN: 50WXA8. DOCUMENT TYPE: Conference; General Review CA Section: 14 (Mammalian Pathological Biochemistry) Section cross-reference(s): 1, 2 A review with 11 refs. on the effects of aspirin, indomethacin, corticosteroids, and stress on gastroduodenal epithelial proliferation and the relation of the data to ulcerogenesis in human and lab. animal. .

Potentiation of nonspecific immunotherapy of experimental lung metastases by indomethacin

Potentiation of nonspecific immunotherapy of experimental lung metastases by indomethacin. Schultz, Richard M.; Altom, Marilyn G. (Dep. Immunol. Res., Lilly Res. Lab., Indianapolis, IN 46285, USA).Some commonly used reagents like 53-86-1 and 27100-68-1 are used in this experiment. J. Immunopharmacol., 5(4), 277-90 (English) 1983. CODEN: JOIMD6. ISSN: 0163-0571. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The effect of indomethacin [53-86-1], a prostaglandin synthetase inhibitor, on the antimetastatic activity of maleic anhydride-divinyl ether copolymer (MVE) [27100-68-1] was detd. An artificial metastasis model was developed in which single-cell suspensions of the M109 tumor were injected i.v. into BALB/c mice. A 52,600 mol. wt. fraction of MVE (MVE-5) was administered, i.p., at 20 mg/kg 2 days prior to tumor inoculation. MVE-5 treatment produced >80 percent redn. in macroscopic lung lesion formation at day 15 and day 19 after tumor inoculation and a resultant 45% increase in lifespan. Chronic administration of indomethacin in the drinking water at 10 mg/mL potentiated the MVE-5 antitumor induced macrophage activation in vivo. In the absence of any evidence for an interaction between indomethacin and circulating M109 cells, it was felt that the potentiating effect could be best explained in terms of interference with PGE-mediated feedback inhibition of macrophage functional activity. .