159 research outputs found
Induced Anticlinic Ordering and Nanophase Segregation of Bow-Shaped Molecules in a Smectic Solvent
Recent experiments indicate that doping low concentrations of bent-core
molecules into calamitic smectic solvents can induce anticlinic and biaxial
smectic phases. We have carried out Monte Carlo (MC) simulations of mixtures of
rodlike molecules (hard spherocylinders with length/breadth ratio ) and bow- or banana-shaped molecules (hard spherocylinder dimers
with length/breadth ratio or 2.5 and opening angle ) to
probe the molecular-scale organization and phase behavior of rod/banana
mixtures. We find that a low concentration (3%) of dimers
induces anticlinic (SmC) ordering in an untilted smectic (SmA) phase for
. For smaller , half of each bow-shaped
molecule is nanophase segregated between smectic layers, and the smectic layers
are untilted. For , no tilted phases are induced. However,
with decreasing we observe a sharp transition from {\sl intralamellar}
nanophase segregation (bow-shaped molecules segregated within smectic layers)
to {\sl interlamellar} nanophase segregation (bow-shaped molecules concentrated
between smectic layers) near . These results demonstrate that
purely entropic effects can lead to surprisingly complex behavior in rod/banana
mixtures.Comment: 5 pages Revtex, 7 postscript figure
Liquid antiferromagnets in two dimensions
It is shown that, for proper symmetry of the parent lattice,
antiferromagnetic order can survive in two-dimensional liquid crystals and even
isotropic liquids of point-like particles, in contradiction to what common
sense might suggest. We discuss the requirements for antiferromagnetic order in
the absence of translational and/or orientational lattice order. One example is
the honeycomb lattice, which upon melting can form a liquid crystal with
quasi-long-range orientational and antiferromagnetic order but short-range
translational order. The critical properties of such systems are discussed.
Finally, we draw conjectures for the three-dimensional case.Comment: 4 pages RevTeX, 4 figures include
Spontaneous chirality through mixing achiral components : A twist-bend nematic phase driven by hydrogen-bonding between unlike components
Acknowledgments: The work was supported by the National Science Centre (Poland) under the grant no. 2016/22/A/ST5/00319. RW gratefully acknowledges the Carnegie Trust for the Universities of Scotland for funding the award of a PhD scholarship.Peer reviewedPostprin
Demographic, multi-morbidity and genetic impact on myocardial involvement and its recovery from COVID-19 : protocol design of COVID-HEART-a UK, multicentre, observational study
Acknowledgements CB acknowledges British Heart Foundation support (RE/18/6134217). GPM is funded by a NIHR Research Professorship (RPâ2017â08âST2â007). CM is funded by a NIHR Clinician Scientist Award (CSâ2015â15â003). VMF and SN acknowledge the NIHR Oxford BRC for support of this study. CBD is in part supported by the NIHR Biomedical Research Centre at University Hospitals Bristol NHS Foundation Trust and the University of Bristol. Additional support was provided by the NIHR Leicester Biomedical Research Centre and the NIHR Leeds Clinical Research Facility. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health and Social Care. We thank the patients and staff who have supported this project. Dr. Warren J. Manning served as a Guest Editor for this manuscript. Study Management and Recruitment centres: Grant applicants: JP Greenwood (chief investigaâ tor), GP McCann, C Berry, M Dweck, J Moon, CM Miller, A Chiribiri, S Prasad, VM Ferreira, C BucciarelliâDucci, D Dawson. Data repository and statistical analysis: Glasgow Clinical Trials Unit. Senior study statistician: Prof A McConnachie, GCTU. Local Principle Investigators and Recruitment Centres: Prof John Greenâ wood, Leeds Teaching Hospitals NHS Trust, UK; Prof Gerry McCann, Glenfield Hospital, Leicester, UK; Prof Dana Dawson, Aberdeen Royal Infirmary, UK; Prof Marc Dweck, Royal Infirmary of Edinburgh, UK; Prof Vanessa Ferreira, JohnRadcliffe Hospital, Oxford, UK; Prof Colin Berry, Queen Elizabeth University Hospital, Glasgow, UK; Dr Peter Swoboda, Pinderfields Hospital, Wakefield, UK; Dr Richard Steeds, Queen