648 research outputs found

    AN APPROACH TO DETERMINE THE EFFECT OF EL NINO ON EXTREME DAILY WEATHER OCCURRENCE

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    We developed a procedure using the chi-square statistic to determine the effect of El Nino- Southern Oscillation on the frequency of extreme daily weather occurrence. Its application is demonstrated for a site in southwestern Montana, located east of the Continental Divide 970 km from the Pacific Ocean. The study used daily weather data focused on a 29-wk period from 3 Dec to 23 Jun in a 100-yr weather record at Montana State University (Bozeman) and compared this weather in relation to November-March sea-surface temperature anomalies in an area of the eastern tropical Pacific Ocean. Daily weather extremes were compared between 25 El Nino years and 50 ‘normal’ years. During El Nino years, December-June weather at Bozeman was characterized by more days of extreme high maximum temperatures, fewer days of extreme low minimum temperatures, fewer days of high precipitation amounts, and fewer days with small diurnal temperature ranges. For the 29-wk period, we determined the difference between El Nino years and normal years to be about 20 percent for each of these four extreme daily weather conditions. An increase or decrease of extreme daily weather occurrences can impact natural resources and a wide range of human activities including agriculture, forestry, recreation, construction, and other businesses

    Slip statistics of dislocation avalanches under different loading modes

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    Slowly compressed microcrystals deform via intermittent slip events, observed as displacement jumps or stress drops. Experiments often use one of two loading modes: an increasing applied stress (stress driven, soft), or a constant strain rate (strain driven, hard). In this work we experimentally test the influence of the deformation loading conditions on the scaling behavior of slip events. It is found that these common deformation modes strongly affect time series properties, but not the scaling behavior of the slip statistics when analyzed with a mean-field model. With increasing plastic strain, the slip events are found to be smaller and more frequent when strain driven, and the slip-size distributions obtained for both drives collapse onto the same scaling function with the same exponents. The experimental results agree with the predictions of the used mean-field model, linking the slip behavior under different loading modes

    Protein kinase C theta is required for efficient induction of IL-10-secreting T cells

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    <div><p>Secretion of interleukin-10 (IL-10) by CD4<sup>+</sup> T cells is an essential immunoregulatory mechanism. The work presented here assesses the role of the signaling molecule protein kinase C theta (PKCθ) in the induction of IL-10 expression in CD4<sup>+</sup> T cells. Using wildtype and PKCθ-deficient Tg4 T cell receptor transgenic mice, we implemented a well-described protocol of repeated doses of myelin basic protein (MBP)Ac1-9[4Y] antigen to induce Tr1-like IL-10<sup>+</sup> T cells. We find that PKCθ is required for the efficient induction of IL-10 following antigen administration. Both serum concentrations of IL-10 and the proportion of IL-10<sup>+</sup> T cells were reduced in PKCθ-deficient mice relative to wildtype mice following [4Y] treatment. We further characterized the T cells of [4Y] treated PKCθ-deficient Tg4 mice and found reduced expression of the transcription factors cMaf, Nfil3 and FoxP3 and the surface receptors PD-1 and Tim3, all of which have been associated with the differentiation or function of IL-10<sup>+</sup> T cells. Finally, we demonstrated that, unlike [4Y] treated wildtype Tg4 T cells, cells from PKCθ-deficient mice were unable to suppress the priming of naïve T cells <i>in vitro</i> and <i>in vivo</i>. In summary, we present data demonstrating a role for PKCθ in the induction of suppressive, IL-10-secreting T cells induced in TCR-transgenic mice following chronic antigen administration. This should be considered when contemplating PKCθ as a suitable drug target for inducing immune suppression and graft tolerance.</p></div

