[Pulmonary adiaspiromycosis: casual finding in a patient who died of yellow fever]. / Adiaspiromicose pulmonar: achado casual em paciente falecido de febre amarela.

During an outbreak of yellow fever (rural form of the infection) occurred recently in the State of Goiás, Brazil, a patient, with clinical manifestations suggestive of the infection, died in the University Hospital of Brasilia, DF, on the fifth day from admission. Postmortem examination revealed, microscopically, the characteristic alterations of the infection, and discovered in the lungs and hilar lymph nodes round microrganisms identified as adiaconidia of Emmonsia parva var. crescens.

Adiaspiromicose pulmonar: achado casual em paciente falecido de febre amarela / Pulmonary adiaspiromycosis: casual finding in a patient who died of yellow fever

During an outbreak of yellow fever (rural form of the infection) occurred recently in the State of Goiás, Brazil, a patient, with clinical manifestations suggestive of the infection, died in the University Hospital of Brasilia, DF, on the fifth day from admission. Postmortem examination revealed, microscopically, the characteristic alterations of the infection, and discovered in the lungs and hilar lymph nodes round microrganisms identified as adiaconidia of Emmonsia parva var. crescens.

Durante um surto de febre amarela (forma rural da infecção) instalado, em fins de 1999, no Estado de Goiás, Brasil, um enfermo, com sintomatologia suspeita, faleceu no Hospital Universitário de Brasília, DF, cinco dias após a admissão. À necropsia, microscopicamente, além das alterações hepáticas características da infecção, encontraram-se nos pulmões e linfonodos hilares, estruturas arredondadas, reconhecidas como adiaconídios de Emmonsia parva var. crescens.

Genetic toxicology of flavonoids: the role of metabolic conditions in the induction of reverse mutation, SOS functions and sister-chromatid exchanges.

Glycosides of flavonols such as quercetin, are found in the edible portions of most food vegetables. Flavonols present in plants as glycosides can be freed during fermentation. We have compared the DNA-damaging activity of quercetin, rutin (3-o-rutinoside of quercetin) and a fermented flavonoid-containing beverage, red wine, for different genetic end-points under different metabolic conditions. The genotoxicity of quercetin, rutin and commercial red wine has been studied for the induction of: (i) reverse mutation in the Ames assay; (ii) SOS functions in the SOS Chromotest; (iii) sister-chromatid exchanges (SCEs) in human lymphocytes. While in the Ames assay the mutagenicity of quercetin is enhanced by the presence of rat liver microsomal enzymes (S9) or the respective cytosolic fraction (S100), genotoxicity is reduced when the induction of SOS responses is assessed using the SOS Chromotest. Similarly, the induction of SCEs is lowered when testing in the presence of liver enzymes. Rutin has no activity whatsoever. Detection of activity of red wine in the three assays is not dependent upon hydrolysis by glycosidases and its content of quercetin accounts almost entirely for the levels of genotoxicity detected. The results suggest that the putative genotoxic metabolites of quercetin vary for different genetic end-points considered and that the metabolic fate of flavonoids might partly account for the conflicting data about their genotoxicity in vivo and carcinogenic activity.

Heat-shock treatment lethal for mammalian cells deprived of glucose and glutamine: protection by alpha-keto acids.

Nil and Nilpy hamster cells exposed to temperatures of 44 degrees C to induce the heat-shock proteins survive such exposure for 2 h or more when incubated in Eagle's Minimum Essential Medium with 10% undialyzed fetal calf serum. If D-glucose and L-glutamine are withdrawn from the medium during heat treatment, nearly all the cells are killed by as little as 20 min at 44 degrees C. Several alpha-keto acids, pyruvate, alpha-ketobutyrate, oxaloacetate, and alpha-ketoglutarate, protect cells from the lethal action of the heat treatment in the absence of D-glucose and L-glutamine. L-Glucose and D-glutamine are without effect. Efforts to reverse lethal effects have not been successful.

Urinary mutagenicity in occupational exposure to mineral oils and iron oxide particles.

Mutagenicity in the urine of workers occupationally exposed to mineral oils and iron oxide particles and age matched workers only exposed to mineral oils was investigated using the Salmonella/mammalian microsome assay. Both groups of workers included smokers and non-smokers. Mutagenicity was significantly higher in the group of workers exposed to both mineral oils and iron oxide particles, the statistical significance of the difference being similar to that found when total non-smokers were compared with total smokers irrespective of occupational exposure. When only non-smokers of both groups of workers were compared, the extent of mutagenicity in the urine of workers exposed to iron oxide particles was still significantly higher, suggesting that smoking did not exhibit a significant enhancing effect on urinary mutagenicity of workers exposed to mineral oils and iron oxide particles, but instead seemed to enhance urinary mutagenicity similarly in both groups of workers. Whether or not this conclusion can be drawn may depend, among other factors, on the variability of the Ames assay. To cope with this particular problem, the possible usefulness of a mutagenicity factor is discussed.