Calculation of the emission power distribution of microstructured OLEDs using the reciprocity theorem

S. Zhang, E.R. Martins, G.A. Turnbull and I.D.W. Samuel are grateful to the Scottish Universities Physics Alliance (SUPA) and the Engineering and Physical Sciences Research Council (EPSRC) for financial support.Integrating photonic microstructures into organic light-emitting diodes (OLEDs) has been a widely used strategy to improve their light out-coupling efficiency. However, there is still a need for optical modelling methods which quantitatively characterise the spatial emission pattern of microstructured OLEDs. In this paper, we demonstrate such rigorous calculation using the reciprocity theorem. The calculation of the emission intensity at each direction in the far field can be simplified into only two simple calculations of an incident plane wave propagating from the far field into a single cell of the periodic structure. The emission from microstructured OLED devices with three different grating periods was calculated as a test of the approach, and the calculated results were in good agreement with experiment. This optical modelling method is a useful calculation tool to investigate and control the spatial emission pattern of microstructured OLEDs.PostprintPeer reviewe

Precision delivery of RAS-inhibiting siRNA to KRAS driven cancer via peptide-based nanoparticles

Over 95% of pancreatic adenocarcinomas (PDACs), as well as a large fraction of other tumor types, such as colorectal adenocarcinoma, are driven by KRAS activation. However, no direct RAS inhibitors exist for cancer therapy. Furthermore, the delivery of therapeutic agents of any kind to PDAC in particular has been hindered by the extensive desmoplasia and resultant drug delivery challenges that accompanies these tumors. Small interfering RNA (siRNA) is a promising modality for anti-neoplastic therapy due to its precision and wide range of potential therapeutic targets. Unfortunately, siRNA therapy is limited by low serum half-life, vulnerability to intracellular digestion, and transient therapeutic effect. We assessed the ability of a peptide based, oligonucleotide condensing, endosomolytic nanoparticle (NP) system to deliver siRNA to KRAS-driven cancers. We show that this peptide-based NP is avidly taken up by cancer cell

A fundamental test of the Higgs Yukawa coupling at RHIC in A+A collisions

Searches for the intermediate boson, $W^{\pm}$, the heavy quantum of the Weak Interaction, via its semi-leptonic decay, $W\to e +\nu$, in the 1970's instead discovered unexpectedly large hadron production at high $p_T$, notably $\pi^0$, which provided a huge background of $e^{\pm}$ from internal and external conversions. Methods developed at the CERN ISR which led to the discovery of direct-single-$e^{\pm}$ in 1974, later determined to be from the semi-leptonic decay of charm which had not yet been discovered, were used by PHENIX at RHIC to make precision measurements of heavy quark production in p-p and Au+Au collisions, leading to the puzzle of apparent equal suppression of light and heavy quarks in the QGP. If the Higgs mechanism gives mass to gauge bosons but not to fermions, then a proposal that all 6 quarks are nearly massless in a QGP, which would resolve the puzzle, can not be excluded. This proposal can be tested with future measurements of heavy quark correlations in A+A collisionsComment: 12 pages, 16 figures, 26th Winter Workshop on Nuclear Dynamics, Ocho Rios, Jamaica WI, January 2-9, 2010. Corrected citation of 1974 direct single lepton discover

Regulation of mitochondrial biogenesis in erythropoiesis by mTORC1-mediated protein translation.

Advances in genomic profiling present new challenges of explaining how changes in DNA and RNA are translated into proteins linking genotype to phenotype. Here we compare the genome-scale proteomic and transcriptomic changes in human primary haematopoietic stem/progenitor cells and erythroid progenitors, and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Mitochondrial factors including TFAM and PHB2 are selectively regulated through protein translation during erythroid specification. Depletion of TFAM in erythroid cells alters intracellular metabolism, leading to elevated histone acetylation, deregulated gene expression, and defective mitochondria and erythropoiesis. Mechanistically, mTORC1 signalling is enhanced to promote translation of mitochondria-associated transcripts through TOP-like motifs. Genetic and pharmacological perturbation of mitochondria or mTORC1 specifically impairs erythropoiesis in vitro and in vivo. Our studies support a mechanism for post-transcriptional control of erythroid mitochondria and may have direct relevance to haematologic defects associated with mitochondrial diseases and ageing

Detection and quantification of angiogenesis in experimental valve disease with integrin-targeted nanoparticles and 19-fluorine MRI/MRS

