[Anti-Trichosporon cutaneum IgG, IgA and s-IgA antibody activities in bronchoalveolar lavage fluids in summer-type hypersensitivity pneumonitis].
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Biomedical subjects
Publications and source records attributed to T Sakata.
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Hypophagia induced by 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA), an endogenous short-chain polyhydroxymonocarboxylic acid, was investigated in rats. Intraperitoneal injection of 2500 mumol 2-DTA did not suppress feeding, but 2.5 mumol 2-DTA injected into the third cerebroventricle did. To efficiently transport exogenous 2-DTA into the brain, its encapsulation and delivery in specially made sulfatide liposomes was attempted. Feeding was suppressed dose-dependently by intraperitoneally injected 2-DTA in liposomes. Injection of 2500 mumol 2-DTA into the common carotid artery also suppressed feeding. Administration by either route prolonged postprandial intermeal interval with no change in meal size, as was observed after central administration of 2-DTA. Injection of 2.5 mumol 2-DTA into the third cerebroventricle elevated plasma glucose level, leaving insulin and free fatty acids unaffected. These findings, together with previous results, indicate that at least one site for the physiological action of 2-DTA is in the hypothalamic centers for food intake.
To clarify the hypophagic action of D-glucose, meal size, postprandial intermeal interval and eating rate were analyzed after infusion of glucose into the third cerebroventricle. The effects of glucose structure modification on feeding modulation were examined by comparing the effects of glucose to those of its epimers, D-mannose, D-allose and D-galactose. Glucose, infused in doses of 6 to 24 mumol, dose relatedly reduced meal size, but did not change other meal parameters. The minimum dose of glucose to induce feeding suppression was between three and 6 mumol. The epimers, at doses of 24 mumol, did not affect food intake or body weight. Drinking patterns and ambulatory activity were not changed by glucose infusion. These findings were consistent with neuronal activity observed in the ventromedial hypothalamic nucleus.
In a study primarily designed to evaluate the inhibitory effects of aspirin on N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT)-initiated and saccharin-promoted bladder carcinogenesis, significant renal lesions were observed. Thus, administration in the diet of aspirin and sodium saccharin to F344 male rats for 68 weeks resulted in significant lesions of the renal papilla. In contrast to the bladder, aspirin enhanced the frequency and severity of the proliferative action of sodium saccharin on the epithelium of the renal papilla (p less than 0.05 compared to rats treated with either compound alone). The majority of rats administered the two chemicals together demonstrated moderate to severe urothelial hyperplasia of the renal papilla. Columnar metaplasia of the papillary epithelium also occurred frequently in rats fed the combination of chemicals. The rats treated with a combination of sodium saccharin and aspirin had a high incidence of renal papillary necrosis which was also present to a lesser extent among rats treated with aspirin only. Papillary calcification was also frequently observed in the rats fed the combination of aspirin and sodium saccharin. Sodium saccharin or aspirin alone reduced the light microscopic incidence and severity of rat nephropathy, a common finding in aging rats. It would appear that the hyperplastic and renal papillary toxic effects of aspirin and sodium saccharin are independent responses, and that the administration of the two chemicals together greatly accentuates these responses.
The modification potentials of ethyl alcohol (EA) and acetaldehyde (AA) on development of immunohistochemical glutathione S-transferase (placental type)-positive (GST-P+) liver cell foci were examined in an in vivo short-term assay system. Rats were given a single intraperitoneal injection of diethylnitrosamine (DEN) and then various concentrations of EA (20, 10, 5%) or AA (5, 2.5%) in their drinking water from week 2 till termination in week 6. All rats were subjected to two-thirds partial hepatectomy in week 3. Animals given EA (20% and 10%) or AA showed significant decrease in liver and body weight. However, only EA caused significant dose-related inhibition of development of areas of foci (mm2/cm2), but AA had no effect on their development.
The effects of D-glucosamine (2-amino-2-deoxy-D-glucose), an endogenous glucose analogue, and 1-deoxy-D-glucosamine on feeding behavior were clarified. Test solutions (24 mumol) were infused into the third cerebroventricle of the rat. Glucosamine induced a feeding episode within 30 min after infusion and then prolonged the ensuing postprandial intermeal interval for the first 4 h of the dark period, while glucose suppressed feeding by decreasing meal size. Ventricular injection of 1-deoxyglucosamine potently suppressed feeding in a dose-related manner by affecting all meal parameters, and oral administration of 2,400 mumol also induced anorexia. Changes in activity of glucose-sensitive neurons in the lateral hypothalamus and glucoreceptor neurons in the ventromedial hypothalamus after electrophoretic application of glucosamine and 1-deoxyglucosamine were compatible with behavior changes. The results indicate that replacement of a hydroxyl group by an amino group at C-2 of the glucose molecule affects feeding behavior and deoxidation of C-1 potently induces anorexia.
