929 resultados para Factor effect


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O objetivo deste estudo foi avaliar o efeito do fator C na resistência adesiva à dentina humana de um compósito à base de silorano, comparando-o com um compósito à base de metacrilato. Foram utilizados 40 molares humanos hígidos. Em metade da amostra foi realizado um preparo do tipo Classe I, com dimensões de 4x4 mm e 2 mm de profundidade, enquanto na outra metade foi realizado um preparo virtual (flat) com auxílio de uma matriz de teflon branco, com as mesmas dimensões da cavidade (4x4x2 mm), apoiada na superfície de dentina exposta. Cada grupo foi divido em dois, de acordo com o sistema restaurador: Sistema Adesivo P90 e resina Filtek P90; Adper Scotchbond Multiuso e resina Filtek Z350 XT (3M ESPE). Após a aplicação do sistema adesivo segundo as especificações do fabricante, as cavidades (real e virtual) foram preenchidas com as resinas (Z350 XT e P90) em dois incrementos. Foi realizada a fotoativação de cada incremento durante 25s. Após uma semana, as coroas foram seccionadas, obtendo-se espécimes constituídos de resina/dente na forma de um paralelepípedo (palitos). Estes palitos foram utilizados para o teste de microtração (Emic), onde a resistência adesiva na unidade MPa foi calculada. Os resultados foram avaliados estatisticamente pelo teste de análise de variância ANOVA One-Way (p = 0,05), e pelo teste de múltiplas comparações Student Newman Keuls. Foi observada uma diferença estatística entre a resina P90 (flat= 16,137,7 MPa e Cavidade= 16,759,0 MPa) e a Z350 XT (flat= 25,8211,6 MPa e Cavidade=24,4713,5 MPa), independentemente do tipo de cavidade restaurada. E não foi possível observar diferença estatística entre os tipos de cavidades (real ou virtual) restauradas com a mesma resina. Através dos testes realizados, foi possível concluir que: o fator C não afetou a resistência adesiva dos dois sistemas restauradores utilizados, e o tipo de sistema restaurador afeta a resistência adesiva, sendo que o sistema à base de silorano apresenta resultados inferiores ao de metacrilato.

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The analytical expressions of quasi-first and second order homogeneous catalytic reactions with different diffusion coefficients at ultramicrodisk electrodes under steady state conditions are obtained by using the reaction layer concept. The method of treatment is simple and its physical meaning is clear. The relationship between the diffusion layer, reaction layer, the electrode dimension and the kinetic rate constant at an ultramicroelectrode is discussed and the factor effect on the reaction order is described. The order of a catalytic reaction at an ultramicroelectrode under steady state conditions is related not only to C(Z)*/C(O)* but also to the kinetic rate constant and the dimension of the ultramicroelectrode; thus the order of reaction can be controlled by the dimension of the ultramicroelectrode. The steady state voltammetry of the ultramicroelectrode is one of the most simple methods available to study the kinetics of fast catalytic reactions.

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The conditions for quasi-first and second order homogeneous catalytic reactions and their variation with each other at an ultramicrodisk electrode in the steady state are discussed in this paper. The order of reaction can be controlled by changing the dimension of the ultramicroelectrode: the second order reaction can be changed to quasi-first by decreasing the dimension of the ultramicroelectrode. An example of this is given. The main factor effect on the reaction order is the dimension of the ultramicroelectrode. The K4Fe(CN)6-aminopyrine system is selected to confirm the theory, the experiments showing that the system is a second order reaction at a 432 mum microelectrode, and a quasi-first order reaction at a 19 mum ultramicroelectrode. The kinetic constant of the system can be determined by applying the previous theory of homogeneous catalytic reaction.

