Influence of the effect pigment size on the sparkle detection distance

5 págs.; 5 figs.In an effort to create more dynamic looking automobiles, there is an ever increasing trend among automobile manufacturers towards the use of gonio-apparent coatings in car bodies. These coatings consist of transparent pigments mixed with metallic or interference flakes. The flakes in the coating cause a change in color and brightness of the finish with viewing and illumination direction. This change in appearance accentuates the 3D shading of a car body, making it visually more attractive. Besides this angular dependence on viewing/illumination direction, the metallic finishes also exhibit a visually complex texture. Depending on the properties of the finish and the viewing and illumination conditions, the flakes exhibit a sparkle like texture, while the glossy clear coat may show a rough or smooth surface. As a result of these complex visual attributes, capturing the appearance and finding a perfect color match for an automotive coating is a non trivial task. The main objective of this work is to evaluate the relationship between the special-effect pigments size, and the maximum distance which is detectable the sparkle texture effect. For this, two different sets of samples with different structural features were evaluated in a lighting booth specifically designed for the visual experiment. The booth allows to vary the lighting conditions, the viewing geometry and the distance at which the sample is perceived. The visual experiment was applied to evaluate the high correlation between a structural parameter (i.e. pigment size) and the visual appearance attribute related with texture (sparkle detection distance). Under some fixed environmental conditions, as light intensity, color temperature and geometry of the light source, the sparkle detection distance was evaluated by applying the adjustment psychophysical method for two panel sets (metallic grays and blues), with known pigment sizes and colorimetry, with a small set of observers. The visual results show that a greater the pigment size, a greater the sparkle detection, but with some considerations. In future, we will extend this method, even reinforced applying the statistical design of experiments (DOE), for understanding the relevance and interplay of structural (size, shape, concentration, orientation, etc.), environmental (illuminance level, color rendering, geometry, etc.) and colorimetric (dark vs. light background, chroma, etc.) factors on the sparkle detection distance. © 2015 Society for Imaging Science and Technology.Authors are grateful to EMRP for funding the project “Multidimensional reflectometry for industry”. The EMRP is jointly funded by the EMRP participating countries within EURAMET and the European Union. We would like to thank the Ministry of Economy and Competitiveness for the coordinated project “New developments in visual optics, vision and color technology” (DPI2011-30090-C02). Omar Gómez would also like to thank the Ministry of Economy and Competitiveness for his pre- doctoral fellowship grant (FPI BES-2012-053080).Peer Reviewe

Influencia del tamaño de pigmento en la distancia de detección del sparkle

XI Reunión Nacional de Óptica Día de la Luz; Facultad de Ciencias • Universidad de Salamanca 1 - 4 Septiembre, 2015; http://rno11.usal.es/programaSe diseñó un experimento psicofísico para evaluar la influencia del tamaño del pigmento de efecto en la distancia de detección del sparkle. Los resultados mostraron que a mayor tamaño de pigmento, mayor distancia de detección. Además, la correlación visual e instrumental (distancia de detección vs. grado de sparkle (SG)) sigue una relación lineal, sin embargo, no existe una relación lineal con el tamaño de pigmento: la distancia es máxima para un tamaño inferior al tamaño máximo.Peer Reviewe

Antitumour activity of a potent MEK inhibitor RDEA119/BAY 869766 combined with rapamycin in human orthotopic primary pancreatic cancer xenografts

<p>Abstract</p> <p>Background</p> <p>Combining MEK inhibitors with other signalling pathway inhibitors or conventional cytotoxic drugs represents a promising new strategy against cancer. RDEA119/BAY 869766 is a highly potent and selective MEK1/2 inhibitor undergoing phase I human clinical trials. The effects of RDEA119/BAY 869766 as a single agent and in combination with rapamycin were studied in 3 early passage primary pancreatic cancer xenografts, OCIP19, 21, and 23, grown orthotopically.</p> <p>Methods</p> <p>Anti-cancer effects were determined in separate groups following chronic drug exposure. Effects on cell cycle and downstream signalling were examined by flow cytometry and western blot, respectively. Plasma RDEA119 concentrations were measured to monitor the drug accumulation <it>in vivo</it>.</p> <p>Results</p> <p>RDEA119/BAY 869766 alone or in combination with rapamycin showed significant growth inhibition in all the 3 models, with a significant decrease in the percentage of cells in S-phase, accompanied by a large decrease in bromodeoxyuridine labelling and cell cycle arrest predominantly in G1. The S6 ribosomal protein was inhibited to a greater extent with combination treatment in all the three models. Blood plasma pharmacokinetic analyses indicated that RDEA119 levels achieved <it>in vivo </it>are similar to those that produce target inhibition and cell cycle arrest <it>in vitro</it>.</p> <p>Conclusions</p> <p>Agents targeting the ERK and mTOR pathway have anticancer activity in primary xenografts, and these results support testing this combination in pancreatic cancer patients.</p

