Regulation of Wages and Hours Prior to 1938

Direct numerical simulations are performed to investigate the transient upstream propagation (flashback) of premixed hydrogen–air flames in the boundary layer of a fully developed turbulent channel flow. Results show that the well-known near-wall velocity fluctuations pattern found in turbulent boundary layers triggers wrinkling of the initially flat flame sheet as it starts propagating against the main flow direction, and that the structure of the characteristic streaks of the turbulent boundary layer ultimately has an important impact on the resulting flame shape and on its propagation mechanism. It is observed that the leading edges of the upstream-propagating premixed flame are always located in the near-wall region of the channel and assume the shape of several smooth, curved bulges propagating upstream side by side in the spanwise direction and convex towards the reactant side of the flame. These leading-edge flame bulges are separated by thin regions of spiky flame cusps pointing towards the product side at the trailing edges of the flame. Analysis of the instantaneous velocity fields clearly reveals the existence, on the reactant side of the flame sheet, of backflow pockets that extend well above the wall-quenching distance. There is a strong correspondence between each of the backflow pockets and a leading edge convex flame bulge. Likewise, high-speed streaks of fast flowing fluid are found to be always colocated with the spiky flame cusps pointing towards the product side of the flame. It is suggested that the origin of the formation of the backflow pockets, along with the subsequent mutual feedback mechanism, is due to the interaction of the approaching streaky turbulent flow pattern with the Darrieus–Landau hydrodynamic instability and pressure fluctuations triggered by the flame sheet. Moreover, the presence of the backflow pockets, coupled with the associated hydrodynamic instability and pressure–flow field interaction, greatly facilitate flame propagation in turbulent boundary layers and ultimately results in high flashback velocities that increase proportionately with pressure

Westerbork Ultra-Deep Survey of HI at z=0.2

In this contribution, we present some preliminary observational results from the completed ultra-deep survey of 21cm emission from neutral hydrogen at redshifts z=0.164-0.224 with the Westerbork Synthesis Radio Telescope. In two separate fields, a total of 160 individual galaxies has been detected in neutral hydrogen, with HI masses varying from 1.1x10^9 to 4.0x10^10 Msun. The largest galaxies are spatially resolved by the synthesized beam of 23x37 arcsec^2 while the velocity resolution of 19 km/s allowed the HI emission lines to be well resolved. The large scale structure in the surveyed volume is traced well in HI, apart from the highest density regions like the cores of galaxy clusters. All significant HI detections have obvious or plausible optical counterparts which are usually blue late-type galaxies that are UV-bright. One of the observed fields contains a massive Butcher-Oemler cluster but none of the associated blue galaxies has been detected in HI. The data suggest that the lower-luminosity galaxies at z=0.2 are more gas-rich than galaxies of similar luminosities at z=0, pending a careful analysis of the completeness near the detection limit. Optical counterparts of the HI detected galaxies are mostly located in the 'blue cloud' of the galaxy population although several galaxies on the 'red sequence' are also detected in HI. These results hold great promise for future deep 21cm surveys of neutral hydrogen with MeerKAT, APERTIF, ASKAP, and ultimately the Square Kilometre Array.Comment: 10 pages, 9 figures, Proceedings of ISKAF2010 Science Meeting: A New Golden Age for Radio Astronomy, June 10-14 2010, Assen, the Netherlands. Edited by J. van Leeuwen. Movies of rendered rotating data cubes are available at http://www.astro.rug.nl/~verheyen/BUDHIES/index.htm

The Neuroscience of Mathematical Cognition and Learning

The synergistic potential of cognitive neuroscience and education for efficient learning has attracted considerable interest from the general public, teachers, parents, academics and policymakers alike. This review is aimed at providing 1) an accessible and general overview of the research progress made in cognitive neuroscience research in understanding mathematical learning and cognition, and 2) understanding whether there is sufficient evidence to suggest that neuroscience can inform mathematics education at this point. We also highlight outstanding questions with implications for education that remain to be explored in cognitive neuroscience. The field of cognitive neuroscience is growing rapidly. The findings that we are describing in this review should be evaluated critically to guide research communities, governments and funding bodies to optimise resources and address questions that will provide practical directions for short- and long-term impact on the education of future generations

Regulation of epithelial plasticity by miR-424 and miR-200 in a new prostate cancer metastasis model

Using an in vivo cycling strategy, we selected metastatic cancer cells from the lymph nodes (LN) of mice bearing orthotopic DU145 human prostate tumors. Repeated rounds of metastatic selection (LN1–LN4) progressively increased the epithelial phenotype, resulting in a new model of tumor cell mesenchymal-epithelial transition (MET). DU145-LN4 showed increased cell-cell adhesions, higher expression of multiple epithelial markers, such as E-cadherin, EpCAM and cytokeratin 18, and reduced expression of mesenchymal markers such as vimentin. The MET in DU145-LN4 cells was accompanied by increased expression of the miR-200 family, and antimiRs to miR-200c and miR-141 induced an EMT. MET also correlated with the loss of miR-424. Ectopic transient and stable miR-424 expression induced EMT, with reduced epithelial marker expression and increased cell scattering. Our model provides evidence for spontaneous MET in vivo. We show that this cellular plasticity can be mediated through the combined action of miR-424 and the miR-200 family

Identification of genes regulating migration and invasion using a new model of metastatic prostate cancer

Background: Understanding the complex, multistep process of metastasis remains a major challenge in cancer research. Metastasis models can reveal insights in tumor development and progression and provide tools to test new intervention strategies. Methods: To develop a new cancer metastasis model, we used DU145 human prostate cancer cells and performed repeated rounds of orthotopic prostate injection and selection of subsequent lymph node metastases. Tumor growth, metastasis, cell migration and invasion were analyzed. Microarray analysis was used to identify cell migration- and cancer-related genes correlating with metastasis. Selected genes were silenced using siRNA, and their roles in cell migration and invasion were determined in transwell migration and Matrigel invasion assays. Results: Our in vivo cycling strategy created cell lines with dramatically increased tumorigenesis and increased ability to colonize lymph nodes (DU145LN1-LN4). Prostate tumor xenografts displayed increased vascularization, enlarged podoplanin-positive lymphatic vessels and invasive margins. Microarray analysis revealed gene expression profiles that correlated with metastatic potential. Using gene network analysis we selected 3 significantly upregulated cell movement and cancer related genes for further analysis: EPCAM (epithelial cell adhesion molecule), ITGB4 (integrin β4) and PLAU (urokinase-type plasminogen activator (uPA)). These genes all showed increased protein expression in the more metastatic DU145-LN4 cells compared to the parental DU145. SiRNA knockdown of EpCAM, integrin-β4 or uPA all significantly reduced cell migration in DU145-LN4 cells. In contrast, only uPA siRNA inhibited cell invasion into Matrigel. This role of uPA in cell invasion was confirmed using the uPA inhibitors, amiloride and UK122. Conclusions: Our approach has identified genes required for the migration and invasion of metastatic tumor cells, and we propose that our new in vivo model system will be a powerful tool to interrogate the metastatic cascade in prostate cancer