Elizabeth Hospital, Birmingham, UK; Prof James Moon, UCL Hospital London, UK; Dr Christopher Miller, Wythenshawe Hospital, Manchester, UK; Dr Timothy Fairbairn, Liverpool Heart and Chest Hospital, UK; Dr Andrew Flett, Southampton General Hospital, UK; Prof Marianna Fontana, Royal Free Hospital, London, UK; Dr Thomas Green, Northumbria NHS Trust, UK; Prof Amedeo Chiribiri, St Thomasâ Hospital, London, UK; Dr Chiara BucciarelliâDucci, University Hospitals Bristol and Weston NHS Trust, UK; Dr Graham Cole, Hammersmith Hospital, London, UK; Prof Sanjay Prasad, Royal Brompton Hospital, London, UK; Dr Adam McDiarmid, Freeman Hospital, Newâ castle Upon Tyne, UK; Dr Nicholas Bunce, St Georges Hospital, London, UK; Dr Prathap Kanagala, Aintree University Hospital, Liverpool, UK; Prof Nicholas Bellenger, The Royal Devon and Exeter Hospital, UK; Dr Tishi Ninan, Swansea Bay University Hospital, UK; Dr Khaled Alfakih, Lewisham University Hospital, London, UK; Prof James Moon, St Bartholomewâs Hospital, London, UK. Funding COVIDâHEART is funded by the National Institute for Health Research (NIHR) and UK Research and Innovation (UKRI) COVIDâ19 Rapid Response Rolling Call (Grant Number COV0254), and sponsored by the University of Leeds, UK. The study has been endorsed by the British Society of Cardiovascular Magnetic Resonance (BSCMR) Research Group, and nationally prioritised, and received both BHFâNIHR Cardiovascular Partnership Flagship Status, and the NIHR Urgent Public Health Group identified it as an Urgent Public Health (UPH) study. Funding for the translation of the patient information leaflets into nonâ English languages was provided by the West Yorkshire and Humber Clinical Research Network (CV070).Peer reviewedPublisher PD
Genotoxic agents promote the nuclear accumulation of annexin A2: role of annexin A2 in mitigating DNA damage
Annexin A2 is an abundant cellular protein that is mainly localized in the cytoplasm and plasma membrane, however a small population has been found in the nucleus, suggesting a nuclear function for the protein. Annexin A2 possesses a nuclear export sequence (NES) and inhibition of the NES is sufficient to cause nuclear accumulation. Here we show that annexin A2 accumulates in the nucleus in response to genotoxic agents including gamma-radiation, UV radiation, etoposide and chromium VI and that this event is mediated by the nuclear export sequence of annexin A2. Nuclear accumulation of annexin A2 is blocked by the antioxidant agent N-acetyl cysteine (NAC) and stimulated by hydrogen peroxide (H2O2), suggesting that this is a reactive oxygen species dependent event. In response to genotoxic agents, cells depleted of annexin A2 show enhanced phospho-histone H2AX and p53 levels, increased numbers of p53-binding protein 1 nuclear foci and increased levels of nuclear 8-oxo-2'-deoxyguanine, suggesting that annexin A2 plays a role in protecting DNA from damage. This is the first report showing the nuclear translocation of annexin A2 in response to genotoxic agents and its role in mitigating DNA damage.Natural Sciences and Engineering Research Council of Canada (NSERC); European Union [PCOFUND-GA-2009-246542]; Foundation for Science and Technology of Portugal; Beatrice Hunter Cancer Research Institute; Terry Fox Foundationinfo:eu-repo/semantics/publishedVersio
Radiative impact of an extreme Arctic biomass-burning event
The aim of the presented study was to investigate the impact on the radiation
budget of a biomass-burning plume, transported from Alaska to the High Arctic
region of Ny-Ă
lesund, Svalbard, in early July 2015. Since the mean
aerosol optical depth increased by the factor of 10 above the average summer
background values, this large aerosol load event is considered particularly
exceptional in the last 25Â years. In situ data with hygroscopic growth
equations, as well as remote sensing measurements as inputs to radiative
transfer models, were used, in order to estimate biases associated with
(i)Â hygroscopicity, (ii)Â variability of single-scattering albedo profiles,
and (iii)Â plane-parallel closure of the modelled atmosphere. A chemical
weather model with satellite-derived biomass-burning emissions was applied to
interpret the transport and transformation pathways.
