Effect of protrin dietary level on repaie tissue genesis in growing rats

Este trabalho teve por objetivo verificar se o teor proteico da dieta, afeta a génese dos tecidos de reparo em ratos que sofreram implante de esponja de policlorovinil (PVC), como também analisar através da histofotometria, as possíveis alterações na síntese de mucopolissacarídeos ácidos (glicosaminoglicanos). Foram utilizados 45 ratos machos wistar, com 21 dias de idade, subdivididos em 3 grupos experimentais, submetidos durante 69 dias a dietas contendo respectivamente 6%, 15% e 40% de proteína. Os animais submetidos á dieta hipoprotéica, contendo 6% de proteína, apresentaram urna inibição na evolução e maturação do tecido de granulação principalmente aos 4 ,7 e 10 dias após o implante da esponja de PVC, apresentando menor infiltração de células inflamatórias, menor proliferarão de fibroblastos, redução da formação de fibras colágenas, neovascularizagáo diminuída e inibição da síntese de mucopolissacarídeos ácidos.424414419The objective of this study was to verify if the diet protein level affects the genesis of the repair tissue in rats submitted to a polychlorovynil (PVC) sponge implantation, as well as to analyse the possible alterations in the synthesis of the mucopolysaccharides acids (glucosam inoglicans) by the histophotometry technique. Forty five Wistar weanling male ratas, at 21 days of age, were divided into three experimental groups; the groups were fed diets al 6%, 15% and 40% protein level from casein source, during at 69 days period. The animals which received the low protein diet (6%) presented an inhibition in the evolution and maturation of the granulation tissue mainly in the 4th, 7th and 10th days after the sponge PVC implantation. It was also observed that there was less infiltration of the inflammatory cells, less fiberblasts proliferation, reduction of othe collagen fibers synthesis, neovascularization decreased and an inhibition of the mucopolysaccharide acids synthesis

Angiotensin-converting enzyme inhibitor protects against cisplatin nephrotoxicity by modulating kinin B1 receptor expression and aminopeptidase P activity in mice

Cisplatin is a highly effective chemotherapeutic agent. However, its use is limited by nephrotoxicity. Enalapril is an angiotensin I-converting enzyme inhibitor used for the treatment of hypertension, mainly through the reduction of angiotensin II formation, but also through the increase of kinins half-life. Kinin B1 receptor is associated with inflammation and migration of immune cells into the injured tissue. We have previously shown that the deletion or blockage of kinin B1 and B2 receptors can attenuate cisplatin nephrotoxicity. In this study, we tested enalapril treatment as a tool to prevent cisplatin nephrotoxicity. Male C57Bl/6 mice were divided into 3 groups: control group; cisplatin (20 mg/kg i.p) group; and enalapril (1.5 mg;kg i.p) + cisplatin group. The animals were treated with a single dose of cisplatin and euthanized after 96 h. Enalapril was able to attenuate cisplatin-induced increase in creatinine and urea, and to reduce tubular injury and upregulation of apoptosis-related genes, as well as inflammatory cytokines in circulation and kidney. The upregulation of B1 receptor was blocked in enalapril + cisplatin group. Carboxypeptidase M expression, which generates B1 receptor agonists, is blunted by cisplatin + enalapril treatment. The activity of aminopeptidase P, a secondary key enzyme able to degrade kinins, is restored by enalapril treatment. These findings were confirmed in mouse renal epithelial tubular cells, in which enalaprilat (5 μM) was capable of decreasing tubular injury and inflammatory markers. We treated mouse renal epithelial tubular cells with cisplatin (100 μM), cisplatin+enalaprilat and cisplatin+enalaprilat+apstatin (10 μM). The results showed that cisplatin alone decreases cell viability, cisplatin plus enalaprilat is able to restore cell viability, and cisplatin plus enalaprilat and apstatin decreases cell viability. In the present study, we demonstrated that enalapril prevents cisplatin nephrotoxicity mainly by preventing the upregulation of B1 receptor and carboxypeptidase M and the increased concentrations of kinin peptides through aminopeptidase activity restoration

Epidemiological situation of bovine brucellosis in the State of Espírito Santo, Brazil

