Environmental exposure effects on composite materials for commercial aircraft

The effects of environmental exposure on composite materials are studied. The environments considered are representative of those experienced by commercial jet aircraft. Initial results have been compiled for the following material systems: T300/5208, T300/5209 and T300/934. Specimens were exposed on the exterior and interior of Boeing 737 airplanes of three airlines, and to continuous ground level exposure at four locations. In addition specimens were exposed in the laboratory to conditions such as: simulated ground-air-ground, weatherometer, and moisture. Residual strength results are presented for specimens exposed for up to two years at three ground level exposure locations and on airplanes from two airlines. Test results are also given for specimens exposed to the laboratory simulated environments. Test results indicate that short beam shear strength is sensitive to environmental exposure and dependent on the level of absorbed moisture

Damage tolerant composite wing panels for transport aircraft

Commercial aircraft advanced composite wing surface panels were tested for durability and damage tolerance. The wing of a fuel-efficient, 200-passenger airplane for 1990 delivery was sized using grahite-epoxy materials. The damage tolerance program was structured to allow a systematic progression from material evaluations to the optimized large panel verification tests. The program included coupon testing to evaluate toughened material systems, static and fatigue tests of compression coupons with varying amounts of impact damage, element tests of three-stiffener panels to evaluate upper wing panel design concepts, and the wing structure damage environment was studied. A series of technology demonstration tests of large compression panels is performed. A repair investigation is included in the final large panel test

Operational Flexibility of Future Generation Portfolios Using High Spatial- and Temporal-Resolution Wind Data

Increasing amounts of variable renewable energy sources will cause fundamental and structural changes to thermal power plant operating regimes. Maintaining key reserve requirements will lead to an increase in power plant start-ups and cycling operations for some units. An enhanced unit commitment model with energy storage and flexible CO2 capture is formulated. High-resolution on-/offshore wind data for the U.K., and probabilistic wind power forecast, model wind imbalances at operational timescales. The strategic use of flexible CO2 capture and energy storage helps maintain reserve levels, decreasing power plant cycling operations and wind curtailment. A temporally explicit variability assessment of net demand illustrates the generation flexibility requirements and the nonlinear impacts of increasing wind capacity on power plant operating regimes

Cobimetinib and trametinib inhibit platelet MEK but do not cause platelet dysfunction

The MEK inhibitors cobimetinib and trametinib are used in combination with BRAF inhibitors to treat metastatic melanoma but increase rates of hemorrhage relative to BRAF inhibitors alone. Platelets express several members of the MAPK signalling cascade including MEK1 and MEK2 and ERK1 and ERK2 but their role in platelet function and haemostasis is ambiguous as previous reports have been contradictory. It is therefore unclear if MEK inhibitors might be causing platelet dysfunction and contributing to increased hemorrhage. In the present study we performed pharmacological characterisation of cobimetinib and trametinib in vitro to investigate potential for MEK inhibitors to cause platelet dysfunction. We report that whilst both cobimetinib and trametinib are potent inhibitors of platelet MEK activity, treatment with trametinib did not alter platelet function. Treatment with cobimetinib results in inhibition of platelet aggregation, integrin activation, alpha-granule secretion and adhesion but only at suprapharmacological concentrations. We identified that the inhibitory effects of high concentrations of cobimetinib are associated with off-target inhibition on Akt and PKC. Neither inhibitor caused any alteration in thrombus formation on collagen under flow conditions in vitro. Our findings demonstrate that platelets are able to function normally when MEK activity is fully inhibited, indicating MEK activity is dispensable for normal platelet function. We conclude that the MEK inhibitors cobimetinib and trametinib do not induce platelet dysfunction and are therefore unlikely to contribute to increased incidence of bleeding reported during MEK inhibitor therapy

Asynchronicity of fine sediment supply and its effects on transport and storage in a regulated river

Open access via Springer Compact Agreement This study was funded by the Environment Agency (EA) and United Utilities (UU) as part of a PhD grant. We would like to thank Gail Butteril, Jane Atkins, Andy Newton and Helen Reid from EA, as well as Kat Liney and Grace Martin from UU for their help and support throughout the project. Damià Vericat is funded by a Ramon y Cajal fellowship (RYC-2010-06264). Authors acknowledge the support from the Economy and Knowledge Department of the Catalan Government through the Consolidated Research Group “Fluvial Dynamics Research Group”—RIUS (2014 SGR 645), and the additional support provided by the CERCA Programme, also from the Catalan Government. We are also thankful to two anonymous reviewers whose comments have helped improve the paper.Peer reviewedPublisher PD

Platelet signaling: a complex interplay between inhibitory and activatory networks

The role of platelets in hemostasis and thrombosis is dependent on a complex balance of activatory and inhibitory signaling pathways. Inhibitory signals released from the healthy vasculature suppress platelet activation in the absence of platelet receptor agonists. Activatory signals present at a site of injury initiate platelet activation and thrombus formation; subsequently, endogenous negative signaling regulators dampen activatory signals to control thrombus growth. Understanding the complex interplay between activatory and inhibitory signaling networks is an emerging challenge in the study of platelet biology and necessitates a systematic approach to utilize experimental data effectively. In this review, we will explore the key points of platelet regulation and signaling that maintain platelets in a resting state, mediate activation to elicit thrombus formation or provide negative feedback. Platelet signaling will be described in terms of key signaling molecules that are common to the pathways activated by platelet agonists and can be described as regulatory nodes for both positive and negative regulators. This article is protected by copyright. All rights reserved

Geomorphological response to system-scale river rehabilitation I : Sediment supply from a reconnected tributary

Funding Information: This study was funded as part of a PhD grant by the Environment Agency UK and United Utilities. DV was funded by a Ramon y Cajal fellowship (RYC-2010-06264) at the time the project was developed, and is now employed as a Serra H?nter Fellow at the University of Lleida. Authors acknowledge the support from the Economy and Knowledge department of the Catalan Government through the Consolidated Research Group ?Fluvial Dynamics Research Group?-RIUS (2017-SGR-459), and the additional support provided by the CERCA Programme, also from the Catalan Government. Publisher Copyright: © 2020 The Authors. River Research and Applications published by John Wiley & Sons Ltd Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Peer reviewe

Geomorphological response to system-scale river rehabilitation II : Main-stem channel adjustments following reconnection of an ephemeral tributary

Open Access via the Jisc Wiley Agreement Research Funders United Utilities Environmental AgencyPeer reviewedPublisher PD