J-PLUS: The Javalambre Photometric Local Universe Survey

The Javalambre Photometric Local Universe Survey (J-PLUS) is an ongoing 12-band photometric optical survey, observing thousands of square degrees of the Northern Hemisphere from the dedicated JAST/T80 telescope at the Observatorio Astrofisico de Javalambre (OAJ). The T80Cam is a camera with a field of view of 2 deg(2) mounted on a telescope with a diameter of 83 cm, and is equipped with a unique system of filters spanning the entire optical range (3500-10 000 angstrom). This filter system is a combination of broad-, medium-, and narrow-band filters, optimally designed to extract the rest-frame spectral features (the 3700-4000 angstrom Balmer break region, H delta, Ca H+K, the G band, and the Mg b and Ca triplets) that are key to characterizing stellar types and delivering a low-resolution photospectrum for each pixel of the observed sky. With a typical depth of AB similar to 21.25 mag per band, this filter set thus allows for an unbiased and accurate characterization of the stellar population in our Galaxy, it provides an unprecedented 2D photospectral information for all resolved galaxies in the local Universe, as well as accurate photo-z estimates (at the delta z/(1 + z) similar to 0.005-0.03 precision level) for moderately bright (up to r similar to 20 mag) extragalactic sources. While some narrow-band filters are designed for the study of particular emission features ([O II]/lambda 3727, H alpha/lambda 6563) up to z < 0.017, they also provide well-defined windows for the analysis of other emission lines at higher redshifts. As a result, J-PLUS has the potential to contribute to a wide range of fields in Astrophysics, both in the nearby Universe (Milky Way structure, globular clusters, 2D IFU-like studies, stellar populations of nearby and moderate-redshift galaxies, clusters of galaxies) and at high redshifts (emission-line galaxies at z approximate to 0.77, 2.2, and 4.4, quasi-stellar objects, etc.). With this paper, we release the first similar to 1000 deg(2) of J-PLUS data, containing about 4.3 million stars and 3.0 million galaxies at r < 21 mag. With a goal of 8500 deg(2) for the total J-PLUS footprint, these numbers are expected to rise to about 35 million stars and 24 million galaxies by the end of the survey

Lack of Clinical Manifestations in Asymptomatic Dengue Infection Is Attributed to Broad Down-Regulation and Selective Up-Regulation of Host Defence Response Genes

<div><p>Objectives</p><p>Dengue represents one of the most serious life-threatening vector-borne infectious diseases that afflicts approximately 50 million people across the globe annually. Whilst symptomatic infections are frequently reported, asymptomatic dengue remains largely unnoticed. Therefore, we sought to investigate the immune correlates conferring protection to individuals that remain clinically asymptomatic.</p><p>Methods</p><p>We determined the levels of neutralizing antibodies (nAbs) and gene expression profiles of host immune factors in individuals with asymptomatic infections, and whose cognate household members showed symptoms consistent to clinical dengue infection.</p><p>Results</p><p>We observed broad down-regulation of host defense response (innate, adaptive and matrix metalloprotease) genes in asymptomatic individuals as against symptomatic patients, with selective up-regulation of distinct genes that have been associated with protection. Selected down-regulated genes include: TNF α (<i>TNF</i>), <i>IL8</i>, <i>C1S</i>, factor B (<i>CFB</i>), <i>IL2</i>, <i>IL3</i>, <i>IL4</i>, <i>IL5</i>, <i>IL8</i>, <i>IL9</i>, <i>IL10</i> and <i>IL13</i>, <i>CD80</i>, <i>CD28</i>, and <i>IL18</i>, <i>MMP8</i>, <i>MMP10</i>, <i>MMP12</i>, <i>MMP15</i>, <i>MMP16</i>, and <i>MMP24</i>. Selected up-regulated genes include: RANTES (<i>CCL5</i>), MIP-1α (<i>CCL3L1/CCL3L3</i>), MIP-1β (<i>CCL4L1</i>), TGFβ (<i>TGFB</i>), and <i>TIMP1</i>.</p><p>Conclusion</p><p>Our findings highlight the potential association of certain host genes conferring protection against clinical dengue. These data are valuable to better explore the mysteries behind the hitherto poorly understood immunopathogenesis of subclinical dengue infection.</p></div

Nutritional care of the older patient with fragility fracture: opportunities for systematised, interdisciplinary approaches across acute care, rehabilitation and secondary prevention settings

Nutritional care of the older patient with fragility fracture is complex. Diagnostic difficulties, multi-morbidities and interdependencies and social complexities all contribute to the wicked problem of malnutrition. Whilst many settings have attempted to address malnutrition through highly specialised care, increasing evidence supports the role of systematised, interdisciplinary approaches across acute care, rehabilitation and secondary prevention settings. Consequently, this chapter is devoted to highlighting why a SIMPLE approach to malnutrition should underpin the nutritional care of the older patient with fragility fracture, regardless of setting or healthcare provider.S Screen for nutrition riskI Interdisciplinary assessmentM Make the diagnosis (es)P Plan with the patientL impLement interventionsE Evaluate ongoing care requirement

Group B Streptococcal Infection and Activation of Human Astrocytes

BACKGROUND:Streptococcus agalactiae (Group B Streptococcus, GBS) is the leading cause of life-threatening meningitis in human newborns in industrialized countries. Meningitis results from neonatal infection that occurs when GBS leaves the bloodstream (bacteremia), crosses the blood-brain barrier (BBB), and enters the central nervous system (CNS), where the bacteria contact the meninges. Although GBS is known to invade the BBB, subsequent interaction with astrocytes that physically associate with brain endothelium has not been well studied. METHODOLOGY/PRINCIPAL FINDINGS:We hypothesize that human astrocytes play a unique role in GBS infection and contribute to the development of meningitis. To address this, we used a well- characterized human fetal astrocyte cell line, SVG-A, and examined GBS infection in vitro. We observed that all GBS strains of representative clinically dominant serotypes (Ia, Ib, III, and V) were able to adhere to and invade astrocytes. Cellular invasion was dependent on host actin cytoskeleton rearrangements, and was specific to GBS as Streptococcus gordonii failed to enter astrocytes. Analysis of isogenic mutant GBS strains deficient in various cell surface organelles showed that anchored LTA, serine-rich repeat protein (Srr1) and fibronectin binding (SfbA) proteins all contribute to host cell internalization. Wild-type GBS also displayed an ability to persist and survive within an intracellular compartment for at least 12 h following invasion. Moreover, GBS infection resulted in increased astrocyte transcription of interleukin (IL)-1β, IL-6 and VEGF. CONCLUSIONS/SIGNIFICANCE:This study has further characterized the interaction of GBS with human astrocytes, and has identified the importance of specific virulence factors in these interactions. Understanding the role of astrocytes during GBS infection will provide important information regarding BBB disruption and the development of neonatal meningitis