Realizou-se um estudo para caracterizar a situação epidemiológica da brucelose bovina no Estado do Espírito Santo. O Estado foi dividido em dois circuitos produtores. Em cada circuito foram amostradas aleatoriamente cerca de 300 propriedades e, dentro dessas, foi escolhido de forma aleatória um número pré-estabelecido de animais, dos quais foi obtida uma amostra de sangue. No total, foram amostrados 5.351 animais, provenientes de 622 propriedades. Em cada propriedade amostrada foi aplicado um questionário epidemiológico para verificar o tipo de exploração e as práticas de criação e sanitárias que poderiam estar associadas ao risco de infecção pela doença. O protocolo de testes utilizado foi o da triagem com o teste do antígeno acidificado tamponado e o reteste dos positivos com o teste do 2-mercaptoetanol. O rebanho foi considerado positivo quando pelo menos um animal foi reagente às duas provas sorológicas. Para o Estado, as prevalências de focos e de animais infectados foram, respectivamente, de 9,0% [7,0-11,6%] e 3,5% [1,9-6,4%]. Para os circuitos, as prevalências de focos e de animais infectados foram, respectivamente, de: circuito 1, 6,8% [4,5-10,2%] e 3,4% [1,3-8,6%]; circuito 2, 10,9% [7,9%-14,8%] e 3,7% [2,1-6,3%]. Os fatores de risco (odds ratio, OR) associados à condição de foco foram: utilização de inseminação artificial (OR = 7,05 [2,51-19,82]) e confinamento/semiconfinamento dos animais (OR = 2,98 [1,22-7,26]). A vacinação de fêmeas entre três e oito meses de idade foi um fator protetor (OR = 0,03 [0,01-0,1]). _____________________________________________________________________________________________________________ ABXTRACTA study to characterize the epidemiological status of brucellosis was carried out in the State of Espírito Santo. The State was divided in two regions. Three hundred herds were randomly sampled in each region and a pre-established number of animals were sampled in each of these herds. A total of 5,351 serum samples from 622 herds were collected. In each herd, it was applied an epidemiological questionnaire focused on herd traits as well as husbandry and sanitary practices that could be associated with the risk of infection. The serum samples were screened for antibodies against Brucella spp. by the Rose-Bengal Test (RBT), and all positive sera were re-tested by the 2-mercaptoethanol test (2-ME). The herd was considered positive if at least one animal was positive on both RBT and 2-ME tests. The prevalence of infected herds and animals in the State were, respectively, 9.0% [7.0-11.6%] and 3.5% [1.9-6.4%]. The prevalence of infected herds and animals in the regions were, respectively: region 1, 6.8% [4.5-10.2%] and 3.4% [1.3-8.6%]; and region 2, 10.9% [7.9-14.8%] and 3.7% [2.1-6.3%]. The risk factors (odds ratio, OR) associated with the presence of the infection were: use of artificial insemination (OR = 7.05 [2.51-19.82]) and intensive/semi-intensive management systems (OR = 2.98 [1.22-7.26]). Vaccination of heifers from three to eight months of age was a protective factor (OR = 0.03 [0.01-0.1])

Kinin B1 receptor controls maternal adiponectin levels and influences offspring weight gain

Given the importance of the kinin B1 receptor in insulin and leptin hormonal regulation, which in turn is crucial in maternal adaptations to ensure nutrient supply to the fetus, we investigated the role of this receptor in maternal metabolism and fetoplacental development. Wild-type and kinin B1 receptor-deficient (B1KO) female mice were mated with male mice of the opposite genotype. Consequently, the entire litter was heterozygous for kinin B1 receptor, ensuring that there would be no influence of offspring genotype on the maternal phenotype. Maternal kinin B1 receptor blockade reduces adiponectin secretion by adipose tissue ex vivo, consistent with lower adiponectin levels in pregnant B1KO mice. Furthermore, fasting insulinemia also increased, which was associated with placental insulin resistance, reduced placental glycogen accumulation, and heavier offspring. Therefore, we propose the combination of chronic hyperinsulinemia and reduced adiponectin secretion in B1KO female mice create a maternal obesogenic environment that results in heavier pups