Karyotype characterization reveals an up and down of 45S and 5S rDNA sites in Crotalaria (Leguminosae-Papilionoideae) species of the section Hedriocarpae subsection Macrostachyae

The genus Crotalaria is one of the largest within the family Leguminosae-Papilionoideae, with more than 600 species. However, few karyotypes have been described. In the present paper, five species belonging to the section Hedriocarpae were studied (subsection Machrostachyae), in order to better understand chromosomal evolution in Crotalaria. The results reveals that all species presented 2n = 2x = 16 with symmetrical karyotypes, and slight differences in the chromosome morphology. A secondary constriction was identified at short arm of the pair 1. The 45S rDNA was mapped in the secondary constriction and adjacent heterochromatin (NOR-heterochromatin) and a minor site was identified in C. ochroleuca. The 5S rDNA was mapped linked to 45S rDNA at chromosome 1 short arm in all species. Additional sites for 5S rDNA were identified in C. pallida, C. striata and C. mucronata. Heterochromatin blocks around the centromeres are not CMA(+) neither DAPI(+). The karyotypes of the subsection Macrostachyae are characterized by an inversion at chromosome pair one in relation to previous specialized floral species analyzed. Additional sites of 45S and 5S rDNA were assumed to be a result of transposition events by different ways. The results suggest heterochromatin differentiation and the position of ribosomal genes indicates chromosomal rearrangements during evolution. Karyotype characteristics corroborate the morphological infrageneric classification.

Down-regulation of ANAPC13 and CLTCL1: Early Events in the Progression of Preinvasive Ductal Carcinoma of the Breast

Alterations in the gene expression profile in epithelial cells during breast ductal carcinoma (DC) progression have been shown to occur mainly between pure ductal carcinoma in situ (DCIS) to the in situ component of a lesion with coexisting invasive ductal carcinoma (DCIS-IDC) implying that the molecular program for invasion is already established in the preinvasive lesion. For assessing early molecular alterations in epithelial cells that trigger tumorigenesis and testing them as prognostic markers for breast ductal carcinoma progression, we analyzed, by reverse transcription-quantitative polymerase chain reaction, eight genes previously identified as differentially expressed between epithelial tumor cells populations captured from preinvasive lesions with distinct malignant potential, pure DCIS and the in situ component of DCIS-IDC. ANAPC13 and CLTCL1 down-regulation revealed to be early events of DC progression that anticipated the invasiveness manifestation. Further down-regulation of ANAPC13 also occurred after invasion appearance and the presence of the protein in invasive tumor samples was associated with higher rates of overall and disease-free survival in breast cancer patients. Furthermore, tumors with low levels of ANAPC13 displayed increased copy number alterations, with significant gains at 1q (1q23.1-1q32.1), 8q, and 17q (17q24.2), regions that display common imbalances in breast tumors, suggesting that down-regulation of ANAPC13 contributes to genomic instability in this disease.

Factors Associated with Height Catch-Up and Catch-Down Growth Among Schoolchildren

In developed countries, children with intrauterine growth restriction (IUGR) or born preterm (PT) tend to achieve catch-up growth. There is little information about height catch-up in developing countries and about height catch-down in both developed and developing countries. We studied the effect of IUGR and PT birth on height catch-up and catch-down growth of children from two cohorts of liveborn singletons. Data from 1,463 children was collected at birth and at school age in Ribeirao Preto (RP), a more developed city, and in Sao Luis (SL), a less developed city. A change in z-score between schoolchild height z-score and birth length z-score >= 0.67 was considered catch-up; a change in z-score <=-0.67 indicated catch-down growth. The explanatory variables were: appropriate weight for gestational age/PT birth in four categories: term children without IUGR (normal), IUGR only (term with IUGR), PT only ( preterm without IUGR) and preterm with IUGR; infant's sex; maternal parity, age, schooling and marital status; occupation of family head; family income and neonatal ponderal index (PI). The risk ratio for catch-up and catch-down was estimated by multinomial logistic regression for each city. In RP, preterms without IUGR (RR = 4.13) and thin children (PI<10th percentile, RR = 14.39) had a higher risk of catch-down; catch-up was higher among terms with IUGR (RR = 5.53), preterms with IUGR (RR = 5.36) and children born to primiparous mothers (RR = 1.83). In SL, catch-down was higher among preterms without IUGR (RR = 5.19), girls (RR = 1.52) and children from low-income families ( RR = 2.74); the lowest risk of catch-down (RR = 0.27) and the highest risk of catch-up (RR = 3.77) were observed among terms with IUGR. In both cities, terms with IUGR presented height catch-up growth whereas preterms with IUGR only had height catch-up growth in the more affluent setting. Preterms without IUGR presented height catch-down growth, suggesting that a better socioeconomic situation facilitates height catch-up and prevents height catch-down growth.

Down-conversion process in Tb3+-Yb3+ co-doped Calibo glasses

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.

Genetic polymorphisms modulate the folate metabolism of Brazilian individuals with Down syndrome

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.

Gene expression down-regulation in CD90+ prostate tumor-associated stromal cells involves potential organ-specific genes

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.

Inflammatory and Immunological parameters in adults with Down syndrome

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.

Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice

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.

Performance of Down syndrome subjects during a coincident timing task

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.

Inclusão escolar de crianças com síndrome de down: experiências contadas pelas famílias

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.

Inclusão de crianças com Síndrome de Down

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.

M-protein is down-regulated in cardiac hypertrophy driven by thyroid hormone in rats

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.

Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice

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