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Natural (NV) and Cobalto60-irradiated (IrV) Crotalus durissus terrificus venom were used to evaluate serum production capacity of sheep and possible hematological and biochemical effects. Freeze-dried venom aliquots were diluted in acidified saline solution (NaCl 150 mM, pH 3.0) and irradiated by a Cobalt 60 source at a dose of 5.54 x 102 Gy/h and a concentration of 2.000 Gy. Twelve sheep were divided into two groups of six animals. One group received irradiated venom (IrV) and the other natural venom (NV). Three antigen doses (venom) were administered at monthly intervals. Blood samples were collected weekly for analysis of serum neutralization potency and capacity, complete blood count (CBC), total plasma protein, fibrinogen, albumin, and globulin. At the end of the experiment, the animals were challenged with a LD50 for sheep and showed no signs of envenoming. The two groups did not present clinical alterations. Results of the total leukocyte count did not present interaction or time factor effect for both groups, but there was a different action between them, with the NV group presenting more cells than the IrV group. The leukocyte increase to 13,000/ml indicates that slight leukocytosis occurred in the week after the first inoculation in the NV group. There was no statistically significant difference between groups in the absolute count of segmented neutrophils, eosinophils, and lymphocytes but there were statistically significant oscillations in values at the different collecting times. The NV group presented an increase in the absolute neutrophil count after the first inoculation that persisted for 5 weeks. In the IrV group, the increase in neutrophils occurred only in the first week returning to normal in the following weeks. The alterations in the neutrophil count are indicative of systemic inflammatory response related to cytokine release; response was more marked in the NV group, showing its greater toxicity.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The close association of excessive alcohol consumption and clinical expression of hemochromatosis has been of widespread interest for many years. In most populations of northern European extraction, more than 90% of patients with overt hemochromatosis are homozygous for the C282Y mutation in the HFE gene. Nevertheless, the strong association of heavy alcohol intake with the clinical expression of hemochromatosis remains. We (individually or in association with colleagues from our laboratories) have performed three relevant studies in which this association was explored. In the first, performed in 1975 before the cloning of the HFE gene, the frequency of clinical symptoms and signs was compared in patients with classical hemochromatosis who consumed 100 g or more of alcohol per day versus in nondrinkers or moderate drinkers who consumed less than 100 g of alcohol per day. The results showed no difference between the two groups except for features of complications of alcoholism in the first group, especially jaundice, peripheral neuritis, and hepatic failure. Twenty-five percent of those with heavy alcohol consumption showed histologic features of alcoholic liver disease (including cirrhosis) together with heavy iron overload. It was concluded that these patients had the genetic disease complicated by alcoholic liver disease. In the second study (2002), 206 subjects with classical HFE-associated hemochromatosis in whom liver biopsy had been performed were evaluated to quantify the contribution of excess alcohol consumption to the development of cirrhosis in hemochromatosis. Cirrhosis was approximately nine times more likely to develop in subjects with hemochromatosis who consumed more than 60 g of alcohol per day than in those who drank less than this amount. In the third study (2002), 371 C282Y-homozygous relatives of patients with HFE-associated hemochromatosis were assessed. Eleven subjects had cirrhosis on liver biopsy and four of these drank 60 g or more of alcohol per day. The reason why heavy alcohol consumption accentuates the clinical expression of hemochromatosis is unclear. Increased dietary iron or increased iron absorption is unlikely. The most likely explanation would seem to be the added co-factor effect of iron and alcohol, both of which cause oxidative stress, hepatic stellate cell activation, and hepatic fibrogenesis. In addition, the cumulative effects of other forms of liver injury may result when iron and alcohol are present concurrently. Clearly, the addition of dietary iron in subjects homozygous for hemochromatosis would be unwise. (C) 2003 Elsevier Inc. All rights reserved.

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Recent studies have demonstrated that IGF-I associates with VN through IGF-binding proteins (IGFBP) which in turn modulate IGF-stimulated biological functions such as cell proliferation, attachment and migration. Since IGFs play important roles in transformation and progression of breast tumours, we aimed to describe the effects of IGF-I:IGFBP:VN complexes on breast cell function and to dissect mechanisms underlying these responses. In this study we demonstrate that substrate-bound IGF-I:IGFBP:VN complexes are potent stimulators of MCF-7 breast cell survival, which is mediated by a transient activation of ERK/MAPK and sustained activation of PI3-K/AKT pathways. Furthermore, use of pharmacological inhibitors of the MAPK and PI3-K pathways confirms that both pathways are involved in IGF-I:IGFBP:VN complex-mediated increased cell survival. Microarray analysis of cells stimulated to migrate in response to IGF-I:IGFBP:VN complexes identified differential expression of genes with previously reported roles in migration, invasion and survival (Ephrin-B2, Sharp-2, Tissue-factor, Stratifin, PAI-1, IRS-1). These changes were not detected when the IGF-I analogue (\[L24]\[A31]-IGF-I), which fails to bind to the IGF-I receptor, was substituted; confirming the IGF-I-dependent differential expression of genes associated with enhanced cell migration. Taken together, these studies have established that IGF-I:IGFBP:VN complexes enhance breast cell migration and survival, processes central to facilitating metastasis. This study highlights the interdependence of ECM and growth factor interactions in biological functions critical for metastasis and identifies potential novel therapeutic targets directed at preventing breast cancer progression.