    Bayesian model comparison in cosmology with Population Monte Carlo

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    We use Bayesian model selection techniques to test extensions of the standard flat LambdaCDM paradigm. Dark-energy and curvature scenarios, and primordial perturbation models are considered. To that end, we calculate the Bayesian evidence in favour of each model using Population Monte Carlo (PMC), a new adaptive sampling technique which was recently applied in a cosmological context. The Bayesian evidence is immediately available from the PMC sample used for parameter estimation without further computational effort, and it comes with an associated error evaluation. Besides, it provides an unbiased estimator of the evidence after any fixed number of iterations and it is naturally parallelizable, in contrast with MCMC and nested sampling methods. By comparison with analytical predictions for simulated data, we show that our results obtained with PMC are reliable and robust. The variability in the evidence evaluation and the stability for various cases are estimated both from simulations and from data. For the cases we consider, the log-evidence is calculated with a precision of better than 0.08. Using a combined set of recent CMB, SNIa and BAO data, we find inconclusive evidence between flat LambdaCDM and simple dark-energy models. A curved Universe is moderately to strongly disfavoured with respect to a flat cosmology. Using physically well-motivated priors within the slow-roll approximation of inflation, we find a weak preference for a running spectral index. A Harrison-Zel'dovich spectrum is weakly disfavoured. With the current data, tensor modes are not detected; the large prior volume on the tensor-to-scalar ratio r results in moderate evidence in favour of r=0. [Abridged]Comment: 11 pages, 6 figures. Matches version accepted for publication by MNRA

    Dark energy constraints and correlations with systematics from CFHTLS weak lensing, SNLS supernovae Ia and WMAP5

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    We combine measurements of weak gravitational lensing from the CFHTLS-Wide survey, supernovae Ia from CFHT SNLS and CMB anisotropies from WMAP5 to obtain joint constraints on cosmological parameters, in particular, the dark energy equation of state parameter w. We assess the influence of systematics in the data on the results and look for possible correlations with cosmological parameters. We implement an MCMC algorithm to sample the parameter space of a flat CDM model with a dark-energy component of constant w. Systematics in the data are parametrised and included in the analysis. We determine the influence of photometric calibration of SNIa data on cosmological results by calculating the response of the distance modulus to photometric zero-point variations. The weak lensing data set is tested for anomalous field-to-field variations and a systematic shape measurement bias for high-z galaxies. Ignoring photometric uncertainties for SNLS biases cosmological parameters by at most 20% of the statistical errors, using supernovae only; the parameter uncertainties are underestimated by 10%. The weak lensing field-to-field variance pointings is 5%-15% higher than that predicted from N-body simulations. We find no bias of the lensing signal at high redshift, within the framework of a simple model. Assuming a systematic underestimation of the lensing signal at high redshift, the normalisation sigma_8 increases by up to 8%. Combining all three probes we obtain -0.10<1+w<0.06 at 68% confidence (-0.18<1+w<0.12 at 95%), including systematic errors. Systematics in the data increase the error bars by up to 35%; the best-fit values change by less than 0.15sigma. [Abridged]Comment: 14 pages, 10 figures. Revised version, matches the one to be published in A&A. Modifications have been made corresponding to the referee's suggestions, including reordering of some section

    Isomer shift and magnetic moment of the long-lived 1/2+^{+} isomer in 3079^{79}_{30}Zn49_{49}: signature of shape coexistence near 78^{78}Ni

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    Collinear laser spectroscopy has been performed on the 3079^{79}_{30}Zn49_{49} isotope at ISOLDE-CERN. The existence of a long-lived isomer with a few hundred milliseconds half-life was confirmed, and the nuclear spins and moments of the ground and isomeric states in 79^{79}Zn as well as the isomer shift were measured. From the observed hyperfine structures, spins I=9/2I = 9/2 and I=1/2I = 1/2 are firmly assigned to the ground and isomeric states. The magnetic moment μ\mu (79^{79}Zn) = −-1.1866(10) μN\mu_{\rm{N}}, confirms the spin-parity 9/2+9/2^{+} with a νg9/2−1\nu g_{9/2}^{-1} shell-model configuration, in excellent agreement with the prediction from large scale shell-model theories. The magnetic moment μ\mu (79m^{79m}Zn) = −-1.0180(12) μN\mu_{\rm{N}} supports a positive parity for the isomer, with a wave function dominated by a 2h-1p neutron excitation across the N=50N = 50 shell gap. The large isomer shift reveals an increase of the intruder isomer mean square charge radius with respect to that of the ground state: δ⟨rc2⟩79,79m\delta \langle r^{2}_{c}\rangle^{79,79m} = +0.204(6) fm2^{2}, providing first evidence of shape coexistence.Comment: 5 pages, 4 figures, 1 table, Accepeted by Phys. Rev. Lett. (2016

    Childhood onset of Scheie syndrome, the attenuated form of mucopolysaccharidosis I

