6,281 research outputs found
Method and apparatus for producing microshells
A method is described for forming hollow particles, or shells, of extremely small size. The shell material is heated to a molten temperature in the presence of a gas that is at least moderately soluble in the shell material, to form a solution of the molten shell material and the soluble gas. The solution is atomized to form a multiplicity of separate droplets that are cooled while in free fall. Cooling of a droplet from the outside traps the desolved gas and forces it to form a gas bubble at the center of the droplet which now forms a gas filled shell. The shell is reheated and then cooled in free fall, in an environment having a lower pressure than the gas pressure in the shell. This causes expansion of the shell and the formation of a shell having a small wall thickness compared to its diameter
Are There Thresholds of Current Account Adjustment in the G7?
We find evidence of threshold behavior in current account adjustment for the G7 countries, such that the dynamics of adjustment towards equilibrium depend upon whether the current-account/ net-output ratio breaches estimated, country specific current account surplus or deficit thresholds. Both the speeds of adjustment and the size of the thresholds are found to differ significantly across countries. In addition, we also find evidence of shifts in means and variances of exchange rate changes, stock returns, and interest differentials that coincide with the current account adjustment regimes identified by the model.
Clinical practice guidelines for the management of atypical haemolytic uraemic syndrome in the United Kingdom
The Transition between Nonorthogonal Polarization Modes in PSR B2016+28 at 1404 MHz
Polarization observations of the radio emission from PSR B2016+28 at 1404 MHz
reveal properties that are consistent with two, very different, interpretations
of the pulsar's viewing geometry. The pulsar's average polarization properties
show a rapid change in position angle (PA) near the pulse center, suggesting
that the observer's sightline nearly intersects the star's magnetic pole. But
single pulse, polarization observations of the pulsar show nearly orthogonal
modes of polarization following relatively flat and parallel PA trajectories
across the pulse, suggesting that the sightline is far from the pole.
Additionally, PA histograms reveal a "modal connecting bridge", of unknown
origin, joining the modal PA trajectories over much of the pulse and following
the rapid PA change shown in the average data. The nonorthogonality of
polarization modes is incorporated in a statistical model of radio polarization
to account for the deviations from mode orthogonality that are observed in the
pulsar. The model is used to interpret the rapid PA change and modal connecting
bridge as a longitudinally-resolved transition between modes of nonorthogonal
polarization. Thus, the modal PA trajectories are argued to reflect the
pulsar's true viewing geometry. This interpretation is consistent with the
pulsar's morphological classification, preserves the Radhakrishnan & Cooke
model of pulsar radio emission, and avoids the complication that the modal
connecting bridge might be produced by some other emission mechanism. The
statistical model's ability to simulate the rich variety of polarization
properties observed in the emission lends additional support to the model's
applicability and its underlying assumption that the polarization modes occur
simultaneously.Comment: Accepted for publication in Ap
Recreation of the terminal events in physiological integrin activation.
Increased affinity of integrins for the extracellular matrix (activation) regulates cell adhesion and migration, extracellular matrix assembly, and mechanotransduction. Major uncertainties concern the sufficiency of talin for activation, whether conformational change without clustering leads to activation, and whether mechanical force is required for molecular extension. Here, we reconstructed physiological integrin activation in vitro and used cellular, biochemical, biophysical, and ultrastructural analyses to show that talin binding is sufficient to activate integrin alphaIIbbeta3. Furthermore, we synthesized nanodiscs, each bearing a single lipid-embedded integrin, and used them to show that talin activates unclustered integrins leading to molecular extension in the absence of force or other membrane proteins. Thus, we provide the first proof that talin binding is sufficient to activate and extend membrane-embedded integrin alphaIIbbeta3, thereby resolving numerous controversies and enabling molecular analysis of reconstructed integrin signaling
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The Term Structure of Forward Exchange Rates and the Forecastability of Spot Exchange Rates: Correcting the Errors
