274 resultados para Neonatal ventral hippocampus lesion
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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O objetivo deste trabalho foi investigar os aspectos morfológicos da bulla tympanica após osteotomia ventral e lateral. Quarenta cães adultos foram distribuídos em dois grupos de 20 animais cada. No grupo A , os animais foram submetidos a osteotomia ventral da bulla tympanica e no grupo B, a osteotomia lateral da bulla tympanica. Cada grupo foi constituído de 2 subgrupos, de acordo com o período de observação: A1 e B1 (6 semanas), A2 e B2 (12 semanas). No exame macroscópico constatou-se que a concavidade de todas as bullae tympanicae operadas era semelhante às normais. Os estudos histológicos mostraram que a regeneração completa da bulla tympanica ocorreu em apenas alguns animais de cada subgrupo. A presença de tecido conjuntivo na área de osteotomia foi verificada na maioria das bullae tympanicae operadas, resultado estatisticamente significante. A análise histológica e a histomorfometria computadorizada não mostraram diferença significante quanto ao estágio de regeneração óssea em todos os subgrupos. Concluiu-se que uma área de ostetomia restrita não causou alterações significantes na conformação da bulla tympanica de cães submetida a osteotomia ventral ou lateral; e que a regeneração total da bulla tympanica geralmente não ocorreu antes de 12 semanas de pós-operatório.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Objective. The aim of this study was to detect the development of experimentally induced periapical lesions using conventional radiography and computed tomography.Study design. The root canals of dogs' teeth were exposed to the oral environment for 7 days for contamination and then sealed for 7 days (GI), 15 days (GII), 30 days (GIII), and 60 days (GIV). Immediately after each experimental period, radiographs and tomograms were taken in order to detect the occurrence of periapical bone resorption. The periapical radiographs were digitized and areas of bone resorption were measured using the VIXWIN 2000 software. Scores were assigned to the tomograms based on the progression of periapical bone resorption. The specimens were evaluated by calibrated examiners who were blinded to the groups. The radiographic results were analyzed by ANOVA and Tukey's test (P <.05) and the tomographic results were analyzed by Kruskal-Wallis and Dunn's tests (P <.05).Results. The radiographic evaluation did not reveal periapical lesions at the 7-day control. Lesions were radiographically visible at 15 and 30 days (47.4% and 77.8% of the cases, respectively) and presented similar dimensions (P <.05). At 60 days, lesions were detected in all specimens, presenting larger dimensions than those of the earlier evaluation periods (P <.05). The tomographic evaluation detected lesions at 7 and 15 days (32.5% and 83.3% of the cases, respectively). Lesions were detected in all specimens at the 30- and 60-day periods, when the greatest values of bone resorption were observed (P <.05).Conclusions. Tomography was able to detect periapical lesion development in its initial stages, even when the lesions were undetectable radiographically.
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Objective. The present study evaluated the dynamics of the development of periapical lesions.Study design. Root canals from dogs' teeth were exposed to the oral environment, and then sealed for 7 days (Group A), 15 days (Group B), 30 days (Group C), and 60 days (Group D). After each experimental period, radiographs were taken to detect periapical bone resorption. In addition, histological sections from the periapical region were prepared. The radiographic and histological results were analyzed by ANOVA and Tukey's, Wilcoxon, and Pearson's tests. Significance level was set at 5%.Results. Lesions were radiographically visible at 15 and 30 days, and had similar size at these periods (P > .05). At 60 days, lesions were larger than in the other periods (P < .05). Bone resorption was detected histologically at 7 days. The greatest values of bone resorption were observed at the 30- and 60-day periods (P < .05). The results of the methods of evaluation were similar only at the 30-day period. There was no correlation between the radiographic and histological results.Conclusions. Periapical radiography did not provide detection of periapical lesion in its initial stages. The periapical lesions became more evident radiographically when the bone resorption area increased. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:442-447)
