[A case of monostotic fibrous dysplasia in the rib (author's transl)].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Arai.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Pholipomycin is a new member of the phosphoglycolipid family of antibiotics. Taxonomic studies of the producing organism revealed that it has morphologically characteristic aerial mycelia in which two to three spores are borne usually on short and clavate side branches. The species name, Streptomyces lividoclavatus, has been proposed. Pholipomycin is produced mainly in the solid residue of the fermentation culture broth and is isolated by methanol extraction of the mycelial cake followed by purification on ion-exchange resin and silica gel chromatography.
Physico-chemical characterization of pholipomycin revealed that this antibiotic is a new member of phosphoglycolipid antibiotics. Pholipomycin was differentiated from other members by the products formed on acid hydrolysis as follows: the presence of glucosamine, a 257 nm chromophore and moenocinol-type C25 lipids, but the absence of glucose, 6-deoxyglucosamine and glycine.
Pholipomycin, a new member of the phosphoglycolipid antibiotics, was primarily active against gram-positive bacteria including clinically isolated resistant bacteria. It differed from other members of the antibiotic family as it also demonstrated activity against gram-negative bacteria. Pholipomycin protected mice from infection with Staphylococcus aureus and was nontoxic to mice having an LD50 (i.v.) of 600 mg/kg. Besides possessing anti-microbiol activity, pholipomycin, when administered orally, appeared to promote growth in chickens and pigs.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Hyperplasia and, ultimately, neoplasia of bladder epithelium were produced by feeding 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) to weaning male Fischer rats. Hyperplasia induced by FANFT feeding for 2, 4, or 6 weeks, followed by feeding control diet until the end of the 84-week experiment, was reversible, and at the end of the experiment bladder epithelium in these animals was normal by light and scanning electron microscopy. Hyperplasia produced by 8 or more weeks of FANFT feeding was irreversible and by 84 weeks had resulted in bladder tumors in all animals fed FANFT for 12 or more weeks and in 4 of 5 and 6 of 7 animals fed FANFT for 8 and 10 weeks, respectively. The epithelial changes after 6 and 8 weeks of FANFT were similar by light microscopy but different by scanning electron microscopy. Pleomorphic microvilli seen with scanning electron microscopy are the hallmark of irreversible, and possibly progressive, epithelial proliferative change.
Urine samples of normal male Fischer rats or rats fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide for 6,8 or 30 weeks were collected and centrifuged 50 weeks after beginning treatment. After being sonicated and assayed (with purified desialylated ovine submaxillary mucin as acceptor glycoprotein), the exfoliated bladder cells obtained from the urines of treated rats showed uridine 5'-diphosphate galactose:glycoprotein transferase activity. The specific enzymatic activity of the enzyme from cells of 30-week-treated rats was about 10 times higher than from normal rats. The enzyme from cells of hyperplastic rats (treated 6 or 8 weeks) was only slightly higher in specific activity than that of normal rats. A similar was obtained at a later stage of bladder tumor induction, when the urines from 30-week-treated rats contained blood. A correction was made for protein contributed by the blood clot. The possibility that the blood clot contributed galactosyl transferase activity was excluded. Activity of the enzyme was detected in normal rat bladder tissue and in normal human urine.
Explore the source record for details and available documents.
Urine specimens obtained periodically from weanling male F344 rats fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) for 25 weeks followed by control diet for an additional 35 weeks, were examined by light microscopy (LM) and scanning electron microscopy (SEM). LM revealed red blood cells and atypical transitional cells in the urine at 25 and 43 weeks, when microinvasive transitional cell carcinoma was present. Malignant transitional cells were seen in the urine by LM at 60 weeks, when muscle invasion was present in histologic sections. However, SEM showed pleomorphic microvilli on exfoliated urothelial cells as early as 10 weeks after the beginning of FANFT administration, and the microvilli became increasingly pleomorphic as the bladder lesions progressed to muscle invasion at 60 weeks. Noninvasive tumors were present in histologic sections of rat bladders examined at the end of 10 weeks of FANFT administration. The numerous microvilli on exfoliated bladder tumor cells were in sharp contrast to the peaked microridges of normal exfoliated superficial cells.
An antibody induced in rabbits against a gentamicin-bovine serum albumin conjugate cross-reacted with the chemically related aminoglycoside, sisomicin, facilitating the development of a sisomicin radioimmunoassay. Sisomicin was labeled with (125)I using an acylating agent [3-(4-hydroxyphenyl)propionic acid-N-hydroxy-succinimide ester]. The resulting assay produced a linear standard curve on a logit-log plot with a sensitivity of 140 pg. Comparison with a microbiological assay showed no significant difference (P < 0.001) in the measurement of sisomicin by these two methods.
Herbicidins A and B, two new antibiotics with selective and contact herbicidal activity, were produced by a new species of Streptomyces designated as S. sagononensis. Among tested microorganisms, herbicidins indicated some activity against fungi in vitro and Xanthomonas oryzae in vivo. Their characteristic features were brought into relief by their selective and contact killing effect on many dicotyledonous plant as well as their inhibition of germination of the plant seeds, such as Chinese cabbage.
Herbicidins were produced in submerged fermentation by Streptomyces sagonomensis. Isolation of the antibiotics from the culture broth was performed by adsorption on resinous adsorbent followed by elution with aqueous acetone. Herbicidins A and B were separated from each other by counter-current distribution on a Ronor column or by silica gel chromatography. Physico-chemical characterization revealed that herbicidins are new antibiotics having an adenine nucleoside moiety in their structures.
