968 resultados para soft tissue alterations


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Objective: This in situ/ex vivo study assessed the effect of titanium tetrafluoride (TiF4) on permanent human enamel subjected to erosion.Design: Ten volunteers took part in this study performed in two phases. In the first phase (ERO), they wore acrylic palatal appliances containing two enamel blocks, divided into two rows: TiF4 (F) and no-TiF4 (no-F). During the 1st day, the formation of a salivary pellicle was allowed. In the 2nd day, the TiF4 solution was applied on one row (ERO + F), whereas on the other row no treatment was performed (ERO + no-F). From 3rd until 7th day, the blocks were subjected to erosion, 4x per day. In the 2nd phase (no-ERO), the volunteers wore acrylic palatal appliances containing one enamel block, during 2 days, to assess the effect of TiF4 only (no-ERO + F). Enamel alterations were determined using profilometry (wear), microhardness (%SMHC) tests, scanning electron microscope and microprobe analysis. The %SMHC and wear were tested using ANOVA and Tukey's post hoc tests (p < 0.05).Results: The mean of %SMHC and wear ( mu m) values ( +/- S.D.) were, respectively: ERO + F -73.32 +/- 5.16(A)/2.40 +/- 0.60(a); ERO + no-F -83.49 +/- 4.59B/1.17 +/- 0.48(b) and no-ERO + F -67.92 +/- 6.16(A)/0.21:E 0.09(c). In microscope analysis, the no-F group showed enamel with honeycomb appearance. For F groups, it was observed a surface coating with microcracks. The microprobe analysis revealed the presence of the following elements (%) in groups ERO + F, ERO + no-F and no-ERO + F, respectively: Ca (69.9, 72.5, 66.25); P (25.9, 26.5, 26.06); Ti (3.0, 0, 5.93).Conclusions: The TiF4 was unable to reduce dental erosion. (c) 2007 Elsevier Ltd. All rights reserved.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The biological response following subcutaneous and bone implantation of beta-wollastonite(beta-W)-doped alpha-tricalcium phosphate bioceramics in rats was evaluated. Tested materials were: tricalciurn phosphate (TCP), consisting of a mixture of alpha- and beta-polymorphs; TCP doped with 5 wt. % of beta-W (TCP5W), composed of alpha-TCP as only crystalline phase; and TCP doped with 15 wt. % of beta-W (TCP15), containing crystalline alpha-TCP and beta-W. Cylinders of 2x1 mm were implanted in tibiae and backs of adult male Rattus norvegicus, Holtzman rats. After 7, 30 and 120 days, animals were sacrificed and the tissue blocks containing the implants were excised, fixed and processed for histological examination. TCP, TCP5W and TCP15W implants were biocompatible but neither bioactive nor biodegradable in rat subcutaneous tissue. They were not osteoinductive in connective tissue either. However, in rat bone tissue beta-W-doped alpha-TCP implants (TCP5W and TCP15W) were bioactive, biodegradable and osteoconductive. The rates of biodegradation and new bone formation observed for TCP5W and TCP15W implants in rat bone tissue were greater than for non-doped TCP.

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Smoking is considered to be the most albeit preventable cause of diseases and premature deaths in the history of mankind. The local action of tobacco on the oral mucosa can cause precancerous and cancerous lesions. However, there is not enough evidence to establish all the systemic effects caused by nicotine on the organism. Thus, the aim of the present study was to characterize the cellular changes of the cheek mucosa of rats submitted to long-term systemic nicotine treatment. Twenty male rats were divided into two experimental groups: a nicotine group and a control group, each consisting of 10 animals. The nicotine group was injected daily with 0.250 mg of nicotine per 100 g of body weight. All animals received a solid diet and water ad libitum. After 90 days of treatment, all animals were weighed and sacrificed. Samples of cheek mucosa were collected for light and transmission electron microscopy. The results revealed oral epithelium containing atypical cells that were characterized by atrophy, cell membrane disorganization and tissue damage. It was concluded that systemic administration of nicotine damaged the cellular integrity of the oral mucosa, impairing tissue function and predisposing the tissue to the action of different pathogenic agents and also to that of other carcinogenic substances present in tobacco. (c) 2006 Elsevier Ltd. All rights reserved.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Phenotypically discordant monozygotic twins offer the possibility of gene discovery through delineation of molecular abnormalities in one member of the twin pair. One proposed mechanism of discordance is postzygotically occurring genomic alterations resulting from mitotic recombination and other somatic changes. Detection of altered genomic fragments can reveal candidate gene loci that can be verified through additional analyses. We investigated this hypothesis using array comparative genomic hybridization; the 50K and 250K Affymetrix GeneChip (R) SNP arrays and an Illumina custom array consisting of 1,536 SNPs, to scan for genomic alterations in a sample of monozygotic twin pairs with discordant cleft lip and/or palate phenotypes. Paired analysis for deletions, amplifications and loss of heterozygosity, along with sequence verification of SNPs with discordant genotype calls did not reveal any genomic discordance between twin pairs in lymphocyte DNA samples. Our results demonstrate that postzygotic genomic alterations are not a common cause of monozygotic twin discordance for isolated cleft lip and/or palate. However, rare or balanced genomic alterations, tissue-specific events and small aberrations beyond the detection level of our experimental approach cannot be ruled out. The stability of genomes we observed in our study samples also suggests that detection of discordant events in other monozygotic twin pairs would be remarkable and of potential disease significance.

