Directive emission of red conjugated polymer embedded within zero index metamaterials

Abstract: We numerically demonstrate an impedance-matched multilayer stacked fishnet metamaterial that has zero index with flat high transmittance from 600nm to 620nm. The effective refractive index

A study on schedule management for BIM projects in the construction industry

There is an advance modelling tool that currently been pushed by the industry is BIM. BIM as known as Building Modelling Information is a computerized process that is used to design, understand and establish the key physical and functional characteristic of a building on a ‘virtual’ computerized model basis at its most basic level [4]. Basically the resulting model is a digital representation of the building which the data can be extracted and analyzed to generate information that can be used for decision making and enhance the process of delivering the building and the entire life cycle use of the building [4]. BIM implementation can help to improve the quality of project especially the schedule management. By implementing BIM into construction project, it can provides schedule visualization which can make the construction planning more efficient. Besides that, through the BIM model clash detection can be detected in the preconstruction phase which save a lot of time on rework during construction phase

Phospholipase Cγ1 (PLCγ1) controls osteoclast numbers via colony-stimulating factor 1 (CSF-1)-dependent diacylglycerol/β-catenin/cyclinD1 pathway

Phospholipases Cγ (PLCγ) 1 and 2 are a class of highly homologous enzymes modulating a variety of cellular pathways through production of inositol 1,4,5-trisphosphate and diacylglycerol (DAG). Our previous studies demonstrated the importance of PLCγ2 in osteoclast (OC) differentiation by modulating inositol 1,4,5-trisphosphate-mediated calcium oscillations and the up-regulation of the transcription factor NFATc1. Surprisingly, despite being expressed throughout osteoclastogenesis, PLCγ1 did not compensate for PLCγ2 deficiency. Because both isoforms are activated during osteoclastogenesis, it is plausible that PLCγ1 modulates OC development independently of PLCγ2. Here, we utilized PLCγ1-specific shRNAs to delete PLCγ1 in OC precursors derived from wild type (WT) mice. Differently from PLCγ2, we found that PLCγ1 shRNA significantly suppresses OC differentiation by limiting colony-stimulating factor 1 (CSF-1)-dependent proliferation and β-catenin/cyclinD1 levels. Confirming the specificity toward CSF-1 signaling, PLCγ1 is recruited to the CSF-1 receptor following exposure to the cytokine. To understand how PLCγ1 controls cell proliferation, we turned to its downstream effector, DAG. By utilizing cells lacking the DAG kinase ζ, which have increased DAG levels, we demonstrate that DAG modulates CSF-1-dependent proliferation and β-catenin/cyclinD1 levels in OC precursors. Most importantly, the proliferation and osteoclastogenesis defects observed in the absence of PLCγ1 are normalized in PLCγ1/DAG kinase ζ double null cells. Taken together, our study shows that PLCγ1 controls OC numbers via a CSF-1-dependent DAG/β-catenin/cyclinD1 pathway