452 resultados para ovine animal model


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The present studies were conducted to determine the role of prostaglandins in the etiology of a rise of body temperature observed in rats after electrolytic lesion made on the dorsal mesencephalic areas. This hyperthermia was abolished by intraperitoneal administration of indomethacin, an inhibitor of prostaglandins synthesis. These results strengthen the suggestion of a similar mechanism for both neurogenic hyperthermia and the fevers produced by pyrogens. However, until further experiments are carried out, the possibility of lesion in producing hyperthermia by different mechanisms cannot be ruled out.

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The authors studied the possible inductive effect of exogenous gangliosides administrated intra-peritoneal and intra-muscular, in 33 rats, after compression and sutures of sciatic nerve. In the animals suffering compression of the sciatic nerve only, the myelin sheath was preserved with good regeneration of the nerve. There was no statistics difference between the two groups with or without the administration of gangliosides. In the group of rats where section of the sciatic nerve and suture were performed, neuroma of amputation as well as dense cicatricial tissue with inflammatory reaction of foreign body type was noted around the sutures. In conclusion, the formation of neuroma of amputation associated with severe inflammatory reaction had an important role in determining the regeneration of the nerve.

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Genetic gains predicted for selection, based on both individual performance and progeny testing, were compared to provide information to be used in implementation of progeny testing for a Nelore cattle breeding program. The prediction of genetic gain based on progeny testing was obtained from a formula, derived from methodology of Young and Weiler (J. Genetics 57: 329-338, 1960) for two-stage selection, which allows prediction of genetic gain per generation when the individuals under test have been pre-selected on the basis of their own performance. The application of this formula also allowed determination of the number of progeny per tested bull needed to maximize genetic gain, when the total number of tested progeny is limited.

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In this study, 90 Wistar rats were used. They were equally divided into three experimental groups - control group (CG), diabetic group (DG) and treated diabetic group (TG). The analyzed parameters were clinical (behavior, activity, general aspect, weight, water ingestion and diuresis) and biochemical (fasting glycemia and urinary glycosis). The diabetes was induced by alloxan and, then, treated with insulin associated to oral hypoglycemic (acarbosis). Observations were made at 5 experimental moments, as it follows: 1, 3, 6, 9, and 12 months after the diabetes induction. The results were submitted to variance analysis, with 5% of significance level. The DG presented lower weight and higher diuresis level than the CG and TG. The water ingestion of the CG was similar to TG. The glycemia levels were higher in DG than in CG, at every experimental moment. The TG, however, presented glycemia similar to the CG, except for the dosages at 3, and 9 months. They urinary glycosis of the DG and TG were similar between themselves, but higher than the one of the CG.

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Protein-calorie malnutrition produces glucose intolerance and reduced insulin release in response to glucose. Rats adapted to low- or high-protein diets show an increased resistance to the diabetogenic action of a single dose of streptozotocin or alloxan. To determine the effects of dietary protein level on pancreatic function, we measured serum glucose levels under basal conditions and during the oral glucose tolerance test (GTT) performed before and after a single dose of alloxan administered to rats fed a 25% or a 6% protein diet for a period of 8 weeks. The incidence of mild hyperglycemia (serum glucose > 250 mg/dl) was greater among the rats fed the 25% protein diet (81%) than among those fed the 6% protein diet (42%). During the GTT performed before alloxan administration the serum glucose levels of the rats fed the 6% protein diet were not found to be significantly different from those of rats fed the 25% protein diet. During the GTT performed after alloxan injection all rats showed intolerance to the substrate (serum glucose > 160 mg/dl 120 min after glucose administration) regardless of whether basal serum glucose was normal or high. In summary, alloxan was less effective in producing basal hyperglycemia in the rats fed the 6% protein diet than in those fed the 25% protein diet but caused glucose intolerance during the oral GTT in both groups. Thus, it seems that feeding a 6% protein diet to rats offers only partial protection against the toxic effects of alloxan.

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The effect of intravenous infusion of hypertonic saline (HS) on the recovery of mean arterial pressure (MAP) during septic shock was studied in sham-operated rats and in rats with electrolytic lesion in the anteroventral third ventricle (AV3V) region. Our results show that intravenous HS infusion in rats treated with endotoxin (Etx) partially restores MAP, but when we have a severe shock produced by Etx, HS was not able to reverse the hypotension. We also show that the integrity of the AV3V region is essential for the protective action of HS in endotoxin shock. It is possible that NO production contributes to the deleterious effect of endotoxin. So, the unraveling of the release of NO by the vascular endothelium and their role as regulators of vascular tone is increasing our understanding of the physiology and pathophysiology of the cardiovascular system and will therefore enhance the possibilities of preventing and treating endotoxin shock.

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Morphological changes of coagulating gland of Wistar rats submitted to the experimental chronic alcoholism were noted. Ultrastructurally, it was observed reduction of the granular endoplasmic reticulum cisternae and nuclei with basal position and irregular shape. The epithelial cells presented pycnotic nuclei and the mitochondrial cristae disappeared, characteristic of cellular degeneration.

