No abstract

Dioctatin A (DotA), a metabolite of Streptomyces, is known to be an inhibitor of human dipeptidyl aminopeptidase II. Here, it was found that DotA strongly inhibited aflatoxin production by Aspergillus parasiticus, with an IC 50 value of 4.0 mM. The mycelial growth of the fungus was not affected by the addition of DotA at a concentration of 50 mM, but inhibition of conidiation was observed at the same concentration. DotA inhibited production of norsolorinic acid, an early biosynthetic intermediate of aflatoxin, and it strongly reduced the mRNA levels of genes encoding aflatoxin biosynthetic enzymes, and significantly decreased the mRNA level of aflR, which encodes a key regulatory protein for aflatoxin biosynthesis. In addition to these genes, the mRNA level of brlA, which encodes a conidiation-specific transcription factor, was also reduced by the addition of DotA. It was also found that DotA dramatically enhanced kojic acid production by the fungus. Furthermore, DotA inhibited production of sterigmatocystin, which is a toxic aflatoxin biosynthetic intermediate, and it also inhibited conidiation in Aspergillus nidulans. These results indicate that DotA has pleiotropic effects on regulatory mechanisms of fungal secondary metabolite production and differentiation, leading to inhibition of aflatoxin production.

Abstract-A standard method for the production of gastric lesions by aspirin in rats was elaborated, and the mechanisms of the deleterious effects of aspirin were inter preted. The method consisted of pylorus ligation of the rat immediately before as pirin dosing, resulting in severe and consistent gastric lesions in the glandular por tion of the rat stomach 7 hr later. Sodium bicarbonate and L-glutamine showed a strong inhibitory effect on the development of aspirin-induced lesions, at almost the same dose level. Aspirin itself reduced the gastric acidity in pylorus-ligated rats. Sodium bicarbonate with or without aspirin markedly lowered the gastric acidity, whereas L-glutamine with or without aspirin restored the reduced acidity by aspirin or increased the acidity more than the normal level. These findings suggest that L glutamine may inhibit the back diffusion of HCl into the gastric mucosa caused by aspirin. Amylopectine sulfate and sulfated glyptide, in a dose sufficient to suppress the peptic activity of gastric contents, slightly inhibited the aspirin-induced lesions. Atropine sulfate, which strongly reduced gastric juice volume but not acidity, did not exert a marked influence on aspirin-induced lesions.It is well known that aspirin is capable of damaging the gastric mucosa in humans and experimental animals, and that this can be detected by a variety of techniques (1, 2). In animals, however, the incidence and severity of gastric lesions induced by aspirin was re portedly rather weak at the time of autopsy. This fact renders the quantitative measure ment of each lesion in the glandular stomach quite difficult, and thus observations of the damage have been performed grossly, frequently employing "all or none" criteria.In a recent review, Cooke (2) concluded that the basis of aspirin damage to the gastric mucosa is the presence of acid in the lumen of the stomach. Thus, an attempt was made to aggravate the aspirin-induced lesions in the rat, by means of ligation of the pylorus im nmediately prior to aspirin dosing, allowing for an easier quantitation of the lesions and in crease in sensitivity of test procedure. By this method hypersecreted gastric juice is accu mulated in the stomach and at the same time the emptying of aspirin into the duodenum is completely prevented. Quite recently, Johnson (3) reported that salicylic acid signifi cantly increased the pepsin output in dogs as a result of accelerated back diffusion of HCI.Several pharmacologic agents, including antipeptic agents, were thus examined for their effects on "standardized" gastric lesions, as well as on gastric secretion in order to test the concept of aspirin-induced damage.

We investigated the pitches of cholesteric liquid crystals prepared by mixing disodium cromoglycate (DSCG) in water with 5 different water-soluble chiral additives. The measurements are based on the Grandjean-Cano wedge cell method. Overall, the twisting effect is weak, and the shortest pitch of 2.9 ± 0.2 μm is obtained using trans-4-hydroxy-l-proline, by which the cholesteric sample is iridescent at certain viewing angles. Freeze-fracture transmission electron microscopy (FFTEM) was also performed for the first time on both the nematic and cholesteric phases, revealing that stacked chromonic aggregates are very long, up to a few hundred nm, which explains why cholesteric chromonic liquid crystals hardly have pitches in the visible wavelength region.

Abstract-Sodium polyacrylate (PANa) is a water-soluble, high-molecular compound, and its aqueous solution shows a very high viscosity and stringiness.In the present study, preventive effects of PANa on three kinds of esophageal lesions induced by gastric juice were examined in comparison with those of aceglutamide aluminium and sodium alginate.