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This was a study on the oxidative stress due to ischaemia (I) and reperfusion (R) in skeletal muscle tissue. Using a tourniquet, groups of rats were submitted to ischaemia for 4 h, followed by different reperfusion periods. The animals were divided in four groups: control; 4 h of ischaemia (IR); 4 h of ischaemia plus 1 h reperfusion (IR-1 h); 4 h of ischaemia plus 24 h reperfusion (IR-24 h); and 4 h of ischaemia plus 72 h reperfusion (IR-72 h). At the end of the procedures, samples of soleus muscle were collected and frozen in n-hexane at -70 degrees C. Cryostat sections were submitted to haematoxylin-eosin, succinate dehydrogenase (SDH) and nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR) stains. An additional muscle sample was processed for electron microscopy. No alterations were found in control animals. IR group showed fibres had normal aspect besides some round, acidophilic and hypertrophic fibres. There were several fibres with angular outlines and smaller diameters in this group compared with control group. NADH-TR/SDH reaction was moderately intense in most fibres. In some fibres, cytoplasm showed areas without activity and other fibres had very intense reactivity. IR-1 h group showed oedema hypercontracted fibres with disorganized myofibrils, mitochondria with focal lesions and dilated sarcoplasmic reticulum. NADH-TR/SDH reaction was moderate to weak. IR-24 h showed intense inflammatory infiltrate in the endomysium and perimysium. NADH-TR/SDH reaction was similar to IR-1 h. IR-72 h showed necrotic fibres, areas with inflammatory infiltrate, reduced muscle fibres at different stages of necrosis and phagocytosis, and many small round and basophilic fibres characterizing a regeneration process. NADH-TR/SDH reaction was weak to negative. Our results suggest that ischaemia and the subsequent 1-, 24- and 72-h reperfusions induced progressive histological damage. Although progressive, it may be reversible because there were ultrastructural signs of recovery after 72-h reperfusion. This recovery could in part be due to the low oxidative stress identified by the morphological and histochemical analysis.

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A implantação do ureter no cólon descendente advém da impossibilidade de reimplantá-lo na vesícula urinária, devido a perdas substanciais do tecido ureteral. O presente trabalho avaliou as alterações macroscópicas, microscópicas e laboratoriais em cães submetidos à ureterocoloanastomose esquerda. Foram utilizados 8 cães adultos, hígidos, de ambos os sexos. A técnica operatória consistiu na ligadura do coto distal do ureter próximo à bexiga e na implantação de um curto seg- mento do coto proximal, através de um túnel submucoso, na face antimesentérica do cólon. Realizou-se dosagens séricas de uréia, creatinina, sódio e potássio no pré-operatório, 2, 7, 15 e 30 dias após a cirurgia. Um total de 6 animais foram observados por 30 dias, e outros dois foram observados durante 7 e 180 dias, res- pectivamente. Todos apresentaram fezes moles durante o decorrer do experimento. Ao exame macroscópico, todos os animais apresentaram dilatação ureteral e pielonefrites. Azotemia transitória e hidronefrose foram observadas no animal mantido por 7 dias, e em mais quatro animais, mantidos por 30 dias, também se observou hidronefrose. O animal mantido por 180 dias demonstrou hidronefrose ao exame ultrasono gráfico aos 30 dias de evolução, mas a mesma não foi observada quando se realizou a necropsia. em um animal, mantido por 30 dias , houve um aumento nos níveis de creatinina nos dias 7, 15 e 30, entretanto estes permaneceram dentro dos limites fisiológicos. Nenhuma alteração foi observada no exame histológico da mucosa intestinal exposta à drenagem de urina. As poucas alterações encontradas nas análises laboratoriais não comprometeram a saúde dos animais, e, considerando que não foram encontradas lesões na mucosa intestinal analisada, é possível concluir que a ureterocoloanastomose é um procedimento viável para ser usada por um curto período de tempo.