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Objective. HLA-DRB1, a major genetic determinant of susceptibility to rheumatoid arthritis (RA), is located within 1,000 kb of the gene encoding tumor necrosis factor (TNF). Because certain HLA-DRB1*04 subtypes increase susceptibility to RA, investigation of the role of the TNF gene is complicated by linkage disequilibrium (LD) between TNF and DRB1 alleles. By adequately controlling for this LD, we aimed to investigate the presence of additional major histocompatibility complex (MHC) susceptibility genes. Methods. We identified 274 HLA-DRB1*04-positive cases of RA and 271 HLA-DRB1*04-positive population controls. Each subject was typed for 6 single-nucleotide polymorphisms within a 4.5-kb region encompassing TNF and lymphotoxin a (LTA). LTA-TNF haplotypes in these unrelated individuals were determined using a combination of family data and the PHASE software program. Results. Significant differences in LTA-TNF haplotype frequencies were observed between different subtypes of HLA-DRB1*04. The LTA-TNF haplotypes observed were very restricted, with only 4 haplotypes constituting 81% of all haplotypes present. Among individuals carrying DRB1*0401, the LTA-TNF 2 haplotype was significantly underrepresented in cases compared with controls (odds ratio 0.5 [95% confidence interval 0.3-0.8], P = 0.007), while in those with DRB1*0404, the opposite effect was observed (P = 0.007). Conclusion. These findings suggest that the MHC contains genetic elements outside the LTA-TNF region that modify the effect of HLA-DRB1 on susceptibility to RA.

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Objectives. To determine whether genetic polymorphisms in or near the transforming growth factor β1 (TGFB1) locus were associated d with susceptibility to or severity of ankylosing spondylitis (AS). Methods. Five intragenic single-nucleotide polymorphisms (SNP) and three microsatellite markers flanking the TGFB1 locus were genotyped. Seven hundred and sixty-two individuals from 184 multiplex families were genotyped for the microsatellite markers and two of the promoter SNPs. One thousand and two individuals from 212 English and 170 Finnish families with AS were genotyped for all five intragenic SNPs. A structured questionnaire was used to assess the age of symptom onset, disease duration and disease severity scores, including the BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) and BASFI (Bath Ankylosing Spondylitis Functional Index). Results. A weak association was noted between the rare TGFB1 + 1632 T allele and AS in the Finnish population (P = 0.04) and in the combined data set (P = 0.03). No association was noted between any other SNPs or SNP haplotype and AS, even among those families with positive non-parametric linkage scores. The TGFB1 +1632 polymorphism was also associated with a younger age of symptom onset (English population, allele 2 associated with age of onset greater by 4.2 yr, P = 0.05; combined data set, allele 2 associated with age of onset greater by 3.2 yr, P = 0.02). A haplotype of coding region SNPs (TGFB1 +869/ +915+1632 alleles 2/1/2) was associated with age of symptom onset in both the English parent-case trios and the combined data set (English data set, haplotype 2/1/2 associated with age of onset greater by 4.9 yr, P = 0.03; combined data set, haplotype 2/1/2 associated with greater age of onset by 4.2 yr, P = 0.006). Weak linkage with AS susceptibility was noted and the peak LOD score was 1.3 at distance 2 cM centromeric to the TGFB1 gene. No other linkage or association was found between quantitative traits and the markers. Conclusion. This study suggests that the polymorphisms within the TGFB1 gene play at most a small role in AS and that other genes encoded on chromosome 19 are involved in susceptibility to the disease.

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Beams with a central edge crack, as well as other noncentral vertical and inclined edge cracks distributed symmetrically, subjected to three-point as well as four-point bending, are analysed using the finite element technique. Values of stress intensity factor K1 at the central crack tip for a crack-to-beam depth ratio Image equal to 0.5, are calculated for various cracked-beam configurations, using the compliance calibration technique as well as method of strain energy release rate. These are compared with the value of K1 for the case of a beam with central edge crack alone. Results of the present parametric study are used to specify the range of values pertaining to basic parameters such as crack-to-beam depth ratios, geometry and position with respect to central edge crack, of other macrocracks for which interaction exists. Accordingly, the macrocracks are classified as either interacting or noninteracting types. Hence for noninteracting types of cracks, analytical expressions available for the determination of K1 in the case of beam with a central edge crack alone, are applicable.