157 resultados para Feral dogs Control


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Many dog owners see homemade diets as a way of increasing the bond with their pets, even though they may not have the convenience of commercial diets. Modifications of ingredients, quality and proportion might change the nutritional composition of the diet, generating nutritional imbalances. The present study evaluated how dog owners use and adhere to homemade diets prescribed by veterinary nutritionists over an extended period of time. Forty-six owners of dogs fed a homemade diet for at least 6 months were selected for the present study. Owners were invited to answer questions by first reading all possible answers and then selecting the one that best indicated their opinion. The results were evaluated through descriptive statistics. Thirty-five owners (76·1 %) found that the diets are easy to prepare. Fourteen owners (30·4 %) admitted to modifying the diets, 40 % did not adequately control the amount of provided ingredients, 73·9 % did not use the recommended amounts of soyabean oil and salt, and 34·8 % did not correctly use the vitamin, mineral or amino acid supplements. Twenty-six owners (56·5 %) reported that their dogs refused to eat at least one food item. All of these alterations make the nutritional composition of the diets unpredictable and likely nutritionally imbalanced. Although homemade diets could be a useful tool for the nutritional management of dogs with certain diseases, not all owners are able to appropriately use this type of diet and adhere to it for an extended period of time and this limitation needs to be considered when recommending the use of homemade diets.

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While methods to evaluate antioxidant capacity in animals exist, one problem with the models is induction of oxidative stress. It is necessary to promote a great enough challenge to induce measurable alterations to oxidative parameters while ensuring the protocol is compatible with animal welfare. The aim of the present study was to evaluate caged transport as a viable short-term stress that would significantly affect oxidative parameters. Twenty adult Beagle dogs, maintained on the same diet for 60 d prior to the transport, were included in the study. To simulate the stress, the dogs were housed in pairs in transport cages (1·0 m × 1·0 m × 1·5 m), placed on a truck coupled to a trailer and transported for a period of 15 min. Blood collection was performed immediately before and again 3 h after the transportation to evaluate oxidative parameters in blood serum, including thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC), sequestration activity of the radical 2,2-diphenyl-1-picryl-hydrazyl (DPPH•), protein carbonylation (PC), total sulfhydryl groups (SH), alpha-tocopherol (αToc) and retinol (Ret). PC, SH and αToc were not significantly changed in the study; however, TBARS, TAC and DPPH increased, whereas Ret decreased after the transport. Although the lack of a control group of dogs not submitted to transport is a limitation to be considered, we conclude that the transport model is effective in inducing an antioxidant response in dogs and relevant blood parameters show sensitivity to this proposed model.

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To compare the effects of dipyrone, meloxicam, and of the combination of these drugs on hemostasis in dogs. Prospective, blinded, randomized crossover study. Research laboratory at a veterinary teaching hospital. Six adult dogs. Animals received 4 intravenous treatments with 15-day washout intervals: control (physiological saline, 0.1 mL/kg), meloxicam (0.2 mg/kg), dipyrone (25 mg/kg), and dipyrone-meloxicam (25 and 0.2 mg/kg, respectively). A jugular catheter was placed for drug injection and for collecting samples for whole blood platelet aggregation (WBPA) and thromboelastometry assays at baseline, 1, 2, 3, 5, and 8 hours after treatment administration. The percent change from baseline of lag time and of the area under the curve (AUC) of impedance changes in response to collagen-induced platelet activation were recorded during WBPA. Thromboelastometry-derived parameters included clotting time, clot formation time, alpha-angle, and maximum clot firmness. The buccal mucosal bleeding time was evaluated by a blinded observer at baseline, 1, 3, and 5 hours after treatment injection. No significant changes in WBPA and thromboelastometry were recorded in the control treatment. Dipyrone significantly (P < 0.05) increased the lag time for 2 hours and decreased the AUC for 3 hours after injection. Meloxicam did not alter WBPA. Dipyrone-meloxicam significantly increased lag time for 2 hours and decreased the AUC for 5 hours after treatment injection. Experimental treatments did not differ from the control treatment for thromboelastometry and buccal mucosal bleeding time. While meloxicam does not alter hemostasis by the methods evaluated, dipyrone inhibits platelet aggregation for up to 3 hours. Meloxicam-dipyrone combination causes more prolonged inhibition of platelet function than dipyrone alone. Decreased platelet aggregation induced by dipyrone and dipyrone-meloxicam does not appear to impact the viscoelastic properties of the blood clot nor increase the risk of bleeding in dogs without preexisting hemostatic disorders.

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To compare peri-implant soft- and hard-tissue integration at implants installed juxta- or sub-crestally. Furthermore, differences in the hard and soft peri-implant tissue dimensions at sites prepared with drills or sonic instruments were to be evaluated. Three months after tooth extraction in six dogs, recipient sites were prepared in both sides of the mandible using conventional drills or a sonic device (Sonosurgery(®) ). Two implants with a 1.7-mm high-polished neck were installed, one with the rough/smooth surface interface placed at the level of the buccal bony crest (control) and the second placed 1.3 mm deeper (test). After 8 weeks of non-submerged healing, biopsies were harvested and ground sections prepared for histological evaluation. The buccal distances between the abutment/fixture junction (AF) and the most coronal level of osseointegration (B) were 1.6 ± 0.6 and 2.4 ± 0.4 mm; between AF and the top of the bony crest (C), they were 1.4 ± 0.4 and 2.2 ± 0.2 mm at the test and control sites, respectively. The top of the peri-implant mucosa (PM) was located more coronally at the test (1.2 ± 0.6 mm) compared to the control sites (0.6 ± 0.5 mm). However, when the original position of the bony crest was taken into account, a higher bone loss and a more apical position of the peri-implant mucosa resulted at the test sites. The placement of implants into a sub-crestal location resulted in a higher vertical buccal bone resorption and a more apical position of the peri-implant mucosa in relation to the level of the bony crest at implant installation. Moreover, peri-implant hard-tissue dimensions were similar at sites prepared with either drills or Sonosurgery(®) .