Occasional submucosal tumors of indeterminate origin and without definite connection to the overlying mucosa have been reported in mice given various carcinogenic agents. Two Swiss mice fed niridazole developed such tumors. Electron microscopy of 1 of the tumors revealed thin myofilaments with oval dense bodies, marginal dense plaques, and gap junctions, identifying the tumor as originating from smooth muscle cells. No desmosomes, tonofilaments, secretory granules, striated muscle, or collagen were present in the tumor cells. Since the biology of these lesions is unknown, classification as benign or malignant cannot be made at this time. Their recognition is important in evaluating possible bladder carcinogens in mice.
N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide (FANFT) fed to male and female Fischer rats at a dose of 0.2% of the diet induces lesions of the urinary bladder which progress from mild hyperplasia at 2 to 4 weeks, to moderate hyperplasia at 6 to 8 weeks, severe nodular and papillary hyperplasia at 10 to 14 weeks, and microinvasive carcinomas by 25 weeks as observed by light microscopy. Male Fischer rats fed FANFT for 2 to 4 weeks and then maintained on control diet show regression of the bladder lesions within 2 weeks to normal-appearing mucosa which persists through 50 weeks. Rats fed FANFT for 6 weeks show regression of the moderately hyperplastic epithelium to normal within 4 weeks after being placed on control diet which persists through 50 weeks. Rats fed FANFT for 8 to 10 weeks show regression of the hyperplastic bladder epithelium within 2 weeks of receiving control diet, but focal areas of mild hyperplasia are detectable through the 20th week of the experiment. By the 50th week the rats fed FANFT for 8 weeks all had moderate to marked hyperplasia, but the rats fed FANFT for 10 weeks had transitional cell tumors, one of which was invasive through the entire thickness of the bladder wall. The lesions present in rats fed FANFT for 12, 14, or 20 weeks continued to progress to invasive tumors (microinvasive or invasion of muscle) after the rats had been maintained on control diet through 50 weeks. Thus, the hyperplastic lesions developing through 6 weeks of FANFT administration appear to be reversible if FANFT is discontinued, but later lesions appear to be irreversible.
The administration of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) at a dose of 0.2% of the diet to male Fischer rats results in the appearance of urinary bladder epithelial lesions progressing from hyperplasia to invasive transitional cell carcinomas. These progressive epithelial alterations have been observed by scanning electron microscopy at 2-week intervals with special attention paid to cells covering the luminal surface. After 2 to 4 weeks of FANFT administration there is mild pleomorphism and moderate swelling of the surface cells giving a cobblestone appearance. The normal pattern of microridges of superficial transitional cells is still present, although occasional cells by 4 weeks of FANFT feeding are covered by small uniform microvilli. By 6 weeks these changes are more extensive and more cells are covered with uniform microvilli. By 8 weeks, cells covered with pleomorphic microvilli are found in discrete foci, and by 10 weeks nodular or papillary lesions are present. The 2- and 4-week lesions regress to normal within 2 to 4 weeks of discontinuing FANFT administration, and the 6- and 8-week lesions regress toward normal in 4 to 6 weeks of being fed control diet. The 6-week lesions have regressed entirely to normal 44 weeks after FANFT was stopped, but the 8-week lesions have progressed to moderate or marked hyperplastic lesions by 42 weeks of control diet with pleomorphic cells covered with pleomorphic microvilli. The results of this study suggest that lesions are reversible up to and including 6 weeks of 0.2% FANFT in the diet, and that, by 8 weeks of 0.2% FANFT, irreversible lesions result which do not revert to normal after 42 weeks of control diet.
Histological studies were made on the nephrotoxic effect of citrinin on the kidneys of rats, with or without previous treatment with the nephrotoxic chemicals, N-(3,5-dichlorophenyl)succinimide (NDPS) and N-nitrosodimethylamine (DMN). Oral administration of 0.02% or 0.05% citrinin alone caused signs of kidney injury but did not induce kidney tumors. On treatment with DMN alone, 8 of 14 rats (57.1%) developed kidney tumors; two (14.3%) were renal cell tumors, eight (57.1%) embryonal cell tumors, and one (7.1%) hemangioendothelioma. On the other hand, kidney tumors developed in 18 of 19 rats (94.7%) and 13 of 15 rats (86.7%) by the administration of 0.02% and 0.05% citrinin, respectively, after DMN. The tumors in these two groups were diagnosed histologically as renal cell tumors in 18 (94.7%) in group IV and 13 (86.7%) in group III, and as embryonal cell tumors in 14 (73.7%) in group IV and 9 (60.0%) in group III. Thus, in groups treated with citrinin after DMN the incidence of renal cell tumors was much greater and the incidence of embryonal cell tumors slightly greater than in the group treated with DMN alone. Kidney tumors developed in 4 of 18 rats (22.2%) treated with 0.02% citrinin after NDPS, but treatment with NDPS alone did not induce kidney tumors. Thus, treatment with citrinin changes the histological type and incidence of kidney tumors in rats induced by DMN. Moreover, this study confirms that citrinin in combination with NDPS can induce kidney tumor in rats, which was renal cell tumor (adenoma) histologically.