Mapping High-velocity H-alpha and Lyman-alpha Emission from Supernova 1987A

We present new {\it Hubble Space Telescope} images of high-velocity H-$\alpha$ and Lyman-$\alpha$ emission in the outer debris of SN~1987A. The H-$\alpha$ images are dominated by emission from hydrogen atoms crossing the reverse shock. For the first time we observe emission from the reverse shock surface well above and below the equatorial ring, suggesting a bipolar or conical structure perpendicular to the ring plane. Using the H$\alpha$ imaging, we measure the mass flux of hydrogen atoms crossing the reverse shock front, in the velocity intervals ($-$7,500~$<$~$V_{obs}$~$<$~$-$2,800 km s$^{-1}$) and (1,000~$<$~$V_{obs}$~$<$~7,500 km s$^{-1}$), $\dot{M_{H}}$ = 1.2~$\times$~10$^{-3}$ M$_{\odot}$ yr$^{-1}$. We also present the first Lyman-$\alpha$ imaging of the whole remnant and new $Chandra$ X-ray observations. Comparing the spatial distribution of the Lyman-$\alpha$ and X-ray emission, we observe that the majority of the high-velocity Lyman-$\alpha$ emission originates interior to the equatorial ring. The observed Lyman-$\alpha$/H-$\alpha$ photon ratio, $\langle$$R(L\alpha / H\alpha)$$\rangle$ $\approx$~17, is significantly higher than the theoretically predicted ratio of $\approx$ 5 for neutral atoms crossing the reverse shock front. We attribute this excess to Lyman-$\alpha$ emission produced by X-ray heating of the outer debris. The spatial orientation of the Lyman-$\alpha$ and X-ray emission suggests that X-ray heating of the outer debris is the dominant Lyman-$\alpha$ production mechanism in SN 1987A at this phase in its evolution.Comment: 6 pages, 5 figures. ApJL - accepte

Season of Grazing Interacts with Soil Texture, Selecting for Associations of Biocrust Morphogroups

Livestock grazing, a widespread land use in semi-arid systems, is often placed in opposition to the perpetuation of biological soil crusts (“biocrusts”: lichens, mosses, and algal crusts including cyanobacteria) that live on the soil surface and provide ecosystem functions. The composition of biocrusts and vascular plants varies with climate, soils, and disturbance. In general, ruderal mosses and light algal crusts make up greater proportions of biocrusts in the presence of disturbance, although morphogroups of biocrusts respond differently to various disturbances. It is unknown if there are scenarios under which grazing can occur and ruderal components of biocrust could be maintained. We examine the hypothesis that soil surface texture-moisture interactions influence the ability of biocrusts to withstand trampling, reasoning that finer-textured soils are firmer (therefore serving as a better substrate for biocrusts) when dry and that coarser-textured are firmer when wet. We test these relationships within Birds of Prey, National Conservation Area (Boise, Idaho, USA). Results demonstrate two associations of biocrusts, dependent on season of grazing: one dominated by light algal crusts and lichens that frequently occurs with wet season grazing, and a second dominated by tall mosses and cup lichens that frequently occurs with dry season grazing. High cover of the invasive annual grass, Bromus tectorum (L.) was observed on sites with coarse-textured soils, and high sand content, that are grazed at relatively high intensities, creating unstable surfaces, and likely putting biocrusts at greater susceptibility to trampling. Results suggest that livestock management that accounts for soil texture and moisture could be used to maintain cover of ruderal biocrusts on fine-textured soils, that are grazed in the dry season, at low intensity. We discuss our findings in the context of managing for species of interest. Our findings are timely as varying the season of grazing is increasingly discussed as a means of favoring desirable native perennial grasses. Although ruderal morphogroups of biocrusts are not interpreted as having equivalent ecosystem functions compared to intact biocrusts, their contributions to soil stability, fertility, hydrology, and weed abatement could increase if they were more intentionally targeted by management

Dental microwear as a behavioral proxy for distinguishing between canids at the Upper Paleolithic (Gravettian) site of Predmostí, Czech Republic

Morphological and genetic evidence put dog domestication during the Paleolithic, sometime between 40,000 and 15,000 years ago, with identification of the earliest dogs debated. We predict that these earliest dogs (referred to herein as protodogs), while potentially difficult to distinguish morphologically from wolves, experienced behavioral shifts, including changes in diet. Specifically, protodogs may have consumed more bone and other less desirable scraps within human settlement areas. Here we apply Dental Microwear Texture Analysis (DMTA) to canids from the Gravettian site of P�redmostí (approx. 28,500 BP), which were previously assigned to the Paleolithic dog or Pleistocene wolf morphotypes. We test whether these groups separate out significantly by diet- related variation in microwear patterning. Results are consistent with differences in dietary breadth, with the Paleolithic dog morphotype showing evidence of greater durophagy than those assigned to the wolf morphotype. This supports the presence of two morphologically and behaviorally distinct canid types at this middle Upper Paleolithic site. Our primary goal here was to test whether these two morphotypes expressed notable differences in dietary behavior. However, in the context of a major Gravettian settlement, this may also support evidence of early stage dog domestication. Dental microwear is a behavioral signal that may appear generations before morphological changes are established in a population. It shows promise for distinguishing protodogs from wolves in the Pleistocene and domesticated dogs from wolves elsewhere in the archaeological record

Multiplex meta-analysis of RNA expression to identify genes with variants associated with immune dysfunction

ObjectiveWe demonstrate a genome-wide method for the integration of many studies of gene expression of phenotypically similar disease processes, a method of multiplex meta-analysis. We use immune dysfunction as an example disease process.DesignWe use a heterogeneous collection of datasets across human and mice samples from a range of tissues and different forms of immunodeficiency. We developed a method integrating Tibshirani's modified t-test (SAM) is used to interrogate differential expression within a study and Fisher's method for omnibus meta-analysis to identify differentially expressed genes across studies. The ability of this overall gene expression profile to prioritize disease associated genes is evaluated by comparing against the results of a recent genome wide association study for common variable immunodeficiency (CVID).ResultsOur approach is able to prioritize genes associated with immunodeficiency in general (area under the ROC curve = 0.713) and CVID in particular (area under the ROC curve = 0.643).ConclusionsThis approach may be used to investigate a larger range of failures of the immune system. Our method may be extended to other disease processes, using RNA levels to prioritize genes likely to contain disease associated DNA variants

Hereditary and Familial Traits in Urological Cancers and Their Underlying Genes

Early recognition of hereditary urological cancers may influence diagnostic and therapeutic decision-making, and potentially alter the fate of patients and family members. Here, we introduce readers to the current knowledge on germline genetic testing and clinical practice in prostate, bladder, renal, and testicular carcinoma. Considering all urological cancer patients, routine inquiries about familial cancer history should become a standard practice in clinical settings. If suspicion arises, patients can opt for two avenues: referral to genetic counseling or undergoing genetic tests after consultation with the treating urologist. Patient summary: Tumors of the urogenital tract (prostate, kidney, bladder, and testes) can sometimes be related to genetic mutations that are present in all the cells of the body. Such mutations can be inherited and run in families. Therefore, it is relevant to obtain information on the incidence of all cancers in the family history. The information obtained may initiate genetic testing, leading to the identification of mutations that are related to cancer in the current or next generation. In addition, these mutations may offer alternative treatment options for patients.</p

Opposing actions of angiopoietin-2 on Tie2 signaling and FOXO1 activation

Angiopoietin-2 (ANG2) regulates blood vessel remodeling in many pathological conditions through differential effects on Tie2 signaling. While ANG2 competes with ANG1 to inhibit Tie2, it can paradoxically also promote Tie2 phosphorylation (p-Tie2). A related paradox is that both inactivation and overactivation of Tie2 can result in vascular remodeling. Here, we reconciled these opposing actions of ANG2 by manipulating conditions that govern its actions in the vasculature. ANG2 drove vascular remodeling during Mycoplasma pulmonis infection by acting as a Tie2 antagonist, which led to p-Tie2 suppression, forkhead box O1 (FOXO1) activation, increased ANG2 expression, and vessel leakiness. These changes were exaggerated by anti-Tie2 antibody, inhibition of PI3K signaling, or ANG2 overexpression and were reduced by anti-ANG2 antibody or exogenous ANG1. In contrast, under pathogen-free conditions, ANG2 drove vascular remodeling by acting as an agonist, promoting high p-Tie2, low FOXO1 activation, and no leakage. Tie1 activation was strong under pathogen-free conditions, but infection or TNF-α led to Tie1 inactivation by ectodomain cleavage and promoted the Tie2 antagonist action of ANG2. Together, these data indicate that ANG2 activation of Tie2 supports stable enlargement of normal nonleaky vessels, but reduction of Tie1 in inflammation leads to ANG2 antagonism of Tie2 and initiates a positive feedback loop wherein FOXO1-driven ANG2 expression promotes vascular remodeling and leakage

Disrupting the spatio-temporal symmetry of the electron dynamics in atmospheric pressure plasmas by voltage waveform tailoring

Single frequency, geometrically symmetric Radio-Frequency (RF) driven atmospheric pressure plasmas exhibit temporally and spatially symmetric patterns of electron heating, and consequently, charged particle densities and fluxes. Using a combination of phase-resolved optical emission spectroscopy and kinetic plasma simulations, we demonstrate that tailored voltage waveforms consisting of multiple RF harmonics induce targeted disruption of these symmetries. This confines the electron heating to small regions of time and space and enables the electron energy distribution function to be tailored

Heterozygous SSBP1 start loss mutation co-segregates with hearing loss and the m.1555A>G mtDNA variant in a large multigenerational family.

The m.1555A>G mtDNA variant causes maternally inherited deafness, but the reasons for the highly variable clinical penetrance are not known. Exome sequencing identified a heterozygous start loss mutation in SSBP1, encoding the single stranded binding protein 1 (SSBP1), segregating with hearing loss in a multi-generational family transmitting m.1555A>G, associated with mtDNA depletion and multiple deletions in skeletal muscle. The SSBP1 mutation reduced steady state SSBP1 levels leading to a perturbation of mtDNA metabolism, likely compounding the intra-mitochondrial translation defect due to m.1555A>G in a tissue-specific manner. This family demonstrates the importance of rare trans-acting genetic nuclear modifiers in the clinical expression of mtDNA disease

Heterozygous SSBP1 start loss mutation co-segregates with hearing loss and the m.1555A>G mtDNA variant in a large multigenerational family

The m.1555A&gt;G mtDNA variant causes maternally inherited deafness, but the reasons for the highly variable clinical penetrance are not known. Exome sequencing identified a heterozygous start loss mutation in SSBP1, encoding the single stranded binding protein 1 (SSBP1), segregating with hearing loss in a multi-generational family transmitting m.1555A&gt;G, associated with mtDNA depletion and multiple deletions in skeletal muscle. The SSBP1 mutation reduced steady state SSBP1 levels leading to a perturbation of mtDNA metabolism, likely compounding the intra-mitochondrial translation defect due to m.1555A&gt;G in a tissue-specific manner. This family demonstrates the importance of rare trans-acting genetic nuclear modifiers in the clinical expression of mtDNA disease