The Effects of Growth Regulators and Apical Bud Removal on Growth, Flowering, and Corms Production of Two Gladiolus Varieties

Gladiolus is commonly propagated from corms. The multiplication rate of corms is low and to increase the propagation rate, we examined a combination of apical bud removal and the application of growth regulators. The experiments were conducted in two varieties, ‘Rose Supreme’ and ‘White Prosperity’, and over two seasons. The apical buds on the planting corms were either removed or left intact before the same corms were soaked in a suspension with either 100 ppm of benzyladenine (BA), 100 ppm of gibberellic acid (GA3), or pure water. The results showed that apical bud removal increased the number of corms and shoots. GA3 had limited the effect on corm and shoot production, but instead resulted in increased total leaf area and leaf weight per shoot. BA, on the other hand, increased the number of corms and shoots. Overall, the removal of the apical bud plus application of BA increased the number of corms and shoots but reduced the average corm diameter and leaf weight per shoot. This was clearer in ‘Rose Supreme’ than in ‘White Prosperity’. To maximize flower production for the coming season, farmers need to produce a high number of planting corms, but they also need to balance this with a sufficient corm size and the production of flowers of good quality. The application of growth regulators in combination with apical bud removal should be fine-tuned to avoid a situation that leads to the production of too many small or too few large corms.publishedVersio

A note on q-Euler numbers and polynomials

The purpose of this paper is to construct q-Euler numbers and polynomials by using p-adic q-integral equations on Zp. Finally, we will give some interesting formulae related to these q-Euler numbers and polynomials.Comment: 6 page

Associations between medical student empathy and personality: A Multi-institutional study

Background: More empathetic physicians are more likely to achieve higher patient satisfaction, adherence to treatments, and health outcomes. In the context of medical education, it is thus important to understand how personality might condition the empathetic development of medical students. Single institutional evidence shows associations between students' personality and empathy. This multi-institutional study aimed to assess such associations across institutions, looking for personality differences between students with high empathy and low empathy levels. Methods: Participants were 472 students from three medical schools in Portugal. They completed validated adaptations to Portuguese of self-report measures of the NEO-Five Factor Inventory(NEO-FFI) and the Jefferson Scale of Physician Empathy(JSPE-spv). Students were categorized into two groups: "Bottom" (low empathy, N = 165) and "Top" (high empathy, N = 169) according to their empathy JSPE-spv total score terciles. Correlation analysis, binary logistic regression analysis and ROC curve analysis were conducted. Results: A regression model with gender, age and university had a predictive power (pseudo R2) for belonging to the top or bottom group of 6.4%. The addition of personality dimensions improved the predictive power to 16.8%. Openness to experience and Agreeableness were important to predict top or bottom empathy scores when gender, age and university were considered." Based on the considered predictors the model correctly classified 69.3% of all students. Conclusions: The present multi-institutional cross-sectional study in Portugal revealed across-school associations between the Big5 dimensions Agreeableness and Openness to experience and the empathy of medical students and that personality made a significant contribution to identify the more empathic students. Therefore, medical schools may need to pay attention to the personality of medical students to understand how to enhance the empathy of medical students

The Association among Literacy, Numeracy, HIV Knowledge and Health-Seeking Behavior: A Population-Based Survey of Women in Rural Mozambique

BACKGROUND: Limited literacy skills are common in the United States (US) and are related to lower HIV knowledge and worse health behaviors and outcomes. The extent of these associations is unknown in countries like Mozambique, where no rigorously validated literacy and numeracy measures exist. METHODS: A validated measure of literacy and numeracy, the Wide Range Achievement Test, version 3 (WRAT-3) was translated into Portuguese, adapted for a Mozambican context, and administered to a cross-section of female heads-of-household during a provincially representative survey conducted from August 8 to September 25, 2010. Construct validity of each subscale was examined by testing associations with education, income, and possession of socioeconomic assets, stratified by Portuguese speaking ability. Multivariable regression models estimated the association among literacy/numeracy and HIV knowledge, self-reported HIV testing, and utilization of prenatal care. RESULTS: Data from 3,557 women were analyzed; 1,110 (37.9%) reported speaking Portuguese. Respondents' mean age was 31.2; 44.6% lacked formal education, and 34.3% reported no income. Illiteracy was common (50.4% of Portuguese speakers, 93.7% of non-Portuguese speakers) and the mean numeracy score (10.4) corresponded to US kindergarten-level skills. Literacy or numeracy was associated (p<0.01) with education, income, age, and other socioeconomic assets. Literacy and numeracy skills were associated with HIV knowledge in adjusted models, but not with HIV testing or receipt of clinic-based prenatal care. CONCLUSION: The adapted literacy and numeracy subscales are valid for use with rural Mozambican women. Limited literacy and numeracy skills were common and associated with lower HIV knowledge. Further study is needed to determine the extent to which addressing literacy/numeracy will lead to improved health outcomes