To assess the diagnostic value of antibody activities to Trichosporon cutaneum antigen in patients with summer-type hypersensitivity pneumonitis in Japan, we measured the serum IgG, IgA, and IgM antibodies to saline-soluble antigen of homogenized T. cutaneum cells by enzyme-linked immunosorbent assay (ELISA). The IgG antibody activity was observed in serum samples from 25 (83%) of the 30 patients and in 9 (82%) of the 11 asymptomatic family members. The IgA antibody activity was found in 25 (83%) of the patients but in only 3 (27%) of asymptomatic family members. Unexpectedly, we found no significant correlation between the IgG and IgA antibody activities to the same antigen in individual patients. Moreover, although the IgG antibody activity was related to the precipitating antibody, the IgA antibody activity was not. The IgM antibody activity by ELISA was found in only 5 (17%) of the patients. The IgG+IgA+IgM antibody activity was demonstrated in 27 (90%) of the 30 patients, and of 3 serum samples that were found negative by the ELISA method, 2 were positive by the IFA method. We conclude that the detection of the serum IgG and IgA antibody activities to T. cutaneum antigen by ELISA is a simple and useful serodiagnostic test for summer-type hypersensitivity pneumonitis. Measurement of the IgA antibody activity is especially helpful in discriminating symptomatic from asymptomatic family members.
Influences of indigestible dietary bulk (kaolin), short chain fatty acids (SCFA), and their interaction on the weight and epithelial cell proliferation rate of digestive organs were studied. Rats with an ileal fistua were fed an elemental diet with or without kaolin (10% w/w). They were given a 3 ml SCFA mixture (acetate, propionate, and butyrate; 100, 20, and 60 mM, respectively; pH 6.1) or a 3 ml NaCl solution (180 mM; pH 6.1) via the fistua twice a day for 14 days. Kaolin, but not SCFA, increased full and empty body weight by 14% and 13%, respectively. Kaolin increased the tissue weight, but not relative tissue weight (tissue weight/empty body weight), of the forestomach, distal colon, liver and heart by 6-14%. SCFA, independent of the presence of kaolin, increased the weight and the relative weight of the cecum, both by 15%. SCFA, but not kaolin, increased the cryptal cell production rate in colonic segments by 50-140%. These results indicate that SCFA accelerates epithelial cell proliferation, thereby increasing cecal tissue weight, kaolin stimulates body weight gain which is accompanied by a proportional increase in the tissue weight of some digestive organs, and the actions of these factors are independent of each other.
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Highly lipophilic trityloxyethylamine (TEAm) or trityloxyethylaniline (TEAn) were prepared and used for the protection of the 5'-terminal phosphate. We synthesized 5'-phosphorylated oligodeoxyribonucleotides by the solid phase synthesis. TEAm or TEAn groups enabled us to isolate the desired oligonucleotide easily by the reversed phase column due to their high lipophilicity and could be removed by the aq. AcOH treatment.
N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide (FANFT) is metabolically activated by several enzyme systems, including prostaglandin H synthase. Aspirin is an inhibitor of prostaglandin H synthase and has been shown to inhibit FANFT-induced bladder carcinogenesis when coadministered in the diet. To further evaluate the effects of aspirin on bladder carcinogenesis in the rat, we have coadministered aspirin with FANFT during the initiation phase and with sodium saccharin during the promotion phase of carcinogenesis. FANFT was administered in the diet at a level of 0.2% for 6 weeks as the initiator and sodium saccharin was administered in the diet at a level of 5% for 61 weeks as promoting stimulus. Aspirin was administered at a level of 0.5% with FANFT or with sodium saccharin, and appropriate control groups were included. Weanling male Fischer 344 rats were utilized and the chemicals were added to Agway Prolab 3000 rat chow. A 1-week interval was included between the FANFT and sodium saccharin administration during which the rats received either aspirin containing diet or control chow, depending on the treatment regimen of the group. Thirty rats were included in each group at the beginning of the experiment, except for the control group which contained 40. Rats given FANFT followed by saccharin had a bladder carcinoma incidence of 83%. Rats given aspirin with FANFT but not with saccharin had a carcinoma incidence of 20% and the rats fed aspirin with the saccharin but not with the FANFT had an incidence of 28%. FANFT followed by control diet resulted in a bladder carcinoma incidence of 10%, as was true for the rats given FANFT plus aspirin followed by control diet. However, the hyperplastic effects induced in the bladder epithelium by saccharin without prior FANFT administration were inhibited by coadministration with aspirin. These results indicate that aspirin inhibits both FANFT initiation and sodium saccharin promotion of bladder carcinogenesis, but the mechanisms involved would most probably be different for each.
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Little is known about in utero urinary bladder embryogenesis and the development of the urothelium of laboratory animals. Previous scanning and transmission electron microscopy studies in rats and mice have indicated that the highly specialized superficial cells of the urothelium complete their differentiation at a very late stage of fetal development or shortly after birth. Limitations in methodology in the past have precluded extensive examination of earlier stages of bladder development. Innovations in preparatory procedures of the bladder of rat fetuses have been developed which make possible detailed scanning and transmission electron microscopic and light microscopic examination of cloaca and urinary bladder as early as day 11 of gestation.
D-glucosamine, 2-amino-2-deoxy-D-glucose, is known to be an endogenous glucose analogue and to antagonize glucose uptake and metabolism. The present experiments were aimed to clarify effects of glucosamine and related chemical substances on ingestive behavior, as well as its direct effects on hypothalamic neurons. Infusion of 24 mumole glucosamine into the third cerebroventricle induced feeding within 30 min in 5 rats out of 7 tested, accompanied by increased ambulatory activity. No periprandial drinking was observed. Plasma glucose level increased, peaking at 30 min after the injection. Plasma insulin level tended to increase, but not significantly. Electrophoretic application of glucosamine activated glucose-sensitive neurons in the lateral hypothalamus and suppressed glucoreceptors in the ventromedial hypothalamus. These facts, together with other reported results, suggest that glucosamine can modulate physiological feeding and that carbon 2 of the glucose molecule is important in feeding modulation by glucose analogues.