Do expanded seven-day NHS services improve clinical outcomes? Analysis of comparative institutional performance from the “NHS Services, Seven Days a Week” project 2013–2016

Background: The cause of adverse weekend clinical outcomes remains unknown. In 2013, the “NHS Services, Seven Days a Week” project was initiated to improve access to services across the seven-day week. Three years on, we sought to analyse the impact of such changes across the English NHS. Methods: Aggregated trust-level data on crude mortality rates, Summary Hospital-Level Mortality Indicator (SHMI), mean length of stay (LOS), A&E admission and four-hour breach rates were obtained from national Hospital Episode Statistics and A&E datasets across the English NHS, excluding mental and community health trusts. Trust annual reports were analysed to determine the presence of any seven-day service reorganisation in 2013–2014. Funnel plots were generated to compare institutional performance and a difference in differences analysis was performed to determine the impact of seven-day changes on clinical outcomes between 2013 and 2014, 2014–2015 and 2015–2016. Data was summarised as mean (SD). Results: Of 159 NHS trusts, 79 (49.7%) instituted seven-day changes in 2013–2014. Crude mortality rates, A&E admission rates and mean LOS remained relatively stable between 2013 and 2016, whilst A&E four-hour breach rates nearly doubled from 5.3 to 9.7%. From 2013 to 2014 to 2014–2015 and 2015–2016, there were no significant differences in the change in crude mortality (2014–2015 p = 0.8, 2015–2016 p = 0.9), SHMI (2014–2015 p = 0.5, 2015–2016 p = 0.5), mean LOS (2014–2015 p = 0.5, 2015–2016 p = 0.4), A&E admission (2014–2015 p = 0.6, 2015–2016 p = 1.0) or four-hour breach rates (2014–2015 p = 0.06, 2015–2016 p = 0.6) between trusts that had implemented seven-day changes compared to those which had not. Conclusions: Adverse weekend clinical outcomes may not be ameliorated by large scale reorganisations aimed at improving access to health services across the week. Such changes may negatively impact care quality without additional financial investment, as demonstrated by worsening of some outcomes. Detailed prospective research is required to determine whether such reallocation of finite resources is clinically effective

Brucellosis remains a neglected disease inthe developing world: a call forinterdisciplinary action

Brucellosis places significant burdens on the human healthcare system and limits the economic growth of individuals, communities, and nations where such development is especially important to diminish the prevalence of poverty. The implementation of public policy focused on mitigating the socioeconomic effects of brucellosis in human and animal populations is desperately needed. When developing a plan to mitigate the associated consequences, it is vital to consider both the abstract and quantifiable effects. This requires an interdisciplinary and collaborative, or One Health, approach that consists of public education, the development of an infrastructure for disease surveillance and reporting in both veterinary and medical fields, and campaigns for control in livestock and wildlife species

Investigating poultry trade patterns to guide avian influenza surveillance and control: a case study in Vietnam

Live bird markets are often the focus of surveillance activities monitoring avian influenza viruses (AIV) circulating in poultry. However, in order to ensure a high sensitivity of virus detection and effectiveness of management actions, poultry management practices features influencing AIV dynamics need to be accounted for in the design of surveillance programmes. In order to address this knowledge gap, a cross-sectional survey was conducted through interviews with 791 traders in 18 Vietnamese live bird markets. Markets greatly differed according to the sources from which poultry was obtained, and their connections to other markets through the movements of their traders. These features, which could be informed based on indicators that are easy to measure, suggest that markets could be used as sentinels for monitoring virus strains circulating in specific segments of the poultry production sector. AIV spread within markets was modelled. Due to the high turn-over of poultry, viral amplification was likely to be minimal in most of the largest markets. However, due to the large number of birds being introduced each day, and challenges related to cleaning and disinfection, environmental accumulation of viruses at markets may take place, posing a threat to the poultry production sector and to public health

Exceptionally large migration length of carbon and topographically-facilitated self-limiting molecular beam epitaxial growth of graphene on hexagonal boron nitride

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Available online 18 December 2016We demonstrate growth of single-layer graphene (SLG) on hexagonal boron nitride (h-BN) by molecular beam epitaxy (MBE), only limited in area by the finite size of the h-BN flakes. Using atomic force microscopy and micro-Raman spectroscopy, we show that for growth over a wide range of temperatures (500◦C – 1000◦C) the deposited carbon atoms spill off the edge of the h-BN flakes. We attribute this spillage to the very high mobility of the carbon atoms on the BN basal plane, consistent with van der Waals MBE. The h-BN flakes vary in size from 30 µm to 100 µm, thus demonstrating that the migration length of carbon atoms on h-BN is greater than 100 µm. When sufficient carbon is supplied to compensate for this loss, which is largely due to this fast migration of the carbon atoms to and off the edges of the h-BN flake, we find that the best growth temperature for MBE SLG on h-BN is ∼950◦C. Self-limiting graphene growth appears to be facilitated by topographic h-BN surface features: We have thereby grown MBE self-limited SLG on an h-BN ridge. This opens up future avenues for precisely tailored fabrication of nano- and hetero-structures on pre-patterned h-BN surfaces for device applications.This work is supported by ONR (N000140610138 and Graphene MURI), AFOSR (FA9550-11-1-0010), EFRC Center for Re-Defining Photovoltaic Efficiency through Molecule Scale Control (award DE-SC0001085), NSF (CHE-0641523), NYSTAR and Spanish Government (AIC-B-2011-0806, MAT2014-54231, MAT2015-67021-R). S.W. and A.P. were supported by the US Department of Energy Office of Science, Division of Materials Science and Engineering (award DE-SC0010695)

Programmed Autophagy in the Fat Body of Aedes aegypti Is Required to Maintain Egg Maturation Cycles