Activity of a novel, dual PI3-kinase/mTor inhibitor NVP-BEZ235 against primary human pancreatic cancers grown as orthotopic xenografts

The phosphatidylinositol-3-kinase (PI3K)/Akt signalling pathway is frequently deregulated in pancreatic cancers, and is believed to be an important determinant of their biological aggression and drug resistance. NVP-BEZ235 is a novel, dual class I PI3K/mammalian target of rapamycin (mTor) inhibitor undergoing phase I human clinical trials. To simulate clinical testing, the effects of NVP-BEZ235 were studied in five early passage primary pancreatic cancer xenografts, grown orthotopically. These tumours showed activated PKB/Akt, and increased levels of at least one of the receptor tyrosine kinases that are commonly activated in pancreatic cancers. Pharmacodynamic effects were measured following acute single doses, and anticancer effects were determined in separate groups following chronic drug exposure. Acute oral dosing with NVP-BEZ235 strongly suppressed the phosphorylation of PKB/Akt, followed by recovery over 24 h. There was also inhibition of Ser235/236 S6 ribosomal protein and Thr37/46 4E-BP1, consistent with the effects of NVP-BEZ235 as a dual PI3K/mTor inhibitor. Chronic dosing with 45 mg kg−1 of NVP-BEZ235 was well tolerated, and produced significant tumour growth inhibition in three models. These results predict that agents targeting the PI3K/Akt/mTor pathway might have anticancer activity in pancreatic cancer patients, and support the testing of combination studies involving chemotherapy or other molecular targeted agents

Histone Deacetylase Inhibitors Downregulate Checkpoint Kinase 1 Expression to Induce Cell Death in Non-Small Cell Lung Cancer Cells

Background: Histone deacetylase inhibitors (HDACis) are promising anticancer drugs; however, the molecular mechanisms leading to HDACi-induced cell death have not been well understood and no clear mechanism of resistance has been elucidated to explain limited efficacy of HDACis in clinical trials. Methods and Findings: Here, we show that protein levels of checkpoint kinase 1 (Chk1), which has a major role in G2 cell cycle checkpoint regulation, was markedly reduced at the protein and transcriptional levels in lung cancer cells treated with pan-and selective HDACis LBH589, scriptaid, valproic acid, apicidin, and MS-275. In HDACi treated cells Chk1 function was impaired as determined by decreased inhibitory phosphorylation of cdc25c and its downstream target cdc2 and increased expression of cdc25A and phosphorylated histone H3, a marker of mitotic entry. In time course experiments, Chk1 downregulation occurred after HDACi treatment, preceding apoptosis. Ectopic expression of Chk1 overcame HDACiinduced cell death, and pretreating cells with the cdc2 inhibitor purvalanol A blocked entry into mitosis and prevented cell death by HDACis. Finally, pharmacological inhibition of Chk1 showed strong synergistic effect with LBH589 in lung cancer cells. Conclusions: These results define a pathway through which Chk1 inhibition can mediate HDACi-induced mitotic entry and cell death and suggest that Chk1 could be an early pharmacodynamic marker to assess HDACi efficacy in clinical samples

RADAR ON RAIA: High frequency radars in the RAIA Observatory

9th International Workshop on Marine Technology (MARTECH), virtual, 16-18 June 2021The RADAR ON RAIA project aims to update and extend beyond the Galician border the High Frequency (HF) radar network that has been operating since 2011 in the framework of the RAIA Observatory. The Project is allowing the establishment of a cross-border collaboration beyond the physical infrastructure itself, developing a sharing strategy of maintenance procedures, validation and data processing on both sides of the border, as well as an easy and public access to all the information. In addition, new products are being developed to exploit the potential of the HF radar technologyN

Ex vivo treatment of patient biopsies as a novel method to assess colorectal tumour response to the MEK1/2 inhibitor, Selumetinib

Abstract Although an array of new therapeutics has emerged for the treatment of colorectal cancer, their use is significantly impacted by variability in patient response. Better pre-clinical models could substantially improve efficacy as it may allow stratification of patients into the correct treatment regime. Here we explore acute, ex vivo treatment of fresh, surgically resected human colorectal tumour biopsies as a novel pre-clinical model for identifying patient response to specific therapeutics. The MEK1/2 inhibitor, Selumetinib (AZD6244, ARRY-142886) was used as a tool compound. Firstly, we established an acute treatment protocol and demonstrated this protocol could differentiate phenotypic and pharmacodynamic responses to Selumetinib (0–3uM). We then used the protocol to evaluate Selumetinib response in tumours from 23 colon cancer patients. These studies revealed that the agent inhibited pERK1/2 phosphorylation in all tumours, caused a significant decrease in proliferation in 5/23 (22%) tumours, and that KRAS/BRAF mutant tumours were particularly sensitive to the anti-proliferative effects of the agent. These data are consistent with data from clinical trials of Selumetinib, suggesting that acute treatment of small tumour biopsies is worthy of further exploration as a pre-clinical model to evaluate colorectal cancer response to novel therapies