482 research outputs found

    Bank performance and noninterest income: evidence from countries in the Asian region

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    Noninterest income (NII) is income generated by banks from sources other than interest payments. Studies conducted on the relationship between NII and bank risk for the USA and Europe have found that emphasis on income diversification lowers risk in European banks but exacerbates it in American banks. Current research on Asian banks has not led to a coherent view of the relationship between NII and bank risk. We employ data over 25 years for 24 Asian countries to examine this relationship. Using the GMM estimation approach we estimate equations for two time-periods, 1996–2007 and 2008–2018, to examine the NII-bank risk relationship in the presence of some controlling financial, macroeconomic and policy variables. Our results show that non-interest income worsens bank risk for all 24 countries as well as for sub-groups of countries. We also find that, by and large, economic growth improves bank risk while inflation above a threshold worsens it. Finally, our proxy measure for monetary policy improves bank risk though fiscal policy seems to have no effect

    Biopython: freely available Python tools for computational molecular biology and bioinformatics

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    Summary: The Biopython project is a mature open source international collaboration of volunteer developers, providing Python libraries for a wide range of bioinformatics problems. Biopython includes modules for reading and writing different sequence file formats and multiple sequence alignments, dealing with 3D macro molecular structures, interacting with common tools such as BLAST, ClustalW and EMBOSS, accessing key online databases, as well as providing numerical methods for statistical learning. Availability: Biopython is freely available, with documentation and source code at www.biopython.org under the Biopython license. Contact: All queries should be directed to the Biopython mailing lists, see www.biopython.org/wiki/[email protected]

    K-Bayes Reconstruction for Perfusion MRI I: Concepts and Application

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    Despite the continued spread of magnetic resonance imaging (MRI) methods in scientific studies and clinical diagnosis, MRI applications are mostly restricted to high-resolution modalities, such as structural MRI. While perfusion MRI gives complementary information on blood flow in the brain, its reduced resolution limits its power for detecting specific disease effects on perfusion patterns. This reduced resolution is compounded by artifacts such as partial volume effects, Gibbs ringing, and aliasing, which are caused by necessarily limited k-space sampling and the subsequent use of discrete Fourier transform (DFT) reconstruction. In this study, a Bayesian modeling procedure (K-Bayes) is developed for the reconstruction of perfusion MRI. The K-Bayes approach (described in detail in Part II: Modeling and Technical Development) combines a process model for the MRI signal in k-space with a Markov random field prior distribution that incorporates high-resolution segmented structural MRI information. A simulation study was performed to determine qualitative and quantitative improvements in K-Bayes reconstructed images compared with those obtained via DFT. The improvements were validated using in vivo perfusion MRI data of the human brain. The K-Bayes reconstructed images were demonstrated to provide reduced bias, increased precision, greater effect sizes, and higher resolution than those obtained using DFT

    The influence of river-derived particles on estuarine and marine elemental cycles: evidence from lithium isotopes

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    To examine the alteration of river-derived sediments through a large estuary and the implications for elemental cycling and global climate, this study analyses lithium (Li) isotopes and elemental concentrations (e.g., Li, Na, Mg, K, Ca, Fe and Al) of both the dissolved load and different phases of the sediment load (i.e., exchangeable, carbonate, oxide, clay and residue) in the Amazon estuary. The results show that river-derived sediments remove Li from the dissolved load, largely due to cation retention in secondary clays. By modelling the Li mass-balance and isotope fractionation, we estimate that the river-derived sediments gain 3–4 μg/g Li from the dissolved load in the Amazon estuary, with a Li isotope fractionation factor (αclay-solution) of approximately 0.975. Considering the whole Amazon estuary, the river-derived sediments remove around 3.6–4.8 × 109 g/yr of Li from the dissolved load. Specifically, around 1.0–1.7 × 108 g/yr of Li is removed from river water (∼1.8–3.0% of the dissolved Li discharge flux of the Amazon River) and around 3.5–4.7 × 109 g/yr of Li is removed from seawater, which represents a significant sink from the ocean. This estuarine Li sink is likely to be related to continental erosion rates; thus, continental weathering and erosion regimes could influence not only riverine Li input, but could also directly affect the Li sink, leading to a dual control on the Li budget and isotope composition in the ocean

    Single-Walled Carbon Nanotube (SWCNT)-induced interstitial fibrosis in the lungs of rats is associated with increased levels of PDGF mRNA and the formation of unique intercellular carbon structures that bridge alveolar macrophages In Situ

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    BACKGROUND: Nanotechnology is a rapidly advancing industry with many new products already available to the public. Therefore, it is essential to gain an understanding of the possible health risks associated with exposure to nanomaterials and to identify biomarkers of exposure. In this study, we investigated the fibrogenic potential of SWCNT synthesized by chemical vapor deposition using cobalt (Co) and molybdenum (Mo) as catalysts. Following a single oropharyngeal aspiration of SWCNT in rats, we evaluated lung histopathology, cell proliferation, and growth factor mRNAs at 1 and 21 days post-exposure. Comparisons were made to vehicle alone (saline containing a biocompatible nonionic surfactant), inert carbon black (CB) nanoparticles, or vanadium pentoxide (V(2)O(5)) as a known inducer of fibrosis. RESULTS: SWCNT or CB caused no overt inflammatory response at 1 or 21 days post-exposure as determined by histopathology and evaluation of cells (>95% macrophages) in bronchoalveolar lavage (BAL) fluid. However, SWCNT induced the formation of small, focal interstitial fibrotic lesions within the alveolar region of the lung at 21 days. A small fraction of alveolar macrophages harvested by BAL from the lungs of SWCNT-exposed rats at 21 days were bridged by unique intercellular carbon structures that extended into the cytoplasm of each macrophage. These "carbon bridge" structures between macrophages were also observed in situ in the lungs of SWCNT-exposed rats. No carbon bridges were observed in CB-exposed rats. SWCNT caused cell proliferation only at sites of fibrotic lesion formation as measured by bromodeoxyuridine uptake into alveolar cells. SWCNT increased platelet-derived growth factor (PDGF)-A, PDGF-B, and PDGF-C mRNA levels significantly at 1 day as measured by Taqman quantitative real-time RT-PCR. At 21 days, SWCNT did not increase any mRNAs evaluated, while V(2)O(5 )significantly increased mRNAs encoding PDGF-A, -B, and -C chains, PDGF-Rα, osteopontin (OPN), connective tissue growth factor (CTGF), and transforming growth factor (TGF)-β1. CONCLUSION: Our findings indicate that SWCNT do not cause lung inflammation and yet induce the formation of small, focal interstital fibrotic lesioins in the alveolar region of the lungs of rats. Of greatest interest was the discovery of unique intercellular carbon structures composed of SWCNT that bridged lung macrophages. These "carbon bridges" offer a novel and easily identifiable biomarker of exposure

    Respiratory syncytial virus infection reduces lung inflammation and fibrosis in mice exposed to vanadium pentoxide

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    <p>Abstract</p> <p>Background</p> <p>Vanadium pentoxide (V<sub>2</sub>O<sub>5</sub>) exposure is a cause of occupational bronchitis and airway fibrosis. Respiratory syncytial virus (RSV) is a ubiquitous pathogen that causes airway inflammation. It is unknown whether individuals with pre-existing respiratory viral infection are susceptible to V<sub>2</sub>O<sub>5</sub>-induced bronchitis. We hypothesized that respiratory viral infection will exacerbate vanadium-induced lung fibrosis.</p> <p>Methods</p> <p>In this study we investigated the effect of RSV pre- or post-exposure to V<sub>2</sub>O<sub>5 </sub>in male AKR mice. Mice were pre-exposed by intranasal aspiration to RSV or media vehicle prior to intranasal aspiration of V<sub>2</sub>O<sub>5 </sub>or saline vehicle at day 1 or day 7. A parallel group of mice were treated first with V<sub>2</sub>O<sub>5 </sub>or saline vehicle at day 1 and day 7 then post-exposed to RSV or media vehicle at day 8.</p> <p>Results</p> <p>V<sub>2</sub>O<sub>5</sub>-induced airway inflammation and fibrosis were decreased by RSV pre- or post-exposure. Real time quantitative RT-PCR showed that V<sub>2</sub>O<sub>5 </sub>significantly increased lung mRNAs encoding pro-fibrogenic growth factors (TGF-β1, CTGF, PDGF-C) and collagen (Col1A2), but also increased mRNAs encoding anti-fibrogenic type I interferons (IFN-α, -β) and IFN-inducible chemokines (CXCL9 and CXCL10). RSV pre- or post-exposure caused a significantly reduced mRNAs of pro-fibrogenic growth factors and collagen, yet reduced RNA levels of anti-fibrogenic interferons and CXC chemokines.</p> <p>Conclusions</p> <p>Collectively these data suggest that RSV infection reduces the severity of V<sub>2</sub>O<sub>5</sub>-induced fibrosis by suppressing growth factors and collagen genes. However, RSV suppression of V<sub>2</sub>O<sub>5</sub>-induced IFNs and IFN-inducible chemokines suggests that viral infection also suppresses the innate immune response that normally serves to resolve V<sub>2</sub>O<sub>5</sub>-induced fibrosis.</p

    Early evolution of the extraordinary Nova Del 2013 (V339 Del)

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    We determine the temporal evolution of the luminosity L(WD), radius R(WD) and effective temperature Teff of the white dwarf (WD) pseudophotosphere of V339 Del from its discovery to around day 40. Another main objective was studying the ionization structure of the ejecta. These aims were achieved by modelling the optical/near-IR spectral energy distribution (SED) using low-resolution spectroscopy (3500 - 9200 A), UBVRcIc and JHKLM photometry. During the fireball stage (Aug. 14.8 - 19.9, 2013), Teff was in the range of 6000 - 12000 K, R(WD) was expanding non-uniformly in time from around 66 to around 300 (d/3 kpc) R(Sun), and L(WD) was super-Eddington, but not constant. After the fireball stage, a large emission measure of 1.0-2.0E+62 (d/3 kpc)**2 cm**(-3) constrained the lower limit of L(WD) to be well above the super-Eddington value. The evolution of the H-alpha line and mainly the transient emergence of the Raman-scattered O VI 1032 A line suggested a biconical ionization structure of the ejecta with a disk-like H I region persisting around the WD until its total ionization, around day 40. It is evident that the nova was not evolving according to the current theoretical prediction. The unusual non-spherically symmetric ejecta of nova V339 Del and its extreme physical conditions and evolution during and after the fireball stage represent interesting new challenges for the theoretical modelling of the nova phenomenon.Comment: 14 pages, 9 figures, 3 tables, accepted for Astronomy and Astrophysic

    Helminth resistance is mediated by differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

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    Macrophages are known to mediate anti-helminth responses, but it remains uncertain which subsets are involved or how macrophages actually kill helminths. Here, we show rapid monocyte recruitment to the lung after infection with the nematode parasite Nippostrongylus brasiliensis. In this inflamed tissue microenvironment, these monocytes differentiate into an alveolar macrophage (AM)-like phenotype, expressing both SiglecF and CD11c, surround invading parasitic larvae, and preferentially kill parasites in vitro. Monocyte-derived AMs (Mo-AMs) express type 2-associated markers and show a distinct remodeling of the chromatin landscape relative to tissue-derived AMs (TD-AMs). In particular, they express high amounts of arginase-1 (Arg1), which we demonstrate mediates helminth killing through L-arginine depletion. These studies indicate that recruited monocytes are selectively programmed in the pulmonary environment to express AM markers and an anti-helminth phenotype
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