The propagation of light pollution in the atmosphere

Methods to map artificial night sky brightness and stellar visibility across large territories or their distribution over the entire sky at any site are based on the computation of the propagation of light pollution with Garstang models, a simplified solution of the radiative transfer problem in the atmosphere which allows a fast computation by reducing it to a ray-tracing approach. We present here up-to-date Extended Garstang Models (EGM) which provide a more general numerical solution for the radiative transfer problem applied to the propagation of light pollution in the atmosphere. We also present the LPTRAN software package, an application of EGM to high-resolution DMSP-OLS satellite measurements of artificial light emissions and to GTOPO30 digital elevation data, which provides an up-to-date method to predict the artificial brightness distribution of the night sky at any site in the World at any visible wavelength for a broad range of atmospheric situations and the artificial radiation density in the atmosphere across the territory. EGM account for (i) multiple scattering, (ii) wavelength from 250 nm to infrared, (iii) Earth curvature and its screening effects, (iv) sites and sources elevation, (v) many kinds of atmosphere with the possibility of custom setup (e.g. including thermal inversion layers), (vi) mix of different boundary layer aerosols and tropospheric aerosols, with the possibility of custom setup, (vii) up to 5 aerosol layers in upper atmosphere including fresh and aged volcanic dust and meteoric dust, (viii) variations of the scattering phase function with elevation, (ix) continuum and line gas absorption from many species, ozone included, (x) up to 5 cloud layers, (xi) wavelength dependant bidirectional reflectance of the ground surface from NASA/MODIS satellites, main models or custom data (snow included), (xii) geographically variable upward light emission function.Comment: 25 pages, 11 figures, accepted for publication in MNRAS, 7 august 201

Naked eye star visibility and limiting magnitude mapped from DMSP-OLS satellite data

We extend the method introduced by Cinzano et al. (2000a) to map the artificial sky brightness in large territories from DMSP satellite data, in order to map the naked eye star visibility and telescopic limiting magnitudes. For these purposes we take into account the altitude of each land area from GTOPO30 world elevation data, the natural sky brightness in the chosen sky direction, based on Garstang modelling, the eye capability with naked eye or a telescope, based on the Schaefer (1990) and Garstang (2000b) approach, and the stellar extinction in the visual photometric band. For near zenith sky directions we also take into account screening by terrain elevation. Maps of naked eye star visibility and telescopic limiting magnitudes are useful to quantify the capability of the population to perceive our Universe, to evaluate the future evolution, to make cross correlations with statistical parameters and to recognize areas where astronomical observations or popularisation can still acceptably be made. We present, as an application, maps of naked eye star visibility and total sky brightness in V band in Europe at the zenith with a resolution of approximately 1 km.Comment: 15 pages, 8 size-reduced PostScript figures, accepted for publication in Monthly Notices of the Royal Astronomical Society, high-resolution original maps will be available as zipped TIFF files from http://www.pd.astro.it/cinzano/page93.htm

Overexpression of lpxT Gene in Escherichia coli Inhibits Cell Division and Causes Envelope Defects without Changing the Overall Phosphorylation Level of Lipid A

LpxT is an inner membrane protein that transfers a phosphate group from the essential lipid undecaprenyl pyrophosphate (C-55PP) to the lipid A moiety of lipopolysaccharide, generating a lipid A tris-phosphorylated species. The protein is encoded by the non-essential lpxT gene, which is conserved in distantly related Gram-negative bacteria. In this work, we investigated the phenotypic effect of lpxT ectopic expression from a plasmid in Escherichia coli. We found that lpxT induction inhibited cell division and led to the formation of elongated cells, mostly with absent or altered septa. Moreover, the cells became sensitive to detergents and to hypo-osmotic shock, indicating that they had cell envelope defects. These effects were not due to lipid A hyperphosphorylation or C-55PP sequestering, but most likely to defective lipopolysaccharide transport. Indeed, lpxT overexpression in mutants lacking the L,D-transpeptidase LdtD and LdtE, which protect cells with outer membrane defects from osmotic lysis, caused cell envelope defects. Moreover, we found that pyrophosphorylated lipid A was also produced in a lpxT deletion mutant, indicating that LpxT is not the only protein able to perform such lipid A modification in E. coli

Proteostasis Regulators in Cystic Fibrosis: Current Development and Future Perspectives

