Virtual Texture Generated using Elastomeric Conductive Block Copolymer in Wireless Multimodal Haptic Glove.

Haptic devices are in general more adept at mimicking the bulk properties of materials than they are at mimicking the surface properties. This paper describes a haptic glove capable of producing sensations reminiscent of three types of near-surface properties: hardness, temperature, and roughness. To accomplish this mixed mode of stimulation, three types of haptic actuators were combined: vibrotactile motors, thermoelectric devices, and electrotactile electrodes made from a stretchable conductive polymer synthesized in our laboratory. This polymer consisted of a stretchable polyanion which served as a scaffold for the polymerization of poly(3,4-ethylenedioxythiophene) (PEDOT). The scaffold was synthesized using controlled radical polymerization to afford material of low dispersity, relatively high conductivity (0.1 S cm-1), and low impedance relative to metals. The glove was equipped with flex sensors to make it possible to control a robotic hand and a hand in virtual reality (VR). In psychophysical experiments, human participants were able to discern combinations of electrotactile, vibrotactile, and thermal stimulation in VR. Participants trained to associate these sensations with roughness, hardness, and temperature had an overall accuracy of 98%, while untrained participants had an accuracy of 85%. Sensations could similarly be conveyed using a robotic hand equipped with sensors for pressure and temperature

The SAMI pilot survey: The kinematic morphology-density relation in Abell 85, Abell 168 and Abell 2399

We examine the kinematic morphology of early-type galaxies (ETGs) in three galaxy clusters Abell 85, 168 and 2399. Using data from the Sydney-AAOMulti-object Integral field spectrograph we measure spatially resolved kinematics for 79 ETGs in these clusters. We calculate λR, a proxy for the projected specific stellar angular momentum, for each galaxy and classify the 79 ETGs in our samples as fast or slow rotators. We calculate the fraction of slow rotators in the ETG populations (fSR) of the clusters to be 0.21 ± 0.08, 0.08 ± 0.08 and 0.12 ± 0.06 for Abell 85, 168 and 2399, respectively, with an overall fraction of 0.15 ± 0.04. These numbers are broadly consistent with the values found in the literature, confirming recent work asserting that the fraction of slow rotators in the ETG population is constant across many orders of magnitude in global environment. We examine the distribution of kinematic classes in each cluster as a function of environment using the projected density of galaxies: the kinematic morphology-density relation.We find that in Abell 85 fSR increases in higher density regions but in Abell 168 and 2399 this trend is not seen. We examine the differences between the individual clusters to explain this. In addition, we find slow rotators on the outskirts of two of the clusters studied, Abell 85 and 2399. These galaxies reside in intermediate to low density regions and have clearly not formed at the centre of a cluster environment. We hypothesize that they formed at the centres of groups and are falling into the clusters for the first time

CHILES: HI morphology and galaxy environment at z=0.12 and z=0.17

We present a study of 16 HI-detected galaxies found in 178 hours of observations from Epoch 1 of the COSMOS HI Large Extragalactic Survey (CHILES). We focus on two redshift ranges between 0.108 <= z <= 0.127 and 0.162 <= z <= 0.183 which are among the worst affected by radio frequency interference (RFI). While this represents only 10% of the total frequency coverage and 18% of the total expected time on source compared to what will be the full CHILES survey, we demonstrate that our data reduction pipeline recovers high quality data even in regions severely impacted by RFI. We report on our in-depth testing of an automated spectral line source finder to produce HI total intensity maps which we present side-by-side with significance maps to evaluate the reliability of the morphology recovered by the source finder. We recommend that this become a common place manner of presenting data from upcoming HI surveys of resolved objects. We use the COSMOS 20k group catalogue, and we extract filamentary structure using the topological DisPerSE algorithm to evaluate the \hi\ morphology in the context of both local and large-scale environments and we discuss the shortcomings of both methods. Many of the detections show disturbed HI morphologies suggesting they have undergone a recent interaction which is not evident from deep optical imaging alone. Overall, the sample showcases the broad range of ways in which galaxies interact with their environment. This is a first look at the population of galaxies and their local and large-scale environments observed in HI by CHILES at redshifts beyond the z=0.1 Universe.Comment: 23 pages, 12 figures, 1 interactive 3D figure, accepted to MNRA