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In vitro rates of overall proteolysis and the activities of four different proteolytic pathways (lysosomal, Ca2+ dependent, ATP dependent, and ATP independent), as well as rates of protein synthesis, were measured in soleus and extensor digitorum longus (EDL) muscles from streptozotocin- diabetic rats. In the acute phase (1-3 days) of diabetes, there was an increase in overall proteolysis that coincided with an increased activity of the Ca2+-dependent pathway in both soleus and EDL and of the ATP-dependent pathway in EDL. After longer periods (5-10 days) of diabetes, the overall rate of protein degradation decreased and reached values similar to or even lower than those of controls as a result of a reduction in the activities of Ca2+-dependent and ATP-dependent pathways. No change was detected at any time interval in the activity of the intralysosomal proteolytic system in muscles from diabetic animals. Rates of protein synthesis were already reduced 24 h after diabetes induction and decreased further thereafter. Insulin treatment restored to normal the activities of the proteolytic pathways and rates of protein synthesis.

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As part of a study of plants involved in crystal-associated hepatogenous photosensitization diseases, samples of Brachiaria decumbens and Panicum dichotomiflorum on which cattle and goats had recently been photosensitized were analyzed. The level of saponins associated with these photosensitization outbreaks were determined by GC-MS. Only low levels of Pithomyces chartarum spores were present on the B decumbens, and all isolates obtained failed to produce sporidesmin.

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The acute, subchronic and chronic toxicities of 2,4- dichlorophenoxyacetic acid (2,4-D) were studied in rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 ± 1.16 mg/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.

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Granulocyte colony-stimulating factor (G-CSF) acts on precursor hematopoietic cells to control the production and maintenance of neutrophils. Recombinant G-CSF (re-G-CSF)is used clinically to treat patients with neutropenia and has greatly reduced the infection risk associated with bone marrow transplantation. Cyclic hematopoiesis, a stem cell defect characterized by severe recurrent neutropenia, occurs in man and grey collie dogs, and can be treated by administration of re-G-CSF. Availability of the rat G-CSF cDNA would benefit the use of rats as models of gene therapy for the treatment of cyclic hematopoiesis. In preliminary rat experiments, retroviral-mediated expression of canine G-CSF caused neutralizing antibody formation which precluded long-term increases in neutrophil counts. To overcome this problem we cloned the rat G-CSF cDNA from RNA isolated from skin fibroblasts. The rat G-CSF sequence shared a high degree of identity in both the coding and non-coding regions with both the murine G-CSF (85%) and human G-CSF (74%). The signal peptides of murine and human G-CSF both contained 30 amino acids (aa), whereas the deduced signal sequence for rat G-CSF possessed 21 aa. A retrovirus encoding the rat G-CSF cDNA synthesized bioactive G-CSF from transduced vascular smooth muscle cells.

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The exoantigen of Paracoccidioides brasiliensis standardized by Camargo et al. [1] (AgR) was used to evaluate the in vivo and in vitro cell immune response of experimental animals and of patients with paracoccidioidomycosis (PBM). Fava Netto antigen (AgF) was tested in parallel as a control antigen. The study was conducted with mice and guinea pigs infected with P. brasiliensis or immunized with its fungal antigens, on patients with PBM and on their respective control groups. The cell immune response was analysed by skin tests, and by the macrophage and leucocyte migration inhibition tests (MMIT and LMIT) in the animals and in the patients, respectively. The skin test with AgR as paracoccidioidin was positive in infected or immunized mice and guinea pigs and negative in control animals. The skin tests with AgR (24 h) showed 96.7% positivity in patients with PBM and were negative in control individuals. Histopathological study of the in vivo tests in the different experimental models was consistent with a delayed hypersensitivity response (DHR). Immunohistochemical study of the skin tests of PBM patients demonstrated a predominance of T lymphocytes, confirming the nature of a DHR to the fungal antigens. The in vitro cell immune response showed variable results for the various experimental models, i.e. significant rates of MMIT in immunized mice, a tendency to positivity in infected guinea pigs, and the absence of migration inhibition in PBM patients. Taken together, the data indicate that the AgR is efficient as paracoccidioidin in the evaluation of DHR in PBM, with an optimum time of reading the test of 24 h.

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Malnutrition is related to diabetes in tropical countries. In experimental animals, protein deficiency may affect insulin secretion. However, the effect of malnutrition on insulin receptor phosphorylation and further intracellular signaling events is not known. Therefore, we decided to evaluate the rate of insulin secretion and the early molecular steps of insulin action in insulin-sensitive tissues of an animal model of protein deficiency. Pancreatic islets isolated from rats fed a standard (17%) or a low (6%) protein diet were studied for their secretory response to increasing concentrations of glucose in the culture medium. Basal as well as maximal rates of insulin secretion were significantly lower in the islets isolated from rats fed a low protein diet. Moreover, the dose-response curve to glucose was significantly shifted to the right in the islets from malnourished rats compared with islets from control rats. During an oral glucose tolerance test, there were significantly lower circulating concentrations of insulin in the serum of rats fed a low protein diet in spite of no difference in serum glucose concentration between the groups, suggesting an increased peripheral insulin sensitivity. Immunoblotting and immunoprecipitation were used to study the phosphorylation of the insulin receptor and the insulin receptor substrate-1 as well as the insulin receptor substrate-1-p85 subunit of phosphatidylinositol 3-kinase association in response to insulin. Values were greater in hind-limb muscle from rats fed a low protein diet compared with controls. No differences were detected in the total amount of protein corresponding to the insulin receptor or insulin receptor substrate-1 between muscle from rats fed the two diets. Therefore, we conclude that a decreased glucose-induced insulin secretion in pancreatic islets from protein-malnourished rats is responsible, at least in part, for an increased phosphorylation of the insulin receptor, insulin receptor substrate-1 and its association with phosphatidylinositol 3-kinase. These might represent some of the factors influencing the equilibrium in glucose concentrations observed in animal models of malnutrition and undernourished subjects.

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