This paper revisits one of the oldest questions in international finance: does the forward exchange rate contain useful information about of the future path of the spot exchange rate? We present a theoretical framework and provide evidence that challenges the common view (Mussa (1979); Dornbusch (1980); Frenkel (1981); Cumby-Obstfeld (1984) that forward premia contain little information regarding subsequent changes in the spot exchange rate. Using weekly dollar-DM and dollar-sterling data on spot exchange rates and 1, 3, 6., and 12 month forward exchange rates, we find that, as predicted by the theoretical framework the term structure of forward exchange rates together with the spot exchange rate comprise a system that is well represented by a vector vector correction model. Employing Johansen's (1991) maximum likelihood approach, we test and confirm for each country the existence of 4 cointegrating relationships as predicted by the theory. We then test and confirm for each country the joint hypothesis that a basis for this cointegrating space is the vector of 4 forward premia. We next test, and reject for each country, the hypothesis that the spot exchange rate is weekly exogenous with respect to the term structure of forward rates. Out-of-sample simulations indicate that the information contained in the term structure of forward premia can be used to reduce the mean squared error in forecasting the spot rate by at least 33 percent at 6 month horizon and 50 percent at a 1 year horizon
Machinery Productivity Estimates from Seed Tenders
Several methods and machines have been introduced during the last five years that can improve the timeliness and productivity of planting operations. Several manufacturers claim these devices can increase productivity by more than 50% over conventional methods. This paper provides insights on the improvement of corn and soybean planting systems, while using a seed tender and other similar devices. A comparison between machine operations is analyzed with the assumptions made by these claims. While the claims may be valid, farm clientele deserve to know the conditions under which these improvements can be expected. The results can assist farmers in evaluating how these purchases influence machine productivity, and how to identify potential operational areas that can improve their productivity with existing machinery systems. It also provides better estimates for parameters currently listed as ranges within the ASABE Standards
Chemotropic guidance facilitates axonal regeneration and synapse formation after spinal cord injury.
A principal objective of spinal cord injury (SCI) research is the restoration of axonal connectivity to denervated targets. We tested the hypothesis that chemotropic mechanisms would guide regenerating spinal cord axons to appropriate brainstem targets. We subjected rats to cervical level 1 (C1) lesions and combinatorial treatments to elicit axonal bridging into and beyond lesion sites. Lentiviral vectors expressing neurotrophin-3 (NT-3) were then injected into an appropriate brainstem target, the nucleus gracilis, and an inappropriate target, the reticular formation. NT-3 expression in the correct target led to reinnervation of the nucleus gracilis in a dose-related fashion, whereas NT-3 expression in the reticular formation led to mistargeting of regenerating axons. Axons regenerating into the nucleus gracilis formed axodendritic synapses containing rounded vesicles, reflective of pre-injury synaptic architecture. Thus, we report for the first time, to the best of our knowledge, the reinnervation of brainstem targets after SCI and an essential role for chemotropic axon guidance in target selection
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The dynamic switch mechanism that leads to activation of LRRK2 is embedded in the DFGÏ motif in the kinase domain.
Leucine-rich repeat kinase 2 (LRRK2) is a large multidomain protein, and LRRK2 mutants are recognized risk factors for Parkinson's disease (PD). Although the precise mechanisms that control LRRK2 regulation and function are unclear, the importance of the kinase domain is strongly implicated, since 2 of the 5 most common familial LRRK2 mutations (G2019S and I2020T) are localized to the conserved DFGÏ motif in the kinase core, and kinase inhibitors are under development. Combining the concept of regulatory (R) and catalytic (C) spines with kinetic and cell-based assays, we discovered a major regulatory mechanism embedded within the kinase domain and show that the DFG motif serves as a conformational switch that drives LRRK2 activation. LRRK2 is quite unusual in that the highly conserved Phe in the DFGÏ motif, which is 1 of the 4 R-spine residues, is replaced with tyrosine (DY2018GI). A Y2018F mutation creates a hyperactive phenotype similar to the familial mutation G2019S. The hydroxyl moiety of Y2018 thus serves as a "brake" that stabilizes an inactive conformation; simply removing it destroys a key hydrogen-bonding node. Y2018F, like the pathogenic mutant I2020T, spontaneously forms LRRK2-decorated microtubules in cells, while the wild type and G2019S require kinase inhibitors to form filaments. We also explored 3 different mechanisms that create kinase-dead pseudokinases, including D2017A, which further emphasizes the highly synergistic role of key hydrophobic and hydrophilic/charged residues in the assembly of active LRRK2. We thus hypothesize that LRRK2 harbors a classical protein kinase switch mechanism that drives the dynamic activation of full-length LRRK2
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