In cystic fibrosis (CF), the deletion of phenylalanine 508 (F508del) in the CF transmembrane conductance regulator (CFTR) leads to misfolding and premature degradation of the mutant protein. These defects can be targeted with pharmacological agents named potentiators and correctors. During the past years, several efforts have been devoted to develop and approve new effective molecules. However, their clinical use remains limited, as they fail to fully restore F508del-CFTR biological function. Indeed, the search for CFTR correctors with different and additive mechanisms has recently increased. Among them, drugs that modulate the CFTR proteostasis environment are particularly attractive to enhance therapy effectiveness further. This Perspective focuses on reviewing the recent progress in discovering CFTR proteostasis regulators, mainly describing the design, chemical structure, and structure-activity relationships. The opportunities, challenges, and future directions in this emerging and promising field of research are discussed, as well

Chromospheric Velocities of a C-class Flare

We use high spatial and temporal resolution observations from the Swedish Solar Telescope to study the chromospheric velocities of a C-class flare originating from active region NOAA 10969. A time-distance analysis is employed to estimate directional velocity components in H-alpha and Ca II K image sequences. Also, imaging spectroscopy has allowed us to determine flare-induced line-of-sight velocities. A wavelet analysis is used to analyse the periodic nature of associated flare bursts. Time-distance analysis reveals velocities as high as 64 km/s along the flare ribbon and 15 km/s perpendicular to it. The velocities are very similar in both the H-alpha and Ca II K time series. Line-of-sight H-alpha velocities are red-shifted with values up to 17 km/s. The high spatial and temporal resolution of the observations have allowed us to detect velocities significantly higher than those found in earlier studies. Flare bursts with a periodicity of approximately 60 s are also detected. These bursts are similar to the quasi-periodic oscillations observed at hard X-ray and radio wavelength data. Some of the highest velocities detected in the solar atmosphere are presented. Line-of-sight velocity maps show considerable mixing of both the magnitude and direction of velocities along the flare path. A change in direction of the velocities at the flare kernel has also been detected which may be a signature of chromospheric evaporation.Comment: Accepted for publication in Astronomy and Astrophysics, 5 figure

Resident Self-Tissue of Proinflammatory Cytokines Rather than Their Systemic Levels Correlates with Development of Myelofibrosis in Gata1low Mice

Serum levels of inflammatory cytokines are currently investigated as prognosis markers in myelofibrosis, the most severe Philadelphia-negative myeloproliferative neoplasm. We tested this hypothesis in the Gata1low model of myelofibrosis. Gata1low mice, and age-matched wild-type littermates, were analyzed before and after disease onset. We assessed cytokine serum levels by Luminex-bead-assay and ELISA, frequency and cytokine content of stromal cells by flow cytometry, and immunohistochemistry and bone marrow (BM) localization of GFP-tagged hematopoietic stem cells (HSC) by confocal microscopy. Differences in serum levels of 32 inflammatory-cytokines between prefibrotic and fibrotic Gata1low mice and their wild-type littermates were modest. However, BM from fibrotic Gata1low mice contained higher levels of lipocalin-2, CXCL1, and TGF-β1 than wild-type BM. Although frequencies of endothelial cells, mesenchymal cells, osteoblasts, and megakar-yocytes were higher than normal in Gata1low BM, the cells which expressed these cytokines the most were malignant megakaryocytes. This increased bioavailability of proinflammatory cytokines was associated with altered HSC localization: Gata1low HSC were localized in the femur diaphysis in areas surrounded by microvessels, neo-bones, and megakaryocytes, while wild-type HSC were localized in the femur epiphysis around adipocytes. In conclusion, bioavailability of inflammatory cytokines in BM, rather than blood levels, possibly by reshaping the HSC niche, correlates with myelofibrosis in Gata1low mice

Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors

Although stem cell factor (SCF)/cKIT interaction plays key functions in erythropoiesis, cKIT signaling in human erythroid cells is still poorly defined. To provide new insights into cKIT-mediated erythroid expansion in development and disease, we performed phosphoproteomic profiling of primary erythroid progenitors from adult blood (AB), cord blood (CB), and Polycythemia Vera (PV) at steady-state and upon SCF stimulation. While AB and CB, respectively, activated transient or sustained canonical cKIT-signaling, PV showed a non-canonical signaling including increased mTOR and ERK1 and decreased DEPTOR. Accordingly, screening of FDA-approved compounds showed increased PV sensitivity to JAK, cKIT, and MEK inhibitors. Moreover, differently from AB and CB, in PV the mature 145kDa-cKIT constitutively associated with the tetraspanin CD63 and was not endocytosed upon SCF stimulation, contributing to unrestrained cKIT signaling. These results identify a clinically exploitable variegation of cKIT signaling/metabolism that may contribute to the great erythroid output occurring during development and in PV