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The down-conversion process in Tb3+-Yb3+ co-doped Calibo glasses was studied. The emission, excitation and time-resolved measurements indicated the existence of an energy conversion through the excitation of Tb3+ ions to near-infrared emission by Yb3+ ions. The emission intensity dependence on excitation power confirms that the one-photon process is responsible for the Yb3+ emission. An enhanced Yb3+ emission was observed with Yb3+ doping and an optimal energy transfer efficiency of 32% was obtained before reaching near-infrared emission quenching. The mechanism of the non-resonant energy transfer from Tb3+ to Yb3+ is discussed in terms of the Tb3+-Yb3+ cross-relaxation and multiphonon decay processes. (C) 2012 Elsevier B.V. All rights reserved.

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Individuals with Down syndrome (DS) carry three copies of the Cystathionine beta-synthase (C beta S) gene. The increase in the dosage of this gene results in an altered profile of metabolites involved in the folate pathway, including reduced homocysteine (Hcy), methionine, S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM). Furthermore, previous studies in individuals with DS have shown that genetic variants in genes involved in the folate pathway influence the concentrations of this metabolism's products. The purpose of this study is to investigate whether polymorphisms in genes involved in folate metabolism affect the plasma concentrations of Hcy and methylmalonic acid (MMA) along with the concentration of serum folate in individuals with DS. Twelve genetic polymorphisms were investigated in 90 individuals with DS (median age 1.29 years, range 0.07-30.35 years; 49 male and 41 female). Genotyping for the polymorphisms was performed either by polymerase chain reaction (PCR) based techniques or by direct sequencing. Plasma concentrations of Hcy and MMA were measured by liquid chromatography-tandem mass spectrometry as previously described, and serum folate was quantified using a competitive immunoassay. Our results indicate that the MTHFR C677T, MTR A2756G, TC2 C776G and BHMT G742A polymorphisms along with MMA concentration are predictors of Hcy concentration. They also show that age and Hcy concentration are predictors of MMA concentration. These findings could help to understand how genetic variation impacts folate metabolism and what metabolic consequences these variants have in individuals with trisomy 21.

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Abstract Background The prostate stroma is a key mediator of epithelial differentiation and development, and potentially plays a role in the initiation and progression of prostate cancer. The tumor-associated stroma is marked by increased expression of CD90/THY1. Isolation and characterization of these stromal cells could provide valuable insight into the biology of the tumor microenvironment. Methods Prostate CD90+ stromal fibromuscular cells from tumor specimens were isolated by cell-sorting and analyzed by DNA microarray. Dataset analysis was used to compare gene expression between histologically normal and tumor-associated stromal cells. For comparison, stromal cells were also isolated and analyzed from the urinary bladder. Results The tumor-associated stromal cells were found to have decreased expression of genes involved in smooth muscle differentiation, and those detected in prostate but not bladder. Other differential expression between the stromal cell types included that of the CXC-chemokine genes. Conclusion CD90+ prostate tumor-associated stromal cells differed from their normal counterpart in expression of multiple genes, some of which are potentially involved in organ development.

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Abstract Background The increase in life expectancy within the general population has resulted in an increasing number of elderly adults, including patients with Down syndrome (DS), with a current life expectancy of about 50 years. We evaluate the parameters of humoral and cellular immune response, the quantitative expression of the regulator of calcineurin1 gene (RCAN1) and the production of cytokines. The study group consisted of adults DS (n = 24) and a control group with intellectual disability without Down syndrome (ID) (n = 21) and living in a similar environmental background. It was evaluated serology, immunophenotyping, the quantitative gene expression of RCAN1 and the production of cytokines. Results In the DS group, the results showed an increase in NK cells, CD8, decreased CD19 (p < 0.05) and an increase spontaneous production of IFNgamma, TNFalpha and IL-10 (p < 0.05). There was not any difference in RCAN1 gene expression between the groups. Conclusions These data suggest a similar humoral response in the two groups. The immunophenotyping suggests sign of premature aging of the immune system and the cytokine production show a proinflammatory profile.

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Abstract Background Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion. Results The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10. Conclusion Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal ischemia/reperfusion.

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Abstract Background The time synchronization is a very important ability for the acquisition and performance of motor skills that generate the need to adapt the actions of body segments to external events of the environment that are changing their position in space. Down Syndrome (DS) individuals may present some deficits to perform tasks with synchronization demand. We aimed to investigate the performance of individuals with DS in a simple Coincident Timing task. Method 32 individuals were divided into 2 groups: the Down syndrome group (DSG) comprised of 16 individuals with average age of 20 (+/− 5 years old), and a control group (CG) comprised of 16 individuals of the same age. All individuals performed the Simple Timing (ST) task and their performance was measured in milliseconds. The study was conducted in a single phase with the execution of 20 consecutive trials for each participant. Results There was a significant difference in the intergroup analysis for the accuracy adjustment - Absolute Error (Z = 3.656, p = 0.001); and for the performance consistence - Variable Error (Z = 2.939, p = 0.003). Conclusion DS individuals have more difficulty in integrating the motor action to an external stimulus and they also present more inconsistence in performance. Both groups presented the same tendency to delay their motor responses.

