21 resultados para INITIAL MASS FUNCTION


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We present all relevant details of our calculation of the complete next-to-leading order O(αS2α) QCD corrections to heavy flavor photoproduction with longitudinally polarized point-like photons and hadrons. In particular we provide analytical results for the virtual plus soft gluon cross section. We carefully address the relevance of remaining theoretical uncertainties by varying, for instance, the factorization and renormalization scales independently. Such studies are of importance for a meaningful first direct determination of the polarized gluon density Δg from the total charm production spin asymmetry by the upcoming COMPASS experiment. It is shown that the scale uncertainty is considerably reduced in next-to-leading order, but the dependence on the charm quark mass is sizable at fixed target energies. Finally, we study several differential single-inclusive heavy quark distributions and, for the polarized HERA option, the total bottom spin asymmetry.

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We study the solutions of the Smoluchowski coagulation equation with a regularization term which removes clusters from the system when their mass exceeds a specified cutoff size, M. We focus primarily on collision kernels which would exhibit an instantaneous gelation transition in the absence of any regularization. Numerical simulations demonstrate that for such kernels with monodisperse initial data, the regularized gelation time decreasesas M increases, consistent with the expectation that the gelation time is zero in the unregularized system. This decrease appears to be a logarithmically slow function of M, indicating that instantaneously gelling kernels may still be justifiable as physical models despite the fact that they are highly singular in the absence of a cutoff. We also study the case when a source of monomers is introduced in the regularized system. In this case a stationary state is reached. We present a complete analytic description of this regularized stationary state for the model kernel, K(m1,m2)=max{m1,m2}ν, which gels instantaneously when M→∞ if ν>1. The stationary cluster size distribution decays as a stretched exponential for small cluster sizes and crosses over to a power law decay with exponent ν for large cluster sizes. The total particle density in the stationary state slowly vanishes as [(ν−1)logM]−1/2 when M→∞. The approach to the stationary state is nontrivial: Oscillations about the stationary state emerge from the interplay between the monomer injection and the cutoff, M, which decay very slowly when M is large. A quantitative analysis of these oscillations is provided for the addition model which describes the situation in which clusters can only grow by absorbing monomers.

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The Eph kinases, EphA4 and EphB1 and their ligand, ephrinB1 have been previously reported to be present in platelets where they contribute to thrombus stability. While thrombus formation allows for Eph-ephrin engagement and bidirectional signalling, the importance specifically of Eph kinase or ephrin signalling in regulating platelet function remained unidentified. In the present study, a genetic approach was used in mice to establish the contribution of signalling orchestrated by the cytoplasmic domain of EphB2 (a newly discovered Eph kinase in platelets) in platelet activation and thrombus formation. We conclude that EphB2 signalling is involved in the regulation of thrombus formation and clot retraction. Furthermore, the cytoplasmic tail of this Eph kinase regulates initial platelet activation in a contact-independent manner in the absence of Eph-ephrin ligation between platelets. Together these data demonstrate that EphB2 signalling not only modulates platelet function within a thrombus but is also involved in the regulation of the function of isolated platelets in a contact-independent manner.

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Background Cluttering is a fluency disorder characterised by overly rapid or jerky speech patterns that compromise intelligibility. The neural correlates of cluttering are unknown but theoretical accounts implicate the basal ganglia and medial prefrontal cortex. Dysfunction in these brain areas would be consistent with difficulties in selection and control of speech motor programs that are characteristic of speech disfluencies in cluttering. There is a surprising lack of investigation into this disorder using modern imaging techniques. Here, we used functional MRI to investigate the neural correlates of cluttering. Method We scanned 17 adults who clutter and 17 normally fluent control speakers matched for age and sex. Brain activity was recorded using sparse-sampling functional MRI while participants viewed scenes and either (i) produced overt speech describing the scene or (ii) read out loud a sentence provided that described the scene. Speech was recorded and analysed off line. Differences in brain activity for each condition compared to a silent resting baseline and between conditions were analysed for each group separately (cluster-forming threshold Z > 3.1, extent p < 0.05, corrected) and then these differences were further compared between the two groups (voxel threshold p < 0.01, extent > 30 voxels, uncorrected). Results In both conditions, the patterns of activation in adults who clutter and control speakers were strikingly similar, particularly at the cortical level. Direct group comparisons revealed greater activity in adults who clutter compared to control speakers in the lateral premotor cortex bilaterally and, as predicted, on the medial surface (pre-supplementary motor area). Subcortically, adults who clutter showed greater activity than control speakers in the basal ganglia. Specifically, the caudate nucleus and putamen were overactive in adults who clutter for the comparison of picture description with sentence reading. In addition, adults who clutter had reduced activity relative to control speakers in the lateral anterior cerebellum bilaterally. Eleven of the 17 adults who clutter also stuttered. This comorbid diagnosis of stuttering was found to contribute to the abnormal overactivity seen in the group of adults who clutter in the right ventral premotor cortex and right anterior cingulate cortex. In the remaining areas of abnormal activity seen in adults who clutter compared to controls, the subgroup who clutter and stutter did not differ from the subgroup who clutter but do not stutter. Conclusions Our findings were in good agreement with theoretical predictions regarding the neural correlates of cluttering. We found evidence for abnormal function in the basal ganglia and their cortical output target, the medial prefrontal cortex. The findings are discussed in relation to models of cluttering that point to problems with motor control of speech.

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Galactic cosmic ray (GCR) flux is modulated by both particle drift patterns and solar wind structures on a range of timescales. Over solar cycles, GCR flux varies as a function of the total open solar magnetic flux and the latitudinal extent of the heliospheric current sheet. Over hours, drops of a few percent in near-Earth GCR flux (Forbush decreases, FDs) are well known to be associated with the near-Earth passage of solar wind structures resulting from corotating interaction regions (CIRs) and transient coronal mass ejections (CMEs). We report on four FDs seen at ground-based neutron monitors which cannot be immediately associated with significant structures in the local solar wind. Similarly, there are significant near-Earth structures which do not produce any corresponding GCR variation. Three of the FDs are during the STEREO era, enabling in situ and remote observations from three well-separated heliospheric locations. Extremely large CMEs passed the STEREO-A spacecraft, which was behind the West limb of the Sun, approximately 2–3 days before each near- Earth FD. Solar wind simulations suggest that the CMEs combined with pre-existing CIRs, enhancing the pre-existing barriers to GCR propagation. Thus these observations provide strong evidence for the modulation of GCR flux by remote solar wind structures.

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Animals are imbued with adaptive mechanisms spanning from the tissue/organ to the cellular scale which insure that processes of homeostasis are preserved in the landscape of size change. However we and others have postulated that the degree of adaptation is limited and that once outside the normal levels of size fluctuations, cells and tissues function in an aberant manner. In this study we examine the function of muscle in the myostatin null mouse which is an excellent model for hypertrophy beyond levels of normal growth and consequeces of acute starvation to restore mass. We show that muscle growth is sustained through protein synthesis driven by Serum/Glucocorticoid Kinase 1 (SGK1) rather than Akt1. Furthermore our metabonomic profiling of hypertrophic muscle shows that carbon from nutrient sources is being channelled for the production of biomass rather than ATP production. However the muscle displays elevated levels of autophagy and decreased levels of muscle tension. We demonstrate the myostatin null muscle is acutely sensitive to changes in diet and activates both the proteolytic and autophagy programmes and shutting down protein synthesis more extensively than is the case for wild-types. Poignantly we show that acute starvation which is detrimental to wild-type animals is beneficial in terms of metabolism and muscle function in the myostatin null mice by normalising tension production.