The provided MODTRAN radiative transfer model (RTM) simulations for the smoke event
(14:00 9Â Julyâ11:30 11Â July) resulted in a mean aerosol
direct radiative forcing at the levels of â78.9 and â47.0âŻWâŻmâ2 at
the surface and at the top of the atmosphere, respectively,
for the mean value of aerosol optical depth equal to 0.64 at 550âŻnm. This
corresponded to the average clear-sky direct radiative forcing of â43.3âŻWâŻmâ2, estimated by radiometer and model simulations at the surface.
Ultimately, uncertainty associated with the plane-parallel atmosphere
approximation altered results by about 2âŻWâŻmâ2. Furthermore,
model-derived aerosol direct radiative forcing efficiency reached on average
â126âŻWâŻmâ2âÏ550 and â71âŻWâŻmâ2âÏ550 at the
surface and at the top of the atmosphere, respectively. The heating rate, estimated at up
to 1.8âŻKâŻdayâ1 inside the biomass-burning plume, implied vertical
mixing with turbulent kinetic energy of 0.3âŻm2âŻsâ2
MerTK expressing hepatic macrophages promote the resolution of inflammation in acute liver failure.
OBJECTIVE: Acute liver failure (ALF) is characterised by overwhelming hepatocyte death and liver inflammation with massive infiltration of myeloid cells in necrotic areas. The mechanisms underlying resolution of acute hepatic inflammation are largely unknown. Here, we aimed to investigate the impact of Mer tyrosine kinase (MerTK) during ALF and also examine how the microenvironmental mediator, secretory leucocyte protease inhibitor (SLPI), governs this response. DESIGN: Flow cytometry, immunohistochemistry, confocal imaging and gene expression analyses determined the phenotype, functional/transcriptomic profile and tissue topography of MerTK+ monocytes/macrophages in ALF, healthy and disease controls. The temporal evolution of macrophage MerTK expression and its impact on resolution was examined in APAP-induced acute liver injury using wild-type (WT) and Mer-deficient (Mer-/-) mice. SLPI effects on hepatic myeloid cells were determined in vitro and in vivo using APAP-treated WT mice. RESULTS: We demonstrate a significant expansion of resolution-like MerTK+HLA-DRhigh cells in circulatory and tissue compartments of patients with ALF. Compared with WT mice which show an increase of MerTK+MHCIIhigh macrophages during the resolution phase in ALF, APAP-treated Mer-/- mice exhibit persistent liver injury and inflammation, characterised by a decreased proportion of resident Kupffer cells and increased number of neutrophils. Both in vitro and in APAP-treated mice, SLPI reprogrammes myeloid cells towards resolution responses through induction of a MerTK+HLA-DRhigh phenotype which promotes neutrophil apoptosis and their subsequent clearance. CONCLUSIONS: We identify a hepatoprotective, MerTK+, macrophage phenotype that evolves during the resolution phase following ALF and represents a novel immunotherapeutic target to promote resolution responses following acute liver injury
Understanding the twist-bend nematic phase: the characterisation of 1-(4-cyanobiphenyl-4'-yloxy)-6-(4-cyanobiphenyl-4'-yl) hexane (CB6OCB) and comparison with CB7CB
Acknowledgements The FFTEM data were obtained at the (Cryo) TEM facility at the Liquid Crystal Institute, Kent State University, supported by the Ohio Research Scholars Program Research Cluster on Surfaces in Advanced Materials. ODL acknowledges the support of NSF DMR-1410378 grant. The authors are grateful for financial support from MINECO/FEDER MAT2015-66208-C3-2-P and from the Gobierno Vasco (GI/IT-449-10) OA via RSC Gold4GoldPeer reviewedPublisher PD
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