Rethinking the red wolf disease: does Protein S suppress systemic lupus erythematosus clinical activity?

In systemic lupus erythematosus, the forces responsible for disease initiation and self-perpetuation in these clinically heterogeneous populations remain poorly understood. Recent studies of the TAM (Tyro3, Axl and MerTK) family of receptor tyrosine kinases may lead to a better understanding of the fundamental control system responsible for the clearance of apoptotic cells and the regulation of inflammation. In a recent report, serum levels of the TAM ligand, Protein S, was found to correlate with certain disease manifestations and with C3 and C4 levels. Protein S levels could provide a quantitative clinical biomarker but it remains to be determined whether this factor directly affects disease activity

Analyzing science education in the U.K.: taking a system-wide approach

Increasing evidence suggests that individuals develop their understanding of science concepts in and out of school, using varied community resources and networks. Thus in contrast to historic research approaches that focus exclusively on single organizations and/or educational events, the current paper presents exploratory research in which we utilized specific community ecology analytical tools and approaches to describe and analyze the U.K. science education community as a whole. Data suggest that overall the U.K. science education community is highly interconnected, and collaborative within individual sectors and moderately interconnected and collaborative between sectors; schools and to a lesser degree universities were outliers to this pattern. An important conclusion was that management to maximize the effectiveness of science education the U.K. science education community would involve support for continued diversification of the number of science education entities in the system and encouragement of reciprocally collaborative, synergistic relationships. We posit that systemic research enables a broader, more comprehensive view of a system's strengths and weaknesses, offering useful insights into the structure and functioning of science education activities; insights that could help researchers, practitioners, and policy makers improve the overall quality of science education delivery for all

Health care costs, utilization and patterns of care following Lyme disease

BACKGROUND:Lyme disease is the most frequently reported vector borne infection in the United States. The Centers for Disease Control have estimated that approximately 10% to 20% of individuals may experience Post-Treatment Lyme Disease Syndrome - a set of symptoms including fatigue, musculoskeletal pain, and neurocognitive complaints that persist after initial antibiotic treatment of Lyme disease. Little is known about the impact of Lyme disease or post-treatment Lyme disease symptoms (PTLDS) on health care costs and utilization in the United States. OBJECTIVES:1) to examine the impact of Lyme disease on health care costs and utilization, 2) to understand the relationship between Lyme disease and the probability of developing PTLDS, 3) to understand how PTLDS may impact health care costs and utilization. METHODS:This study utilizes retrospective data on medical claims and member enrollment for persons aged 0-64 years who were enrolled in commercial health insurance plans in the United States between 2006-2010. 52,795 individuals treated for Lyme disease were compared to 263,975 matched controls with no evidence of Lyme disease exposure. RESULTS:Lyme disease is associated with $2,968 higher total health care costs (95$3,798 higher total health care costs (95% CI: 3,542-4,055, p<.001) and 66% more outpatient visits (95% CI: 64%-69%, p<.001) over a 12-month period, relative to those with no PTLDS-related diagnoses. CONCLUSIONS:Lyme disease is associated with increased costs above what would be expected for an easy to treat infection. The presence of PTLDS-related diagnoses after treatment is associated with significant health care costs and utilization

Self-Tracking, Governmentality, and Nursing and Midwifery Council's (2016) Revalidation Policy

In April 2016 the Nursing and Midwifery Council (NMC) introduced a new revalidation continuous professional development (CPD) policy. This policy states that revalidation is the responsibility of nurses, and although employers are urged to support the revalidation process, the NMC clearly states that employers have no legal requirement to provide either time or funds for the CPD activities of nurses and midwives (NMC, 2014, 2016; Royal College of Nursing, 2016). The aim of this professional development policy is to ensure that nurses and midwives maintain their professional competency and to promote public safety and confidence in nurses and midwives. A closer look at the process of revalidation suggests that several measures have been introduced to ensure that nurses and midwives conform to the CPD policy, and this paper examines the influence of governmentality and neoliberalism on the NMC's self-tracking revalidation policy. It will be recommended that the responsibility for the revalidation process should be shared by nurses, midwives, and their employers, and that time and money should be allocated for the professional development of nurses and midwives

