O objetivo deste trabalho foi estimar o nível e a distribuição da variabilidade genética em reprodutores brasileiros do camarão marinho (Litopenaeus vannamei). Nove dos maiores laboratórios de maturação do país foram analisados por meio de marcadores microssatélites codominantes e altamente polimórficos. Os resultados obtidos a partir da genotipagem de dez locos de microssatélites são indicativos de variabilidade genética compatível com aquela encontrada em populações naturais de L. vannamei no México e na América Central. Uma possível explicação é a origem altamente diversificada e relativamente recente dos plantéis disponíveis. A análise bayesiana detectou sinal correspondente a cinco populações originais. A distribuição das distâncias genéticas reflete parcialmente a localização geográfica, e essa informação será útil na formação de novos plantéis. Portanto, a variabilidade genética de L. vannamei entre nove dos maiores laboratórios de maturação nacionais pode ser considerada alta.

The objective of this work was to estimate the genetic variability level and distribution in Brazilian broodstocks of marine shrimp (Litopenaeus vannamei). Nine of the country's largest hatcheries were evaluated using codominant and highly polymorphic microsatellite markers. The results obtained from genotyping of ten microsatellite loci are indicative of genetic variability that is compatible with that found in wild populations of L. vannamei in Mexico and Central America. A possible explanation is the highly diversified and relatively recent origin of the available broodstocks. Bayesian analysis detected a signal for five founding populations. The distribution of genetic distances partially reflects geographical location, and this information will be useful for the creation of new broodstocks. Therefore, L. vannamei genetic variability among nine of the largest national hatcheries can be considered high.

Several motile processes are responsible for the movement of proteins into and within the flagellar membrane, but little is known about the process by which specific proteins (either actin-associated or not) are targeted to protozoan flagellar membranes. Actin is a major cytoskeleton protein, while polymerization and depolymerization of parasite actin and actin-interacting proteins (AIPs) during both processes of motility and host cell entry might be key events for successful infection. For a better understanding the eukaryotic flagellar dynamics, we have surveyed genomes, transcriptomes and proteomes of pathogenic Leishmania spp. to identify pertinent genes/proteins and to build in silico models to properly address their putative roles in trypanosomatid virulence. In a search for AIPs involved in flagellar activities, we applied computational biology and proteomic tools to infer from the biological meaning of coronins and Arp2/3, two important elements in phagosome formation after parasite phagocytosis by macrophages. Results presented here provide the first report of Leishmania coronin and Arp2/3 as flagellar proteins that also might be involved in phagosome formation through actin polymerization within the flagellar environment. This is an issue worthy of further in vitro examination that remains now as a direct, positive bioinformatics-derived inference to be presented.

Este trabalho investigou a margem de segurança do inibidor COX-2, meloxicam, em cães, enfocando seus efeitos deletérios nas células sangüíneas e no trato gastrintestinal. Para tanto, após uma avaliação clínico-laboratorial, os cães foram distribuídos nos seguintes grupos: I (placebo; n= 3), II (piroxicam; 1,0mg kg-1; n= 5), III (meloxicam; 0,2mg kg-1; n= 5), IV (meloxicam;1,0mg kg-1; n= 5) e V (meloxicam; 2,0mg kg-1; n= 5). Os fármacos foram usados, por via oral, por 16 dias. No 17º dia, repetiu-se o hemograma completo e, então, procedeu-se a eutanásia seguida pela necrópsia. No grupo I, não houve alterações dignas de nota. No grupo II, todos os cães apresentaram episódios moderados de vômito e diarréia. O perfil celular sangüíneo não foi significativamente modificado. Em dois cães, houve redução no hematócrito e na hemoglobina. Na necropsia, observaram-se focos hemorrágicos e lesões gastriduodenais moderadas. A análise microscópica revelou a presença de gastrite e enterite ulcerativa. No grupo III, quatro cães (80%) apresentaram vômito e diarréia, sem alteração no perfil celular sangüíneo. Na análise macroscópica, observaram-se lesões brandas na mucosa gástrica e focos hemorrágicos no duodeno em quatro cães. Na histopatologia, observaram-se lesões sugestivas de discreta gastroenterite. No grupo IV, os cinco cães tiveram vômito e diarréia sanguinolenta. Quatro deles (80%) apresentaram anemia (p < 0,05). Quatro e cinco cães apresentaram redução no hematócrito e hemoglobina, respectivamente. Ocorreram, ainda, leucocitose, neutrofilia e linfopenia significantes (p < 0,05), em 60% dos cães. Na necrópsia, evidenciaram-se hiperemia, hemorragia e úlceras gástricas severas em 100% dos animais. Verificou-se na microscopia um quadro de gastroenterite ulcerativa nos cinco cães. No grupo V, todos os cães apresentaram sérios episódios de vômito, diarréia e melena. Os quatro (80%) cães que suportaram o tratamento apresentaram anemia e leucocitose com neutrofilia e linfopenia significativas (p< 0,05). Houve, ainda, uma redução no hematócrito e hemoglobina desses cães. Na necropsia, foram visualizadas hemorragias e graves ulcerações gastroduodenais. À histopatologia, evidenciou-se severa gastroenterite. Conclui-se que o meloxicam, mesmo sendo COX-2 seletivo, induz efeitos deletérios no trato gastrintestinal e células sangüíneas de cães, quando administrado em concentrações cinco e dez vezes a dose terapêutica, que demonstram sua estreita margem de segurança nesta espécie.

This study investigated the margin of safety of the COX-2e inhibitor, meloxicam on blood cells and gastrointestinal tract of dogs. After a clinical and laboratorial examination, the dogs were distributed in the following groups: I (placebo; n=3), II (piroxicam: 1.0mg kg-1; n=5), III (meloxicam: 0.2mg kg-1; n=5), IV (meloxican: 1.0mg kg-1; n=5) and V (meloxican: 2.0mg kg-1; n=5). The drugs were given orally for 16 days. On the 17th day the complete hemogram was repeated and the euthanasia and necropsy were then accomplished. In group I there were no significative alterations. In group II, all the dogs showed moderate episodes of vomit and diarrhea. The blood-cell profile was not modified. Two dogs had hematocrit and hemoglobin reduction. In the necropsy, hemorrhagic spots and moderate gastroduodenal lesions were seen. The microscopic analysis revealed the presence of gastritis and ulcerative enteritis. In group III, four dogs (80%) showed vomit and diarrhea, without alteration in blood-cell profile. The microscopic analysis showed mild lesions in the gastric mucosa and hemorrhagic spots in the duodenum of four dogs. Histology showed lesions suggesting mild gastroenteritis. In group IV, all the dogs (n=5) showed vomit and blood diarrhea. Four of them showed anemia (p <0.05). Four and five dogs, respectively, had hematocrit and hemoglobin reduction. In addition, there was a significant (p<0.05) leukocytosis, neutrophilia and linfopenia in 60% of the dogs. The necropsy showed hiperemia, hemorrhage and severe gastric ulcers in all the dogs. In the microscopic analyses, gastroenteritis ulcerative was present in all the animals. In group V, the dogs (n=5) had serious vomit, diarrhea and melena episodes. The dogs that bore the treatment (n=4) had anemia and leukocytosis with neutrophilia and linfopenia significatives (p<0.05). All the dogs had hematocrit and hemoglobin reduction. In the necropsy, hemorrhages and severe gastroduodenal ulceration were seen. The microscopic analysis showed severe gastroenteritis. It can be concluded that, although meloxicam is a COX-2 selective inhibitor, it induces deleterious effects on gastrointestinal tract and blood cells of dogs, when given five or ten times the therapeutic dose, which demonstrate its low margin of safety in this animal specie.

Nitric oxide (NO) is an important effector molecule involved in immune regulation and defense. NO produced by cytokine-activated macrophages was reported to be cytotoxic against the helminth Schistosoma mansoni. Identification and characterization of S. mansoni antigens that can provide protective immunity is crucial for understanding the complex immunoregulatory events that modulate the immune response in schistosomiasis. It is, then, essential to have available defined, purified parasite antigens. Previous work by our laboratory identified a fraction of S. mansoni soluble adult worm antigenic preparation (SWAP), named PIII, able to elicit significant in vitro cell proliferation and at the same time lower in vitro and in vivo granuloma formation when compared either to SEA (soluble egg antigen) or to SWAP. In the present work we report the effect of different in vivo trials with mice on their spleen cells ability to produce NO. We demonstrate that PIII-immunization is able to significantly increase NO production by spleen cells after in vitro stimulation with LPS. These data suggest a possible role for NO on the protective immunity induced by PIII.