Autophagy plays a pivotal role by allowing cells to recycle cellular components under conditions of stress, starvation, development and cancer. In this work, we have demonstrated that programmed autophagy in the mosquito fat body plays a critical role in maintaining of developmental switches required for normal progression of gonadotrophic cycles. Mosquitoes must feed on vertebrate blood for their egg development, with each gonadotrophic cycle being tightly coupled to a separate blood meal. As a consequence, some mosquito species are vectors of pathogens that cause devastating diseases in humans and domestic animals, most importantly malaria and Dengue fever. Hence, deciphering mechanisms to control egg developmental cycles is of paramount importance for devising novel approaches for mosquito control. Central to egg development is vitellogenesis, the production of yolk protein precursors in the fat body, the tissue analogous to a vertebrate liver, and their subsequent specific accumulation in developing oocytes. During each egg developmental cycle, the fat body undergoes a developmental program that includes previtellogenic build-up of biosynthetic machinery, intense production of yolk protein precursors, and termination of vitellogenesis. The importance of autophagy for termination of vitellogenesis was confirmed by RNA interference (RNAi) depletions of several autophagic genes (ATGs), which inhibited autophagy and resulted in untimely hyper activation of TOR and prolonged production of the major yolk protein precursor, vitellogenin (Vg). RNAi depletion of the ecdysone receptor (EcR) demonstrated its activating role of autophagy. Depletion of the autophagic genes and of EcR led to inhibition of the competence factor, betaFTZ-F1, which is required for ecdysone-mediated developmental transitions. Moreover, autophagy-incompetent female mosquitoes were unable to complete the second reproductive cycle and exhibited retardation and abnormalities in egg maturation. Thus, our study has revealed a novel function of programmed autophagy in maintaining egg maturation cycles in mosquitoes

Electronic Spin Transport in Dual-Gated Bilayer Graphene

The elimination of extrinsic sources of spin relaxation is key in realizing the exceptional intrinsic spin transport performance of graphene. Towards this, we study charge and spin transport in bilayer graphene-based spin valve devices fabricated in a new device architecture which allows us to make a comparative study by separately investigating the roles of substrate and polymer residues on spin relaxation. First, the comparison between spin valves fabricated on SiO2 and BN substrates suggests that substrate-related charged impurities, phonons and roughness do not limit the spin transport in current devices. Next, the observation of a 5-fold enhancement in spin relaxation time in the encapsulated device highlights the significance of polymer residues on spin relaxation. We observe a spin relaxation length of ~ 10 um in the encapsulated bilayer with a charge mobility of 24000 cm2/Vs. The carrier density dependence of spin relaxation time has two distinct regimes; n<4 x 1012 cm-2, where spin relaxation time decreases monotonically as carrier concentration increases, and n>4 x 1012 cm-2, where spin relaxation time exhibits a sudden increase. The sudden increase in the spin relaxation time with no corresponding signature in the charge transport suggests the presence of a magnetic resonance close to the charge neutrality point. We also demonstrate, for the first time, spin transport across bipolar p-n junctions in our dual-gated device architecture that fully integrates a sequence of encapsulated regions in its design. At low temperatures, strong suppression of the spin signal was observed while a transport gap was induced, which is interpreted as a novel manifestation of impedance mismatch within the spin channel

Identification of novel subgroup a variants with enhanced receptor binding and replicative capacity in primary isolates of anaemogenic strains of feline leukaemia virus

&lt;b&gt;BACKGROUND:&lt;/b&gt; The development of anaemia in feline leukaemia virus (FeLV)-infected cats is associated with the emergence of a novel viral subgroup, FeLV-C. FeLV-C arises from the subgroup that is transmitted, FeLV-A, through alterations in the amino acid sequence of the receptor binding domain (RBD) of the envelope glycoprotein that result in a shift in the receptor usage and the cell tropism of the virus. The factors that influence the transition from subgroup A to subgroup C remain unclear, one possibility is that a selective pressure in the host drives the acquisition of mutations in the RBD, creating A/C intermediates with enhanced abilities to interact with the FeLV-C receptor, FLVCR. In order to understand further the emergence of FeLV-C in the infected cat, we examined primary isolates of FeLV-C for evidence of FeLV-A variants that bore mutations consistent with a gradual evolution from FeLV-A to FeLV-C.&lt;p&gt;&lt;/p&gt; &lt;b&gt;RESULTS:&lt;/b&gt; Within each isolate of FeLV-C, we identified variants that were ostensibly subgroup A by nucleic acid sequence comparisons, but which bore mutations in the RBD. One such mutation, N91D, was present in multiple isolates and when engineered into a molecular clone of the prototypic FeLV-A (Glasgow-1), enhanced replication was noted in feline cells. Expression of the N91D Env on murine leukaemia virus (MLV) pseudotypes enhanced viral entry mediated by the FeLV-A receptor THTR1 while soluble FeLV-A Env bearing the N91D mutation bound more efficiently to mouse or guinea pig cells bearing the FeLV-A and -C receptors. Long-term in vitro culture of variants bearing the N91D substitution in the presence of anti-FeLV gp70 antibodies did not result in the emergence of FeLV-C variants, suggesting that additional selective pressures in the infected cat may drive the subsequent evolution from subgroup A to subgroup C.&lt;p&gt;&lt;/p&gt; &lt;b&gt;CONCLUSIONS:&lt;/b&gt; Our data support a model in which variants of FeLV-A, bearing subtle differences in the RBD of Env, may be predisposed towards enhanced replication in vivo and subsequent conversion to FeLV-C. The selection pressures in vivo that drive the emergence of FeLV-C in a proportion of infected cats remain to be established