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Objectives: This in vitro study assessed the effect of an experimental 4%TiF4 varnish on enamel erosion.Methods: Sixty bovine enamel blocks were randomly allocated to each type of varnish:Duraphat((R)) -D (NaF, 2.26%F), Duofluorid((R))-F(NaF, 2.71% F), TiF4-T(2.45%F) and no-fluoride-P. After application of the varnishes, the blocks were subjected to six sequential pH cycles (cola drink for 10 min and artificial saliva for 50 min, each) per day, during 4 days. After the pH cycles, the blocks were maintained in artificial saliva for 18 h. Enamel alterations were determined in the 2nd and 4th days, using profilometry (wear) and microhardness (%SMHC) tests. Data were tested using ANOVA and Tukey's tests (p < 0.05).Results: the mean %SMHC (+/- S.D.) at the 2nd and 4th day was, respectively, D (-77.26 +/- 5.04(a) and -88.59 +/- 5.11(A)), F (-76.79 +/- 7.82(a) and -88.78 +/- 6.10(A)), T(-88.28 +/- 3.19(b) and -92.04 +/- 2.54(A,B)) and P (-87.96 +/- 2.23(b) and -94.15 +/- 1.14(B)). The mean wear (mu m +/- S.D.) at the 2nd and 4th day was, respectively, D (3.16 +/- 0.32(a) and 7.56 +/- 0.90(A)), F(3.35 +/- 0.78(a,b) and 7.92 +/- 0.98(A)), T (3.81 +/- 0.43(b) and 7.69 +/- 0.76(A)) and P (3.43 +/- 1.13(a,b) and 7.31 +/- 0.53(A)).Conclusions: the NaF varnishes reduced the softening, but had no effect on the reduction of the wear. The TiF4 varnish was not able to reduce the softening and wear. (C) 2007 Elsevier Ltd. All rights reserved.

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The aim of the present study was to determine the effects of ad lib, overfeeding and of dietary restriction (DR) on oxidative stress in cardiac tissue. Lipoperoxide concentrations ere decreased and antioxidant enzymes ere increased in moderate-DR-fed rats. Severe-DR induced increased lipoperoxide concentrations. Overfeeding increased lipoperoxide levels in cardiac tissue. Total superoxide dismutase (SOD) and Cu-Zn superoxide dismutase (Cu-Zn SOD) activities were decreased in cardiac tissue at 35 days of overfeeding. As no changes in glutathione peroxidase (GSH-Px) ere observed in overfed rats, awhile SOD and Cu-Zn SOD activities were decreased in these animals. it is assumed that superoxide anion is an important intermediate in the toxicity of ad lib, overfeeding. Overfeeding induced alterations in markers of oxidative stress in cardiac tissue. (C) 2002 Elsevier B.V. Ltd. All rights reserved.

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There has been persistent controversy regarding the nature of cell differentiation in alveolar soft-part sarcoma (ASPS) since its first description in 1952. Some studies suggest that ASPS might represent an unusual variant of skeletal muscle tumor, Given the availability of new monoclonal antibodies to probe for skeletal muscle differentiation and the rapid advance in immunocytochemical techniques for deparaffinized, formalin-fixed tissue sections, we wished to test the proposed hypothesis that ASPS might represent a new type of rhabdomyosarcoma Twelve archival samples of ASPS were retrieved, and we investigated the expression of two myogenic regulatory proteins, MyoD1 and myogenin, as rvell as other muscle-associated proteins, using sensitive immunocytochemical techniques. Despite the presence of desmin immunostaining in six ASPSs, no tumors were positive for either muscle actin or myoglobin Most importantly, no specimen showed nuclear expression of MyoD1 or myogenin, In 11 tumors, however, there was considerable granular immunostaining in the tumor cell cytoplasm with the anti-MyoD1 monoclonal antibody 5.8A, a phenomenon observed in various nonmuscle normal and neoplastic tissues with this antibody, To analyze the exact nature of immunostaining of MyoD1 and desmin in ASPS, biochemical analyses using available fresh frozen tumor tissue were performed, Although a 53-kDa band was noted with antidesmin antibody on Western blot analysis, no specific protein band that corresponds to the 45-kDa MyoD1 was detected with antibody 5.8A. These results confirm the presence of desmin in ASPS but argue against authentic expression of MyoD1, They also suggest that the cytoplasmic immunostaining observed with anti-MyoD1 antibody 5.8A most likely represents a nonspecific cross-reaction with an unknown cytoplasmic antigen, Considering the master role that MyoD1 and myogenin play in skeletal muscle commitment and differentiation and the lack of expression of these two proteins in ASPS as determined immunocytochemically and biochemically, we think that the histogenesis of ASPS remains unknown.