Characterization of Chromosomal Instability in Murine Colitis-Associated Colorectal Cancer

Patients suffering from ulcerative colitis (UC) bear an increased risk for colorectal cancer. Due to the sparsity of colitis-associated cancer (CAC) and the long duration between UC initiation and overt carcinoma, elucidating mechanisms of inflammation-associated carcinogenesis in the gut is particularly challenging. Adequate murine models are thus highly desirable. For human CACs a high frequency of chromosomal instability (CIN) reflected by aneuploidy could be shown, exceeding that of sporadic carcinomas. The aim of this study was to analyze mouse models of CAC with regard to CIN. Additionally, protein expression of p53, beta-catenin and Ki67 was measured to further characterize murine tumor development in comparison to UC-associated carcinogenesis in men.The AOM/DSS model (n = 23) and IL-10(-/-) mice (n = 8) were applied to monitor malignancy development via endoscopy and to analyze premalignant and malignant stages of CACs. CIN was assessed using DNA-image cytometry. Protein expression of p53, beta-catenin and Ki67 was evaluated by immunohistochemistry. The degree of inflammation was analyzed by histology and paralleled to local interferon-γ release.CIN was detected in 81.25% of all murine CACs induced by AOM/DSS, while all carcinomas that arose in IL-10(-/-) mice were chromosomally stable. Beta-catenin expression was strongly membranous in IL-10(-/-) mice, while 87.50% of AOM/DSS-induced tumors showed cytoplasmatic and/or nuclear translocation of beta-catenin. p53 expression was high in both models and Ki67 staining revealed higher proliferation of IL-10(-/-)-induced CACs.AOM/DSS-colitis, but not IL-10(-/-) mice, could provide a powerful murine model to mechanistically investigate CIN in colitis-associated carcinogenesis

Cigarette smoke promotes dendritic cell accumulation in COPD; a Lung Tissue Research Consortium study

<p>Abstract</p> <p>Background</p> <p>Abnormal immune responses are believed to be highly relevant in the pathogenesis of chronic obstructive pulmonary disease (COPD). Dendritic cells provide a critical checkpoint for immunity by their capacity to both induce and suppress immunity. Although evident that cigarette smoke, the primary cause of COPD, significantly influences dendritic cell functions, little is known about the roles of dendritic cells in the pathogenesis of COPD.</p> <p>Methods</p> <p>The extent of dendritic cell infiltration in COPD tissue specimens was determined using immunohistochemical localization of CD83+ cells (marker of matured myeloid dendritic cells), and CD1a+ cells (Langerhans cells). The extent of tissue infiltration with Langerhans cells was also determined by the relative expression of the CD207 gene in COPD <it>versus </it>control tissues. To determine mechanisms by which dendritic cells accumulate in COPD, complimentary studies were conducted using monocyte-derived human dendritic cells exposed to cigarette smoke extract (CSE), and dendritic cells extracted from mice chronically exposed to cigarette smoke.</p> <p>Results</p> <p>In human COPD lung tissue, we detected a significant increase in the total number of CD83+ cells, and significantly higher amounts of CD207 mRNA when compared with control tissue. Human monocyte-derived dendritic cells exposed to CSE (0.1-2%) exhibited enhanced survival <it>in vitro </it>when compared with control dendritic cells. Murine dendritic cells extracted from mice exposed to cigarette smoke for 4 weeks, also demonstrated enhanced survival compared to dendritic cells extracted from control mice. Acute exposure of human dendritic cells to CSE induced the cellular pro-survival proteins heme-oxygenase-1 (HO-1), and B cell lymphoma leukemia-x(L) (Bcl-xL), predominantly through oxidative stress. Although activated human dendritic cells conditioned with CSE expressed diminished migratory CCR7 expression, their migration towards the CCR7 ligand CCL21 was not impaired.</p> <p>Conclusions</p> <p>These data indicate that COPD is associated with increased numbers of cells bearing markers associated with Langerhans cells and mature dendritic cells, and that cigarette smoke promotes survival signals and augments survival of dendritic cells. Although CSE suppressed dendritic cell CCR7 expression, migration towards a CCR7 ligand was not diminished, suggesting that reduced CCR7-dependent migration is unlikely to be an important mechanism for dendritic cell retention in the lungs of smokers with COPD.</p