A comprehensive approach to analyze discrepancies between land surface models and in-situ measurements: a case study over the US and Illinois with SECHIBA forced by NLDAS

The purpose of this study is to test the ability of the Land Surface Model SECHIBA to simulate water budget and particularly soil moisture at two different scales: regional and local. The model is forced by NLDAS data set at 1/8th degree resolution over the 1997–1999 period. SECHIBA gives satisfying results in terms of evapotranspiration and runoff over the US compared with four other land surface models, all forced by NLDAS data set for a common time period. The simulated soil moisture is compared to in-situ data from the Global Soil Moisture Database across Illinois by computing a soil wetness index. A comprehensive approach is performed to test the ability of SECHIBA to simulate soil moisture with a gradual change of the vegetation parameters closely related to the experimental conditions. With default values of vegetation parameters, the model overestimates soil moisture, particularly during summer. Sensitivity tests of the model to the change of vegetation parameters show that the roots extraction parameter has the largest impact on soil moisture, other parameters such as LAI, height or soil resistance having a minor impact. Moreover, a new evapotranspiration computation including bare soil evaporation under vegetation has been introduced into the model. The results point out an improvement of the soil moisture simulation when this effect is taken into account. Finally, soil moisture sensitivity to precipitation variation is addressed and it is shown that soil moisture observations can be rather different, depending on the method of measuring field capacity. When the observed field capacity is deducted from the observed volumetric water profiles, simulated soil wetness index is closer to the observations

Beyond scaling and locality in turbulence

An analytic perturbation theory is suggested in order to find finite-size corrections to the scaling power laws. In the frame of this theory it is shown that the first order finite-size correction to the scaling power laws has following form $S(r) \cong cr^{\alpha_0}[\ln(r/\eta)]^{\alpha_1}$, where $\eta$ is a finite-size scale (in particular for turbulence, it can be the Kolmogorov dissipation scale). Using data of laboratory experiments and numerical simulations it is shown shown that a degenerate case with $\alpha_0 =0$ can describe turbulence statistics in the near-dissipation range $r > \eta$, where the ordinary (power-law) scaling does not apply. For moderate Reynolds numbers the degenerate scaling range covers almost the entire range of scales of velocity structure functions (the log-corrections apply to finite Reynolds number). Interplay between local and non-local regimes has been considered as a possible hydrodynamic mechanism providing the basis for the degenerate scaling of structure functions and extended self-similarity. These results have been also expanded on passive scalar mixing in turbulence. Overlapping phenomenon between local and non-local regimes and a relation between position of maximum of the generalized energy input rate and the actual crossover scale between these regimes are briefly discussed.Comment: extended versio

Abortigenic but not neurotropic equine herpes virus 1 modulates the interferon antiviral defense

Equine herpesvirus 1 (EHV1) is considered as a major pathogen of Equidae, causing symptoms from mild respiratory disease to late-termabortion and neurological disorders. Different EHV1 strains circulating in the field have been characterized to be of abortigenic or neurovirulent phenotype. Both variants replicate in a plaque-wise manner in the epithelium of the upper respiratory tract (URT), where the abortigenic strains induce more prominent viral plaques, compared to the neurovirulent strains. Considering the differences in replication at the URT, we hypothesized that abortigenic strains may show an increased ability to modulate the type I IFN secretion/signaling pathway, compared to strains that display the neurovirulent phenotype. Here, we analyze IFN levels induced by abortigenic and neurovirulent EHV1 using primary respiratory epithelial cells (EREC) and respiratory mucosa ex vivo explants. Similar levels of IFN alpha (similar to 70 U/ml) were detected in explants inoculated with both types of EHV1 strains from 48 to 72 hpi. Second, EREC and mucosa explants were treated with recombinant equine IFN alpha (rEqIFN alpha) or Ruxolitinib (Rux), an IFN signaling inhibitor, prior to and during inoculation with abortigenic or neurovirulent EHV1. Replication of both EHV1 variants was suppressed by rEqIFN alpha. Further, addition of Rux increased replication in a concentration-dependent manner, indicating an IFN-susceptibility for both variants. However, in two out of three horses, at a physiological concentration of 100 U/ml of rEqIFN alpha, an increase in abortigenic EHV1 replication was observed compared to 10 U/ml of rEqIFN alpha, which was not observed for the neurovirulent strains. Moreover, in the presence of Rux, the plaque size of the abortigenic variants remained unaltered, whereas the typically smaller viral plaques induced by the neurovirulent variants became larger. Overall, our results demonstrate the importance of IFN alpha in the control of EHV1 replication in the URT for both abortigenic and neurovirulent variants. In addition, our findings support the speculation that abortigenic variants of EHV1 may have developed anti-IFN mechanisms that appear to be absent or less pronounced in neurovirulent EHV1 strains

Extented ionized gas emission and kinematics of the compact group galaxies in HCG 16: Signatures of mergers

We report on kinematic observations of Ha emission line from four late-type galaxies of Hickson Compact Group 16 (H16a,b,c and d) obtained with a scanning Fabry-Perot interferometer and samplings of 16 km/s and 1". The velocity fields show kinematic peculiarities for three of the four galaxies: H16b, c and d. Misalignments between the kinematic and photometric axes of gas and stellar components (H16b,c,d), double gas systems (H16c) and severe warping of the kinematic major axis (H16b and c) were some of the peculiarities detected. We conclude that major merger events have taken place in at least two of the galaxies group. H16c and d, based on their significant kinematic peculiarities, their double nuclei and high infrared luminosities. Their Ha gas content is strongly spatially concentred - H16d contains a peculiar bar-like structure confined to the inner $\sim$ 1 h^-1 kpc region. These observations are in agreement with predictions of simulations, namely that the gas flows towards the galaxy nucleus during mergers, forms bars and fuel the central activity. Galaxy H16b, and Sb galaxy, also presents some of the kinematic evidences for past accretion events. Its gas content, however, is very spare, limiting our ability to find other kinematic merging indicators, if they are present. We find that isolated mergers, i.e., they show an anormorphous morphology and no signs of tidal tails. Tidal arms and tails formed during the mergers may have been stripped by the group potential (Barnes & Hernquist 1992) ar alternatively they may have never been formed. Our observations suggest that HCG 16 may be a young compact group in formation throught the merging of close-by objects in a dense environment.Comment: Accepted for publication in ApJ. 35 pages, 13 figures. tar file gzipped and uuencode