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    Scheie syndrome is the most attenuated and rarest form of mucopolysaccharidosis type I (MPS I), an inherited lysosomal storage disorder. Only small patient series have previously been reported. Using natural history data from the uniquely large population of 78 Scheie patients enrolled in the MPS I Registry, we characterized the onset and prevalence of clinical manifestations and explored reasons for delayed diagnosis of the disease. Median patient age was 17.5 years; 46% of the patients were male, and 88% were Caucasian. Of 25 MPS I-related clinical features, cardiac valve abnormalities, joint contractures, and corneal clouding were each reported by >80% and all three by 53% of patients. Carpal tunnel syndrome, hernia, coarse facial features, and hepatomegaly were each reported by >50% of patients. Age at onset of the clinical features varied widely between individuals, but the median age at onset was 3 years for hernia and between 5 and 12 years for most features, including coarse facial features, hepatomegaly, joint contractures, bone deformities, cardiac valve abnormalities, cognitive impairment, and corneal clouding. Carpal tunnel syndrome, cardiomyopathy, and myelopathy arose more commonly during adolescence or adulthood. Delays up to 47 years intervened between symptom onset and disease diagnosis, and the longest delays were associated with later age at symptom onset and symptom onset before 1980. In summary, Scheie syndrome usually emerges during childhood, and recognition of attenuated MPS I requires awareness of the multisystemic disease manifestations and their diverse presentation. Given the availability of etiologic treatment, prompt diagnosis is important

    Lock-in Amplifier as a Sensitive Instrument for Biomedical Measurement : Analysis and Implementation

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    A measuring instrument plays important role in the biomedical measurement since the biological process in living organism generates very weak signal. Therefore, a reliable and sensitive measuring instrument is needed. In this study, a lock-in amplifier was analysed and tested. This paper presents an experiment to investigate the lock-in amplifier for biomedical measurement. An experiment using RC (resistor capacitor) tissue model to measure the voltage change related to impedance change was performed using a lock-in amplifier to evaluate the accuracy of the lock-in amplifier. Three different values of the capacitor in the RC tissue model were applied regarding to simulate small impedance changes. The measurement results were compared with the theoretical calculation and an impedance measurement system. An error analysis was conducted to investigate the accuracy of the measurement. The comparison result showed that impedance measurement using lock-in amplifier is an effective technique, which could able to measure very small voltage regarding impedance change in the RC tissue model

    Atherogenic Lipid Stress Induces Platelet Hyperactivity Through CD36-Mediated Hyposensitivity To Prostacyclin-; The Role Of Phosphodiesterase 3A

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    Prostacyclin (PGI2) controls platelet activation and thrombosis through a cyclic adenosine monophosphate (cAMP) signalling cascade. However, in patients with cardiovascular diseases this protective mechanism fails for reasons that are unclear. Using both pharmacological and genetic approaches we describe a mechanism by which oxidised low density lipoproteins (oxLDL) associated with dyslipidaemia promote platelet activation through impaired PGI2 sensitivity and diminished cAMP signalling. In functional assays using human platelets, oxLDL modulated the inhibitory effects of PGI2, but not a PDE-insensitive cAMP analogue, on platelet aggregation, granule secretion and in vitro thrombosis. Examination of the mechanism revealed that oxLDL promoted the hydrolysis of cAMP through the phosphorylation and activation of phosphodiesterase 3A (PDE3A), leading to diminished cAMP signalling. PDE3A activation by oxLDL required Src family kinases, Syk and protein kinase C. The effects of oxLDL on platelet function and cAMP signalling were blocked by pharmacological inhibition of CD36, mimicked by CD36-specific oxidised phospholipids and ablated in CD36-/- murine platelets. The injection of oxLDL into wild type mice strongly promoted FeCl3 induced carotid thrombosis in vivo, which was prevented by pharmacological inhibition of PDE3A. Furthermore, blood from dyslipidaemic mice was associated with increased oxidative lipid stress, reduced platelet sensitivity to PGI2 ex vivo and diminished PKA signalling. In contrast, platelet sensitivity to a PDE-resistant cAMP analogue remained normal. Genetic deletion of CD36, protected dyslipidaemic animals from PGI2 hyposensitivity and restored PKA signalling. These data suggest that CD36 can translate atherogenic lipid stress into platelet hyperactivity through modulation of inhibitory cAMP signalling.  
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