Mannose-binding lectin genotypes: lack of association with susceptibility to thoracic empyema

<p>Abstract</p> <p>Background</p> <p>The role of the innate immune protein mannose-binding lectin (MBL) in host defence against severe respiratory infection remains controversial. Thoracic empyema is a suppurative lung infection that arises as a major complication of pneumonia and is associated with a significant mortality. Although the pathogenesis of thoracic empyema is poorly understood, genetic susceptibility loci for this condition have recently been identified. The possible role of MBL genotypic deficiency in susceptibility to thoracic empyema has not previously been reported.</p> <p>Methods</p> <p>To investigate this further we compared the frequencies of the six functional <it>MBL </it>polymorphisms in 170 European individuals with thoracic empyema and 225 healthy control individuals.</p> <p>Results</p> <p>No overall association was observed between MBL genotypic deficiency and susceptibility to thoracic empyema (2 × 2 Chi square = 0.02, <it>P </it>= 0.87). Furthermore, no association was seen between MBL deficiency and susceptibility to the Gram-positive or pneumococcal empyema subgroups. MBL genotypic deficiency did not associate with progression to death or requirement for surgery.</p> <p>Conclusions</p> <p>Our results suggest that MBL genotypic deficiency does not associate with susceptibility to thoracic empyema in humans.</p

Who needs what from a national health research system: Lessons from reforms to the English Department of Health's R&D system

This article has been made available through the Brunel Open Access Publishing Fund.Health research systems consist of diverse groups who have some role in health research, but the boundaries around such a system are not clear-cut. To explore what various stakeholders need we reviewed the literature including that on the history of English health R&D reforms, and we also applied some relevant conceptual frameworks. We first describe the needs and capabilities of the main groups of stakeholders in health research systems, and explain key features of policymaking systems within which these stakeholders operate in the UK. The five groups are policymakers (and health care managers), health professionals, patients and the general public, industry, and researchers. As individuals and as organisations they have a range of needs from the health research system, but should also develop specific capabilities in order to contribute effectively to the system and benefit from it. Second, we discuss key phases of reform in the development of the English health research system over four decades - especially that of the English Department of Health's R&D system - and identify how far legitimate demands of key stakeholder interests were addressed. Third, in drawing lessons we highlight points emerging from contemporary reports, but also attempt to identify issues through application of relevant conceptual frameworks. The main lessons are: the importance of comprehensively addressing the diverse needs of various interacting institutions and stakeholders; the desirability of developing facilitating mechanisms at interfaces between the health research system and its various stakeholders; and the importance of additional money in being able to expand the scope of the health research system whilst maintaining support for basic science. We conclude that the latest health R&D strategy in England builds on recent progress and tackles acknowledged weaknesses. The strategy goes a considerable way to identifying and more effectively meeting the needs of key groups such as medical academics, patients and industry, and has been remarkably successful in increasing the funding for health research. There are still areas that might benefit from further recognition and resourcing, but the lessons identified, and progress made by the reforms are relevant for the design and coordination of national health research systems beyond England.This article is available through the Brunel Open Access Publishing Fund

Human neutrophil clearance of bacterial pathogens triggers anti-microbial gamma delta T cell responses in early infection