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The cholinergic agonist pilocarpine injected intraperitoneally (ip) increases mean arterial pressure (MAP) and superior mesenteric (SM) vascular resistance and reduces submandibular/sublingual gland (SSG) vascular resistance. In the present study, we investigated the effects of electrolytic lesions of the anteroventral third ventricle (AV3V) region on the changes in MAP, SM, and SSG vascular resistances induced by ip pilocarpine. Male Holtzman rats anesthetized with urethane (1.0 g/kg) and chloralose (60 mg/kg) were submitted to sham or electrolytic AV3V lesions and bad pulsed Doppler flow probes implanted around the arteries. Contrary to sham rats, in 1-h and 2-day AV3V-lesioned rats, pilocarpine (4 mu mol/kg) ip decreased MAP (-41 +/- 4 and -26 4 mm Hg, respectively, vs. sham: 19 +/- 4 mm Hg) and SM (-48 +/- 11 and -45 +/- 10%, respectively, vs. sham: 41 +/- 10%) and hindlimb vascular resistances (-65 +/- 32 and -113 +/- 29%, respectively, vs. sham: 19 +/- 29%). In 7-day AV3V-lesioned rats, pilocarpine produced no changes on MAP and SM and hindlimb vascular resistances. Similar to sham rats, pilocarpine reduced SSG vascular resistance 1 h after AV3V lesions (-46 +/- 6%, vs. sham: -40 +/- 6%), but it produced no effect 2 days after AV3V lesions and increased SSG vascular resistance (37 6%) in 7-day AV3V-lesioned rats. The responses to ip pilocarpine were similar in 15-day sham and AV3V-lesioned rats. The cholinergic antagonist atropine methyl bromide (10 nmol) iv slightly increased the pressor response to ip pilocarpine in sham rats and abolished for 40 min the fall in MAP induced by ip pilocarpine in 1-h AV3V-lesioned rats. The results suggest that central mechanisms dependent on the AV3V region are involved in the pressor responses to ip pilocarpine. Although it was impaired 2 and 7 days after AV3V lesions, pilocarpine-induced salivary gland vasodilation was not altered 1 h after AV3V lesions which suggests that this vasodilation is not directly dependent on the AV3V region. (c) 2005 Elsevier B.V. All rights reserved.
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Water and sodium chloride intake was studied in male Holtzman rats weighing 250-300 g that had been subjected to electrolytic and chemical lesions of the septal area (SA). Water intake increased in animals with electrolytic lesion of the SA bilaterally from 169.37 +/- 8.55 (sham) to 214.87 +/- 23.10 ml/5 days (lesioned). Water intake decreased after ibotenic acid lesion of the SA from 229.33 +/- 27.60 to 127.33 +/- 22.84 ml/5 days. Sodium chloride intake (1.5%) increased in animals with electrolytic lesion of the SA from 10.0 +/- 1.73 to 15.5 +/- 1.95 ml/5 days after lesion. Also sodium chloride (1.5%) intake increased after ibotenic acid injection into the SA to a greater extent (from 7.83 +/- 1.25 to 14.33 +/- 1.87 ml/5 days). The results indicate that the water intake response may be due to lesions that involve cell bodies and fibers of passage and that the sodium intake response can also be induced by lesions which involve only cell bodies. Finally, these results led us to conclude that the SA uses its cell bodies and afferent bodies and fibers for processing inputs mediating water intake and salt appetite and that the cells bodies of the SA are implicated in increased water intake. (C) 1998 Elsevier B.V.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Diseases. such as cancer and benign prostatic hyperplasia, are related to disruption of the mechanism regulating the balance between cell proliferation and apoptosis in prostatic cells. Since castration and vasectomy might alter that balance, this study evaluates the cell proliferation, apoptosis and height of the secretory epithelium of the ventral-prostate ductal system post-castration and vasectomy. Immunohistochemical (PCNA and Ki67), cytochemical (Fuelgen reaction) and morphometric investigation have been carried out. Cell proliferation indices decreased significantly in both regions of the ventral-prostate ductal system after castration compared to the sham-operated group. The apoptotic index increased significantly after 48 h, declining 7 days post-castration. The cell proliferation indices did not differ after 48 h significantly; however, they increased 7 days post-vasectomy in both regions. The apoptotic index did not differ significantly in either time post-vasectomy. Castration caused an imbalance in favor of apoptosis, whereas vasectomy caused an imbalance in favor of cell proliferation. (c) 2005 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Could neonatal testosterone replacement prevent alterations induced by prenatal stress in male rats?
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The present study was designed to examine whether testosterone replacement is able to prevent some effects of maternal restraint stress during the period of brain sexual differentiation - on endocrine system and sexual behavior in male rat descendants. Pregnant rats were exposed to restraint stress for 1 h/day from gestational days 18 to 22. At birth, some male pups from these stressed rats received testosterone propionate. The neonatal testosterone replacement was able to prevent the reduction in anogenital distance at 22 days of age observed in pups from stressed pregnant rats as well as prevents the decrease in testosterone levels during the adulthood of these animals. Testosterone replacement in these males also presented an improvement in sexual performance. In this way, testosterone replacement probably through increasing neonatal level of this hormone was able to prevent the later alterations caused by the prenatal stress during the period of brain sexual differentiation. (c) 2005 Published by Elsevier B.V.