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Este trabalho teve como objetivo explorar as experiências de famílias no processo de inclusão de crianças com síndrome de Down na rede regular de ensino. O objetivo foi conhecer as potencialidades e limitações vividas por essa clientela, no período de transição da instituição especializada para a escola regular e, assim, levantar as necessidades de cuidado, com vistas à promoção de saúde dessas famílias. Trata-se de um estudo de casos múltiplos, de abordagem qualitativa. Participaram da pesquisa 11 mães e um pai de crianças com Síndrome de Down, cujas crianças frequentaram uma instituição especializada e foram encaminhadas para a rede regular de ensino de um município do interior paulista. Os resultados evidenciaram a necessidade de acompanhamento das famílias, antes, durante e após a inclusão propriamente dita, de modo a apoiá-las nos momentos de busca e escolha da escola, de adaptação da criança ao novo ambiente e de transição dos atendimentos oferecidos pela instituição especializada para outros setores. O conhecimento produzido neste estudo tem a intenção de tornar o processo de inclusão da criança com Síndrome de Down, na rede regular de ensino, uma etapa a ser vivida por ela e sua família da melhor forma possível, sentindo-se preparadas e acolhidas.

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O objetivo deste trabalho foi explorar as experiências de famílias no processo de inclusão escolar de crianças com síndrome de Down, com vistas à promoção de saúde dessas famílias. Trata-se de um estudo de casos múltiplos, de abordagem qualitativa, em que participaram onze famílias de crianças com síndrome de Down. Os dados foram coletados por meio de entrevista semiestruturada e submetidos à análise de conteúdo. Os resultados demonstraram que, na perspectiva dos participantes, os professores não estão preparados para a inclusão, porém, ainda assim, esse processo vem se demonstrando benéfico na educação infantil. Ficou evidente a necessidade de articulação entre os setores da educação e saúde e de uma mudança de paradigma no modelo educacional. A pesquisa aponta aspectos que merecem atenção por parte dos profissionais envolvidos, de modo a tornar a inclusão um processo a ser vivido da melhor forma possível.

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Although it is well known that the thyroid hormone (T3) is an important positive regulator of cardiac function over a short term and that it also promotes deleterious effects over a long term, the molecular mechanisms for such effects are not yet well understood. Because most alterations in cardiac function are associated with changes in sarcomeric machinery, the present work was undertaken to find novel sarcomeric hot spots driven by T3 in the heart. A microarray analysis indicated that the M-band is a major hot spot, and the structural sarcomeric gene coding for the M-protein is severely down-regulated by T3. Real-time quantitative PCR-based measurements confirmed that T3 (1, 5, 50, and 100 physiological doses for 2 days) sharply decreased the M-protein gene and protein expression in vivo in a dose-dependent manner. Furthermore, the M-protein gene expression was elevated 3.4-fold in hypothyroid rats. Accordingly, T3 was able to rapidly and strongly reduce the M-protein gene expression in neonatal cardiomyocytes. Deletions at the M-protein promoter and bioinformatics approach suggested an area responsive to T3, which was confirmed by chromatin immunoprecipitation assay. Functional assays in cultured neonatal cardiomyocytes revealed that depletion of M-protein (by small interfering RNA) drives a severe decrease in speed of contraction. Interestingly, mRNA and protein levels of other M-band components, myomesin and embryonic-heart myomesin, were not altered by T3. We concluded that the M-protein expression is strongly and rapidly repressed by T3 in cardiomyocytes, which represents an important aspect for the basis of T3-dependent sarcomeric deleterious effects in the heart.

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Experimental two-phase frictional pressure drop and flow boiling heat transfer results are presented for a horizontal 2.32-mm ID stainless-steel tube using R245fa as working fluid. The frictional pressure drop data was obtained under adiabatic and diabatic conditions. Experiments were performed for mass velocities ranging from 100 to 700 kg m−2 s−1 , heat flux from 0 to 55 kW m−2 , exit saturation temperatures of 31 and 41◦C, and vapor qualities from 0.10 to 0.99. Pressures drop gradients and heat transfer coefficients ranging from 1 to 70 kPa m−1 and from 1 to 7 kW m−2 K−1 were measured. It was found that the heat transfer coefficient is a strong function of the heat flux, mass velocity, and vapor quality. Five frictional pressure drop predictive methods were compared against the experimental database. The Cioncolini et al. (2009) method was found to work the best. Six flow boiling heat transfer predictive methods were also compared against the present database. Liu and Winterton (1991), Zhang et al. (2004), and Saitoh et al. (2007) were ranked as the best methods. They predicted the experimental flow boiling heat transfer data with an average error around 19%.

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BACKGROUND: Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion. RESULTS: The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10. CONCLUSION: Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal