1,170 research outputs found
Fine Points for Broad Bumps: The Extension of Rietveld Refinement for Benchtop Powder XRD Analysis of Ultra-Small Supported Nanoparticles
The goal of this work is to demonstrate the capabilities of benchtop Bragg diffraction in characterizing ultra-small (\u3c 2nm) nanoparticles. To this end we have established a method for accurately separating the background, adjusting for relevant intensity effects, and analyzing the results with Rietveld refinement. This method is applied to the characterization of six silica-supported “noble” metals under ambient conditions: Pt, Pd, Ir, Rh, Ru, and Au. Surprisingly, Bragg diffraction is capable of shining light on this difficult-to-characterize size region – revealing the propensity of these metal nanoparticles to oxidize at room temperature. Preliminary findings for future work are also discussed: extending our method to crystalline supports and fluorescent samples
Structure factors of harmonic and anharmonic Fibonacci chains by molecular dynamics simulations
The dynamics of quasicrystals is characterized by the existence of phason
excitations in addition to the usual phonon modes. In order to investigate
their interplay on an elementary level we resort to various one-dimensional
model systems. The main observables are the static, the incoherent, and the
coherent structure factor, which are extracted from molecular dynamics
simulations. For the validation of the algorithms, results for the harmonic
periodic chain are presented. We then study the Fibonacci chain with harmonic
and anharmonic interaction potentials. In the dynamic Fibonacci chain
neighboring atoms interact by double-well potentials allowing for phason flips.
The difference between the structure factors of the dynamic and the harmonic
Fibonacci chain lies in the temperature dependence of the phonon line width. If
a bias is introduced in the well depth, dispersionless optic phonon bands split
off.Comment: 12 pages, 15 figure
Parallel suppression of superconductivity and Fe moment in the collapsed tetragonal phase of Ca0.67Sr0.33Fe2As2 under pressure
Using non-resonant Fe K-beta x-ray emission spectroscopy, we reveal that
Sr-doping of CaFe2As2 decouples the Fe moment from the volume collapse
transition, yielding a collapsed-tetragonal, paramagnetic normal state out of
which superconductivity develops. X-ray diffraction measurements implicate the
c-axis lattice parameter as the controlling criterion for the Fe moment,
promoting a generic description for the appearance of pressure-induced
superconductivity in the alkaline-earth-based 122 ferropnictides (AFe2As2). The
evolution of the superconducting critical temperature with pressure lends
support to theories for superconductivity involving unconventional pairing
mediated by magnetic fluctuations
Human pathogen shown to cause disease in the threatened elkhorn coral Acropora palmata
Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch\u27s postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine “reverse zoonosis” involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival
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Calcium puffs are generic InsP<sub>3</sub>-activated elementary calcium signals and are downregulated by prolonged hormonal stimulation to inhibit cellular calcium responses
Elementary Ca2+ signals, such as "Ca2+ puffs", which arise from the activation of inositol 1,4,5-trisphosphate receptors, are building blocks for local and global Ca2+ signalling. We characterized Ca2+ puffs in six cell types that expressed differing ratios of the three inositol 1,4,5-trisphosphate receptor isoforms. The amplitudes, spatial spreads and kinetics of the events were similar in each of the cell types. The resemblance of Ca2+ puffs in these cell types suggests that they are a generic elementary Ca2+ signal and, furthermore, that the different inositol 1,4,5-trisphosphate isoforms are functionally redundant at the level of subcellular Ca2+ signalling. Hormonal stimulation of SH-SY5Y neuroblastoma cells and HeLa cells for several hours downregulated inositol 1,4,5-trisphosphate expression and concomitantly altered the properties of the Ca2+ puffs. The amplitude and duration of Ca2+ puffs were substantially reduced. In addition, the number of Ca2+ puff sites active during the onset of a Ca2+ wave declined. The consequence of the changes in Ca2+ puff properties was that cells displayed a lower propensity to trigger regenerative Ca2+ waves. Therefore, Ca2+ puffs underlie inositol 1,4,5-trisphosphate signalling in diverse cell types and are focal points for regulation of cellular responses
Human Pathogen Shown to Cause Disease in the Threatened Elkhorn Coral Acropora palmata
Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch\u27s postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine \u27\u27reverse zoonosis\u27\u27 involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival
Linalool inhibits the angiogenic activity of endothelial cells by downregulating intracellular ATP levels and activating TRPM8
Angiogenesis crucially contributes to various diseases, such as cancer and diabetic retinopathy. Hence, anti-angiogenic therapy is considered as a powerful strategy against these diseases. Previous studies reported that the acyclic monoterpene linalool exhibits anticancer, anti-inflammatory and anti-oxidative activity. However, the effects of linalool on angiogenesis still remain elusive. Therefore, we investigated the action of (3R)-(−)-linalool, a main enantiomer of linalool, on the angiogenic activity of human dermal microvascular endothelial cells (HDMECs) by a panel of angiogenesis assays. Non-cytotoxic doses of linalool significantly inhibited HDMEC proliferation, migration, tube formation and spheroid sprouting. Linalool also suppressed the vascular sprouting from rat aortic rings. In addition, Matrigel plugs containing linalool exhibited a significantly reduced microvessel density 7 days after implantation into BALB/c mice. Mechanistic analyses revealed that linalool promotes the phosphorylation of extracellular signal-regulated kinase (ERK), downregulates the intracellular level of adenosine triphosphate (ATP) and activates the transient receptor potential cation channel subfamily M (melastatin) member (TRPM)8 in HDMECs. Inhibition of ERK signaling, supplementation of ATP and blockade of TRPM8 significantly counteracted linalool-suppressed HDMEC spheroid sprouting. Moreover, ATP supplementation completely reversed linalool-induced ERK phosphorylation. In addition, linalool-induced ERK phosphorylation inhibited the expression of bone morphogenetic protein (BMP)-2 and linalool-induced TRPM8 activation caused the inhibition of β1 integrin/focal adhesion kinase (FAK) signaling. These findings indicate an anti-angiogenic effect of linalool, which is mediated by downregulating intracellular ATP levels and activating TRPM8
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