Passive Aeroelastic Tailored Wing Modal Test Using the Fixed Base Correction Method

In modal testing and finite element model correlation, analysts desire modal results using free-free or rigid boundary conditions to ease comparisons of test versus analytical data. It is often expensive both in cost and schedule to build and test with boundary conditions that replicate the free-free or rigid boundaries. Static test fixtures for load testing are often large, heavy, and unyielding, but do not provide adequate boundaries for modal tests because they are dynamically too flexible and often contain natural frequencies within the frequency range of interest of the test article. Dynamic coupling between the test article and test fixture complicates the model updating process because significant effort is required to model the test fixture and boundary conditions in addition to the test article. If there were a way to correct the modal results for fixture coupling, then setups used for other structural testing could be adequate for modal testing. In the case described in this paper, a partial static loads testing setup was used, which allowed significant schedule and cost savings by eliminating a unique setup for a modal test. A fixed base correction technique was investigated during modal testing of a flexible wing cantilevered from part of a static test fixture. The technique was successfully used to measure the wing modes de-coupled from the dynamically active test fixture. The technique is promising for future aircraft applications, but more research is needed

Skin and soft tissue infections in hospitalized and critically ill patients: a nationwide population-based study

<p>Abstract</p> <p>Background</p> <p>The proportional distributions of various skin and soft tissue infections (SSTIs) with/without intensive care are unclear. Among SSTI patients, the prevalence and significance of complicating factors, such as comorbidities and infections other than skin/soft tissue (non-SST infections), remain poorly understood. We conducted this population-based study to characterize hospitalized SSTI patients with/without intensive care and to identify factors associated with patient outcome.</p> <p>Methods</p> <p>We analyzed first-episode SSTIs between January 1, 2005 and December 31, 2007 from the hospitalized claims data of a nationally representative sample of 1,000,000 people, about 5% of the population, enrolled in the Taiwan National Health Insurance program. We classified 18 groups of SSTIs into three major categories: 1) superficial; 2) deeper or healthcare-associated; and 3) gangrenous or necrotizing infections. Multivariate logistic regression models were applied to identify factors associated with intensive care unit (ICU) admission and hospital mortality.</p> <p>Results</p> <p>Of 146,686 patients ever hospitalized during the 3-year study period, we identified 11,390 (7.7%) patients having 12,030 SSTIs. Among these SSTI patients, 1,033 (9.1%) had ICU admission and 306 (2.7%) died at hospital discharge. The most common categories of SSTIs in ICU and non-ICU patients were "deeper or healthcare-associated" (62%) and "superficial" (60%) infections, respectively. Of all SSTI patients, 45.3% had comorbidities and 31.3% had non-SST infections. In the multivariate analyses adjusting for demographics and hospital levels, the presence of several comorbid conditions was associated with ICU admission or hospital mortality, but the results were inconsistent across most common SSTIs. In the same analyses, the presence of non-SST infections was consistently associated with increased risk of ICU admission (adjusted odds ratios [OR] 3.34, 95% confidence interval [CI] 2.91-3.83) and hospital mortality (adjusted OR 5.93, 95% CI 4.57-7.71).</p> <p>Conclusions</p> <p>The proportional distributions of various SSTIs differed between ICU and non-ICU patients. Nearly one-third of hospitalized SSTI patients had non-SST infections, and the presence of which predicted ICU admission and hospital mortality.</p

Evidence for a Rad18-Independent Frameshift Mutagenesis Pathway in Human Cell-Free Extracts

Bypass of replication blocks by specialized DNA polymerases is crucial for cell survival but may promote mutagenesis and genome instability. To gain insight into mutagenic sub-pathways that coexist in mammalian cells, we examined N-2-acetylaminofluorene (AAF)-induced frameshift mutagenesis by means of SV40-based shuttle vectors containing a single adduct. We found that in mammalian cells, as previously observed in E. coli, modification of the third guanine of two target sequences, 5'-GGG-3' (3G) and 5'-GGCGCC-3' (NarI site), induces –1 and –2 frameshift mutations, respectively. Using an in vitro assay for translesion synthesis, we investigated the biochemical control of these events. We showed that Pol eta, but neither Pol iota nor Pol zeta, plays a major role in the frameshift bypass of the AAF adduct located in the 3G sequence. By complementing PCNA-depleted extracts with either a wild-type or a non-ubiquitinatable form of PCNA, we found that this Pol eta-mediated pathway requires Rad18 and ubiquitination of PCNA. In contrast, when the AAF adduct is located within the NarI site, TLS is only partially dependent upon Pol eta and Rad18, unravelling the existence of alternative pathways that concurrently bypass this lesion

π0\pi^0 photoproduction on the proton for photon energies from 0.675 to 2.875 GeV

Differential cross sections for the reaction $\gamma p \to p \pi^0$ have been measured with the CEBAF Large Acceptance Spectrometer (CLAS) and a tagged photon beam with energies from 0.675 to 2.875 GeV. The results reported here possess greater accuracy in the absolute normalization than previous measurements. They disagree with recent CB-ELSA measurements for the process at forward scattering angles. Agreement with the SAID and MAID fits is found below 1 GeV. The present set of cross sections has been incorporated into the SAID database, and exploratory fits have been extended to 3 GeV. Resonance couplings have been extracted and compared to previous determinations.Comment: 18 pages, 48 figure

An Advanced Method to Assess the Diet of Free-Ranging Large Carnivores Based on Scats

<div><h3>Background</h3><p>The diet of free-ranging carnivores is an important part of their ecology. It is often determined from prey remains in scats. In many cases, scat analyses are the most efficient method but they require correction for potential biases. When the diet is expressed as proportions of consumed mass of each prey species, the consumed prey mass to excrete one scat needs to be determined and corrected for prey body mass because the proportion of digestible to indigestible matter increases with prey body mass. Prey body mass can be corrected for by conducting feeding experiments using prey of various body masses and fitting a regression between consumed prey mass to excrete one scat and prey body mass (correction factor 1). When the diet is expressed as proportions of consumed individuals of each prey species and includes prey animals not completely consumed, the actual mass of each prey consumed by the carnivore needs to be controlled for (correction factor 2). No previous study controlled for this second bias.</p> <h3>Methodology/Principal Findings</h3><p>Here we use an extended series of feeding experiments on a large carnivore, the cheetah (<em>Acinonyx jubatus</em>), to establish both correction factors. In contrast to previous studies which fitted a linear regression for correction factor 1, we fitted a biologically more meaningful exponential regression model where the consumed prey mass to excrete one scat reaches an asymptote at large prey sizes. Using our protocol, we also derive correction factor 1 and 2 for other carnivore species and apply them to published studies. We show that the new method increases the number and proportion of consumed individuals in the diet for large prey animals compared to the conventional method.</p> <h3>Conclusion/Significance</h3><p>Our results have important implications for the interpretation of scat-based studies in feeding ecology and the resolution of human-wildlife conflicts for the conservation of large carnivores.</p> </div

Search for new phenomena in final states with an energetic jet and large missing transverse momentum in pp collisions at √ s = 8 TeV with the ATLAS detector

Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses 20.3 fb−1 of √ s = 8 TeV data collected in 2012 with the ATLAS detector at the LHC. Events are required to have at least one jet with pT > 120 GeV and no leptons. Nine signal regions are considered with increasing missing transverse momentum requirements between Emiss T > 150 GeV and Emiss T > 700 GeV. Good agreement is observed between the number of events in data and Standard Model expectations. The results are translated into exclusion limits on models with either large extra spatial dimensions, pair production of weakly interacting dark matter candidates, or production of very light gravitinos in a gauge-mediated supersymmetric model. In addition, limits on the production of an invisibly decaying Higgs-like boson leading to similar topologies in the final state are presente

Lymphoid Tissue Damage in HIV-1 Infection Depletes Naïve T Cells and Limits T Cell Reconstitution after Antiretroviral Therapy

Highly active antiretroviral therapy (HAART) can suppress HIV-1 replication and normalize the chronic immune activation associated with infection, but restoration of naïve CD4+ T cell populations is slow and usually incomplete for reasons that have yet to be determined. We tested the hypothesis that damage to the lymphoid tissue (LT) fibroblastic reticular cell (FRC) network contributes to naïve T cell loss in HIV-1 infection by restricting access to critical factors required for T cell survival. We show that collagen deposition and progressive loss of the FRC network in LTs prior to treatment restrict both access to and a major source of the survival factor interleukin-7 (IL-7). As a consequence, apoptosis within naïve T cell populations increases significantly, resulting in progressive depletion of both naïve CD4+ and CD8+ T cell populations. We further show that the extent of loss of the FRC network and collagen deposition predict the extent of restoration of the naïve T cell population after 6 month of HAART, and that restoration of FRC networks correlates with the stage of disease at which the therapy is initiated. Because restoration of the FRC network and reconstitution of naïve T cell populations are only optimal when therapy is initiated in the early/acute stage of infection, our findings strongly suggest that HAART should be initiated as soon as possible. Moreover, our findings also point to the potential use of adjunctive anti-fibrotic therapies to avert or moderate the pathological consequences of LT fibrosis, thereby improving immune reconstitution

A novel aspect of the structure of the avian thymic medulla.

We provide evidence for the compartmentalization of the avian thymic medulla and identify the avian thymic dendritic cell. The thymic anlage develops from an epithelial cord of the branchial endoderm. Branches of the cord are separated by primary septae of neural crest origin. The dilation of the primary septae produces the keratin-negative area (KNA) of the thymic medulla and fills the gaps of the keratin-positive network (KPN). Morphometric analysis indicates that the KNA takes up about half of the volume of the thymic medulla, which has reticular connective tissue, like peripheral lymphoid organs. The KNA receives blood vessels and in addition to pericytes, the myoid cells of striated muscle structure occupy this area. The myoid cells are of branchial arch or prechordal plate origin providing indirect evidence for the neural crest origin of the KNA. The marginal epithelial cells of the KPN co-express keratin and vimentin intermediate filaments, which indicate their functional peculiarity. The basal lamina of the primary septum is discontinuous on the surface of the KPN providing histological evidence for the loss of the blood-thymus barrier in the medulla. In the center of the KNA, the dendritic cells lie in close association with blood vessels, whereas the B-cells accumulate along the KPN. The organization of the KPN and KNA increases the "surface" of the so-called cortico-medullary border, thereby contributing to the efficacy of central tolerance

CD133 Is a Marker of Bioenergetic Stress in Human Glioma

Mitochondria dysfunction and hypoxic microenvironment are hallmarks of cancer cell biology. Recently, many studies have focused on isolation of brain cancer stem cells using CD133 expression. In this study, we investigated whether CD133 expression is regulated by bioenergetic stresses affecting mitochondrial functions in human glioma cells. First, we determined that hypoxia induced a reversible up-regulation of CD133 expression. Second, mitochondrial dysfunction through pharmacological inhibition of the Electron Transport Chain (ETC) produced an up-regulation of CD133 expression that was inversely correlated with changes in mitochondrial membrane potential. Third, generation of stable glioma cells depleted of mitochondrial DNA showed significant and stable increases in CD133 expression. These glioma cells, termed rho0 or ρ0, are characterized by an exaggerated, uncoupled glycolytic phenotype and by constitutive and stable up-regulation of CD133 through many cell passages. Moreover, these ρ0 cells display the ability to form “tumor spheroids” in serumless medium and are positive for CD133 and the neural progenitor cell marker, nestin. Under differentiating conditions, ρ0 cells expressed multi-lineage properties. Reversibility of CD133 expression was demonstrated by transfering parental mitochondria to ρ0 cells resulting in stable trans-mitochondrial “cybrid” clones. This study provides a novel mechanistic insight about the regulation of CD133 by environmental conditions (hypoxia) and mitochondrial dysfunction (genetic and chemical). Considering these new findings, the concept that CD133 is a marker of brain tumor stem cells may need to be revised