Scaling laws and vortex profiles in 2D decaying turbulence

We use high resolution numerical simulations over several hundred of turnover times to study the influence of small scale dissipation onto vortex statistics in 2D decaying turbulence. A self-similar scaling regime is detected when the scaling laws are expressed in units of mean vorticity and integral scale, as predicted by Carnevale et al., and it is observed that viscous effects spoil this scaling regime. This scaling regime shows some trends toward that of the Kirchhoff model, for which a recent theory predicts a decay exponent $\xi=1$. In terms of scaled variables, the vortices have a similar profile close to a Fermi-Dirac distribution.Comment: 4 Latex pages and 4 figures. Submitted to Phys. Rev. Let

Prior history of feeding–swallowing difficulties in children with language impairment

Purpose This study updated and extended our previous investigation (Malas et al., 2015) of feeding–swallowing difficulties and concerns (FSCs) in children with language impairments (LI) by using more stringent inclusion criteria and targeting children earlier in the care delivery pathway. Method Retrospective analyses were performed on the clinical files of 29 children (average age: 60 months, SD = 9.0) diagnosed as having LI using standardized testing, nonstandardized testing and final speech-language pathologist judgment. The files of children born prematurely or with a history of anatomical, structural, neurodevelopmental, cognitive, sensory, motor, or speech disorders were excluded. Literature-based indicators were used to determine the prevalence of difficulties in sucking, food transition, food selectivity, and salivary control. Values were compared with the general population estimate of Lindberg et al. (1992). Results A significantly higher percentage of histories of FSCs (48%) were found in the files of children with LI when compared with the population estimate (χ2 = 13.741, df = 1, p < .001). Difficulties in food transition (31%) and food selectivity (14%) were the most frequent. Data confirm and extend our previous findings and suggest that a previous history of FSCs may characterize children with LI early in their care delivery pathway

Kang-Redner Anomaly in Cluster-Cluster Aggregation

The large time, small mass, asymptotic behavior of the average mass distribution \pb is studied in a $d$-dimensional system of diffusing aggregating particles for $1\leq d \leq 2$. By means of both a renormalization group computation as well as a direct re-summation of leading terms in the small reaction-rate expansion of the average mass distribution, it is shown that \pb \sim \frac{1}{t^d} (\frac{m^{1/d}}{\sqrt{t}})^{e_{KR}} for $m \ll t^{d/2}$, where $e_{KR}=\epsilon +O(\epsilon ^2)$ and $\epsilon =2-d$. In two dimensions, it is shown that \pb \sim \frac{\ln(m) \ln(t)}{t^2} for $m \ll t/ \ln(t)$. Numerical simulations in two dimensions supporting the analytical results are also presented.Comment: 11 pages, 6 figures, Revtex

The cell envelope subtilisin-like proteinase is a virulence determinant for Streptococcus suis

<p>Abstract</p> <p>Background</p> <p><it>Streptococcus suis </it>is a major swine pathogen and zoonotic agent that mainly causes septicemia, meningitis, and endocarditis. It has recently been suggested that proteinases produced by <it>S. suis </it>(serotype 2) are potential virulence determinants. In the present study, we screened a <it>S. suis </it>mutant library created by the insertion of Tn<it>917 </it>transposon in order to isolate a mutant deficient in a cell surface proteinase. We characterized the gene and assessed the proteinase for its potential as a virulence factor.</p> <p>Results</p> <p>Two mutants (G6G and M3G) possessing a single Tn<it>917 </it>insertion were isolated. The affected gene coded for a protein (SSU0757) that shared a high degree of identity with <it>Streptococccus thermophilus </it>PrtS (95.9%) and, to a lesser extent, with <it>Streptococcus agalactiae </it>CspA (49.5%), which are cell surface serine proteinases. The SSU0757 protein had a calculated molecular mass of 169.6 kDa and contained the catalytic triad characteristic of subtilisin family proteinases: motif I (Asp₂₀₀), motif II (His₂₃₉), and motif III (Ser₅₆₈). SSU0757 also had the Gram-positive cell wall anchoring motif (Leu-Pro-X-Thr-Gly) at the carboxy-terminus, which was followed by a hydrophobic domain. All the <it>S. suis </it>isolates tested, which belonged to different serotypes, possessed the gene encoding the SSU0757 protein. The two mutants devoid of subtilisin-like proteinase activity had longer generation times and were more susceptible to killing by whole blood than the wild-type parent strain P1/7. The virulence of the G6G and M3G mutants was compared to the wild-type strain in the CD1 mouse model. Significant differences in mortality rates were noted between the P1/7 group and the M3G and G6G groups (<it>p </it>< 0.001).</p> <p>Conclusion</p> <p>In summary, we identified a gene coding for a cell surface subtilisin-like serine proteinase that is widely distributed in <it>S. suis</it>. Evidences were brought for the involvement of this proteinase in <it>S. suis </it>virulence.</p