Human blood Vc9/Vd2 T cells, monocytes and neutrophils share a responsiveness toward inflammatory chemokines and are rapidly recruited to sites of infection. Studying their interaction in vitro and relating these findings to in vivo observations in patients may therefore provide crucial insight into inflammatory events. Our present data demonstrate that Vc9/Vd2 T cells provide potent survival signals resulting in neutrophil activation and the release of the neutrophil chemoattractant CXCL8 (IL-8). In turn, Vc9/Vd2 T cells readily respond to neutrophils harboring phagocytosed bacteria, as evidenced by expression of CD69, interferon (IFN)-c and tumor necrosis factor (TNF)-a. This response is dependent on the ability of these bacteria to produce the microbial metabolite (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMB-PP), requires cell-cell contact of Vc9/Vd2 T cells with accessory monocytes through lymphocyte function-associated antigen-1 (LFA-1), and results in a TNF-a dependent proliferation of Vc9/Vd2 T cells. The antibiotic fosmidomycin, which targets the HMB-PP biosynthesis pathway, not only has a direct antibacterial effect on most HMB-PP producing bacteria but also possesses rapid anti-inflammatory properties by inhibiting cd T cell responses in vitro. Patients with acute peritoneal-dialysis (PD)-associated bacterial peritonitis – characterized by an excessive influx of neutrophils and monocytes into the peritoneal cavity – show a selective activation of local Vc9/Vd2 T cells by HMB-PP producing but not by HMB-PP deficient bacterial pathogens. The cd T celldriven perpetuation of inflammatory responses during acute peritonitis is associated with elevated peritoneal levels of cd T cells and TNF-a and detrimental clinical outcomes in infections caused by HMB-PP positive microorganisms. Taken together, our findings indicate a direct link between invading pathogens, neutrophils, monocytes and microbe-responsive cd T cells in early infection and suggest novel diagnostic and therapeutic approaches.Martin S. Davey, Chan-Yu Lin, Gareth W. Roberts, Sinéad Heuston, Amanda C. Brown, James A. Chess, Mark A. Toleman, Cormac G.M. Gahan, Colin Hill, Tanya Parish, John D. Williams, Simon J. Davies, David W. Johnson, Nicholas Topley, Bernhard Moser and Matthias Eber

On-chip picosecond pulse detection and generation using graphene photoconductive switches

We report on the use of graphene for room temperature on-chip detection and generation of pulsed terahertz (THz) frequency radiation, exploiting the fast carrier dynamics of light-generated hot carriers, and compare our results with conventional low-temperature-grown gallium arsenide (LT-GaAs) photoconductive (PC) switches. Coupling of picosecond-duration pulses from a biased graphene PC switch into Goubau line waveguides is also demonstrated. A Drude transport model based on the transient photoconductance of graphene is used to describe the mechanism for both detection and generation of THz radiation

Alternative Splicing Events Are a Late Feature of Pathology in a Mouse Model of Spinal Muscular Atrophy

Spinal muscular atrophy is a severe motor neuron disease caused by inactivating mutations in the SMN1 gene leading to reduced levels of full-length functional SMN protein. SMN is a critical mediator of spliceosomal protein assembly, and complete loss or drastic reduction in protein leads to loss of cell viability. However, the reason for selective motor neuron degeneration when SMN is reduced to levels which are tolerated by all other cell types is not currently understood. Widespread splicing abnormalities have recently been reported at end-stage in a mouse model of SMA, leading to the proposition that disruption of efficient splicing is the primary mechanism of motor neuron death. However, it remains unclear whether splicing abnormalities are present during early stages of the disease, which would be a requirement for a direct role in disease pathogenesis. We performed exon-array analysis of RNA from SMN deficient mouse spinal cord at 3 time points, pre-symptomatic (P1), early symptomatic (P7), and late-symptomatic (P13). Compared to littermate control mice, SMA mice showed a time-dependent increase in the number of exons showing differential expression, with minimal differences between genotypes at P1 and P7, but substantial variation in late-symptomatic (P13) mice. Gene ontology analysis revealed differences in pathways associated with neuronal development as well as cellular injury. Validation of selected targets by RT–PCR confirmed the array findings and was in keeping with a shift between physiologically occurring mRNA isoforms. We conclude that the majority of splicing changes occur late in SMA and may represent a secondary effect of cell injury, though we cannot rule out significant early changes in a small number of transcripts crucial to motor neuron survival