Decoupling Environment-Dependent and Independent Genetic Robustness across Bacterial Species

The evolutionary origins of genetic robustness are still under debate: it may arise as a consequence of requirements imposed by varying environmental conditions, due to intrinsic factors such as metabolic requirements, or directly due to an adaptive selection in favor of genes that allow a species to endure genetic perturbations. Stratifying the individual effects of each origin requires one to study the pertaining evolutionary forces across many species under diverse conditions. Here we conduct the first large-scale computational study charting the level of robustness of metabolic networks of hundreds of bacterial species across many simulated growth environments. We provide evidence that variations among species in their level of robustness reflect ecological adaptations. We decouple metabolic robustness into two components and quantify the extents of each: the first, environmental-dependent, is responsible for at least 20% of the non-essential reactions and its extent is associated with the species' lifestyle (specialized/generalist); the second, environmental-independent, is associated (correlation = ∼0.6) with the intrinsic metabolic capacities of a species—higher robustness is observed in fast growers or in organisms with an extensive production of secondary metabolites. Finally, we identify reactions that are uniquely susceptible to perturbations in human pathogens, potentially serving as novel drug-targets

Family learning and the socio-spatial practice of 'supportive' power

Family learning has been an important mode of education deployed by governments in the United Kingdom over the past 20 years, and is positioned at the nexus of various social policy areas whose focus stretch beyond education. Drawing on qualitative research exploring mothers' participation in seven different family learning programmes across West London, this paper looks at how this type of education is mobilised; that is, how mothers are 'encouraged' to participate and benefit from this type of programme. Framed by a neo-liberal policy climate and Foucauldian writings on governmentality and surveillance, we explore how participating mothers are carefully 'targeted' for this type of learning through their children and through school/ nursery spaces, and how programmes themselves then operate as a supportive social space aimed at facilitating social networks, friendship and personal development linked to positions of gender, ethnicity, class and migrant status. It is the socio-spatial workings of 'supportive' power and power relations that enable family learning to be mobilised that ensures its popularity as a social policy initiative.The British Academy (small research grant SG42092)

The CARMENES search for exoplanets around M dwarfs High-resolution optical and near-infrared spectroscopy of 324 survey stars

The CARMENES radial velocity (RV) survey is observing 324 M dwarfs to search for any orbiting planets. In this paper, we present the survey sample by publishing one CARMENES spectrum for each M dwarf. These spectra cover the wavelength range 520–1710 nm at a resolution of at least R >80 000, and we measure its RV, Hα emission, and projected rotation velocity. We present an atlas of high-resolution M-dwarf spectra and compare the spectra to atmospheric models. To quantify the RV precision that can be achieved in low-mass stars over the CARMENES wavelength range, we analyze our empirical information on the RV precision from more than 6500 observations. We compare our high-resolution M-dwarf spectra to atmospheric models where we determine the spectroscopic RV information content, Q, and signal-to-noise ratio. We find that for all M-type dwarfs, the highest RV precision can be reached in the wavelength range 700–900 nm. Observations at longer wavelengths are equally precise only at the very latest spectral types (M8 and M9). We demonstrate that in this spectroscopic range, the large amount of absorption features compensates for the intrinsic faintness of an M7 star. To reach an RV precision of 1 m s−1 in very low mass M dwarfs at longer wavelengths likely requires the use of a 10 m class telescope. For spectral types M6 and earlier, the combination of a red visual and a near-infrared spectrograph is ideal to search for low-mass planets and to distinguish between planets and stellar variability. At a 4 m class telescope, an instrument like CARMENES has the potential to push the RV precision well below the typical jitter level of 3–4 m s−1

The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

BACKGROUND: A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. PRESENTATION OF THE HYPOTHESIS: Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia. TESTING THE HYPOTHESIS: Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. IMPLICATIONS OF THE HYPOTHESIS: The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments