Reference

Nocardicin A antibiotic

Nocardicin A antibiotic. Mori, Shigeru; Ohsawa, Shigeyoshi; Aoki, Hatsuo; Imanaka, Hiroshi (Fujisawa Pharmaceutical Co., Ltd., Japan). Ger. Offen. DE 2652686 2 Jun 1977, 25 pp. (German). (Germany). CODEN: GWXXBX. CLASS: IC: C12D009-08. PRIORITY: JP 75-139405 19 Nov 1975. DOCUMENT TYPE: Patent CA Section: 16 (Fermentations) Nocardicin A (I) [39391-39-4] was produced by Nocardia uniformis subspecies tsuyamanensis ATCC 12,301, on a complex culture medium supplemented with shikimic acid [138-59-0], II, where A = an alkylene residue with an amino-, hydroxy-, acylamino-, or oxo-group and n is a whole no. from 0 to 4, or a carboxyl group deriv. of II and 1 compd. of the group glycine [56-40-6], alanine [56-41-7], serine [56-45-1], homoserine [672-15-1], .alpha.-aminobutyric acid [80-60-4], and(or) .alpha.,.beta.-diaminopropionic acid [515-94-6]. Thus, 1 L of seed culture of the above organism was inoculated to 20 L to an aq. prodn. medium consisting of starch, cotton seed meal, salts, glycine, and L-tyrosine [60-18-4], and cultured for 6 days at 30.degree. with agitation and aeration. The culture broth was then acidified to pH 4, filtered, and passed through Diaion HP20 from which I was eluted with MeOH, concd., and crystd. at pH 2.5 to yield 2.9 g colorless cryst. I.

Effects of diaminopropionate, deoxyadenosine, and theophylline on stimulated formation of cyclic AMP and GMP by depolarizing agents in slices of guinea pig cerebral cortex

Effects of diaminopropionate, deoxyadenosine, and theophylline on stimulated formation of cyclic AMP and GMP by depolarizing agents in slices of guinea pig cerebral cortex. Shimizu, H.; Yamamura, Y. (Dep. Biochem., Nippon Roche Res. Cent., Kamakura, Japan). J. Neurochem., 28(2), 383-8 (English) 1977. CODEN: JONRA9. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) 2,3-Diaminopropionate [515-94-6] (5mM) and 2'-deoxyadenosine [958-09-8] (1mM) inhibited by .apprx.50% the 50- to 80-fold increases in cyclic AMP [60-92-4] content of guinea pig cerebral cortex induced by depolarizing agents and by adenosine [58-61-7] and glutamate [56-86-0] (0.1 and 5mM resp.). Theophylline [58-55-9] and 1-methyl-3-isobutylxanthine [28822-58-4] (1 and 0.5mM resp.) also inhibited the depolarization-induced increases in cyclic AMP. Thus, releases of both glutamate and adenosine appear to be involved in the depolarization-elicited increases in cyclic AMP levels. Cyclic GMP [7665-99-8] levels in the slices were increased by the depolarizing agent veratridine [71-62-5] (0.05mM) and by 5mM glutamate, but the increases were always less than those of cyclic AMP. The responses for cyclic GMP both to veratridine and glutamate were augmented by methylxanthines and not inhibited by 2,3-diaminopropionate. Glutamate appears to increase cyclic GMP levels by a different mechanism or site of action from that for cyclic AMP.