<p>Abstract</p> <p>Background</p> <p>Angiogenesis is a critical early feature of atherosclerotic plaque development and may also feature prominently in the pathogenesis of aortic valve stenosis. It has been shown that MRI can detect and quantify specific molecules of interest expressed in cardiovascular disease and cancer by measuring the unique fluorine signature of appropriately targeted perfluorocarbon (PFC) nanoparticles. In this study, we demonstrated specific binding of α_νβ₃integrin targeted nanoparticles to neovasculature in a rabbit model of aortic valve disease. We also showed that fluorine MRI could be used to detect and quantify the development of neovasculature in the excised aortic valve leaflets.</p> <p>Methods</p> <p>New Zealand White rabbits consumed a cholesterol diet for ~180 days and developed aortic valve thickening, inflammation, and angiogenesis mimicking early human aortic valve disease. Rabbits (n = 7) were treated with α_νβ₃integrin targeted PFC nanoparticles or control untargeted PFC nanoparticles (n = 6). Competitive inhibition <it>in vivo </it>of nanoparticle binding (n = 4) was tested by pretreatment with targeted nonfluorinated nanoparticles followed 2 hours later by targeted PFC nanoparticles. 2 hours after treatment, aortic valves were excised and ¹⁹F MRS was performed at 11.7T. Integrated ¹⁹F spectral peaks were compared using a one-way ANOVA and Hsu's MCB (multiple comparisons with the best) post hoc t test. In 3 additional rabbits treated with α_νβ₃integrin targeted PFC nanoparticles, ¹⁹F spectroscopy was performed on a 3.0T clinical scanner. The presence of angiogenesis was confirmed by immunohistochemistry.</p> <p>Results</p> <p>Valves of rabbits treated with targeted PFC nanoparticles had 220% more fluorine signal than valves of rabbits treated with untargeted PFC nanoparticles (p < 0.001). Pretreatment of rabbits with targeted oil-based nonsignaling nanoparticles reduced the fluorine signal by 42% due to competitive inhibition, to a level not significantly different from control animals. Nanoparticles were successfully detected in all samples scanned at 3.0T. PECAM endothelial staining and α_νβ₃integrin staining revealed the presence of neovasculature within the valve leaflets.</p> <p>Conclusion</p> <p>Integrin-targeted PFC nanoparticles specifically detect early angiogenesis in sclerotic aortic valves of cholesterol fed rabbits. These techniques may be useful for assessing atherosclerotic components of preclinical aortic valve disease in patients and could assist in defining efficacy of medical therapies.</p

Trap-Assisted Charge Injection into Large Bandgap Polymer Semiconductors.

The trap-assisted charge injection in polyfluorene-poly(3,4-ethylenedioxythiophene): poly(styrenesulfonate) (PEDOT:PSS) model systems with an Al or Al/LiF cathode is investigated. We find that inserting 1.3 nm LiF increases electron and hole injections simultaneously and the increase of holes is greater than electrons. The evolution of internal interfaces within polymer light-emitting diodes is observed by transmission electron microscopy, which reveals that the introduction of LiF improves the interface stability at both the cathode (cathode/polymer) and the anode (indium tin oxide (ITO)/PEDOT:PSS). Above-mentioned experimental results have been compared to the numerical simulations with a revised Davids model and potential physical mechanisms for the trap-assisted charge injection are discussed

Activation of Human Stearoyl-Coenzyme A Desaturase 1 Contributes to the Lipogenic Effect of PXR in HepG2 Cells

The pregnane X receptor (PXR) was previously known as a xenobiotic receptor. Several recent studies suggested that PXR also played an important role in lipid homeostasis but the underlying mechanism remains to be clearly defined. In this study, we found that rifampicin, an agonist of human PXR, induced lipid accumulation in HepG2 cells. Lipid analysis showed the total cholesterol level increased. However, the free cholesterol and triglyceride levels were not changed. Treatment of HepG2 cells with rifampicin induced the expression of the free fatty acid transporter CD36 and ABCG1, as well as several lipogenic enzymes, including stearoyl-CoA desaturase-1 (SCD1), long chain free fatty acid elongase (FAE), and lecithin-cholesterol acyltransferase (LCAT), while the expression of acyl:cholesterol acetyltransferase(ACAT1) was not affected. Moreover, in PXR over-expressing HepG2 cells (HepG2-PXR), the SCD1 expression was significantly higher than in HepG2-Vector cells, even in the absence of rifampicin. Down-regulation of PXR by shRNA abolished the rifampicin-induced SCD1 gene expression in HepG2 cells. Promoter analysis showed that the human SCD1 gene promoter is activated by PXR and a novel DR-7 type PXR response element (PXRE) response element was located at -338 bp of the SCD1 gene promoter. Taken together, these results indicated that PXR activation promoted lipid synthesis in HepG2 cells and SCD1 is a novel PXR target gene. © 2013 Zhang et al

Green Tea Extract and (−)-Epigallocatechin-3-Gallate Inhibit Mast Cell-Stimulated Type I Collagen Expression in Keloid Fibroblasts via Blocking PI-3K/Akt Signaling Pathways

Keloid, a chronic fibro-proliferative disease, exhibits distinctive histological features characterized by an abundant extracellular matrix stroma, a local infiltration of inflammatory cells including mast cells (MCs), and a milieu of enriched cytokines. Previous studies have demonstrated that co-culture with MCs stimulate type I collagen synthesis in fibroblasts, but the signaling mechanisms remain largely unknown. In this study, we investigated the signaling pathways involved in MC-stimulated type I collagen synthesis and the effects of green tea extract (GTE) and its major catechin, (-)-epigallocatechin-3-gallate (EGCG), on collagen homeostasis in keloid fibroblasts. Our results showed that MCs significantly stimulated type I collagen expression in keloid fibroblasts, and the upregulation of type I collagen was significantly attenuated by blockade of phosphatidylinositol-3-kinase (PI-3K), mammalian target of rapamycin (mTOR), and p38 MAPK signaling pathways, but not by blockade of ERK1/2 pathway. Furthermore, GTE and EGCG dramatically inhibited type I collagen production possibly by interfering with the PI-3K/Akt/mTOR signaling pathway. Our findings suggest that interaction between MCs and keloid fibroblasts may contribute to excessive collagen accumulation in keloids and imply a therapeutic potential of green tea for the intervention and prevention of keloids and other fibrotic diseases. © 2006 The Society for Investigative Dermatology