Quark charge balance function and hadronization effects in relativistic heavy ion collisions

We calculate the charge balance function of the bulk quark system before hadronization and those for the directly produced and the final hadron system in high energy heavy ion collisions. We use the covariance coefficient to describe the strength of the correlation between the momentum of the quark and that of the anti-quark if they are produced in a pair and fix the parameter by comparing the results for hadrons with the available data. We study the hadronization effects and decay contributions by comparing the results for hadrons with those for the bulk quark system. Our results show that while hadronization via quark combination mechanism slightly increases the width of the charge balance functions, it preserves the main features of these functions such as the longitudinal boost invariance and scaling properties in rapidity space. The influence from resonance decays on the width of the balance function is more significant but it does not destroy its boost invariance and scaling properties in rapidity space either. The balance functions in azimuthal direction are also presented.Comment: 9 figure

Quark number scaling of hadronic pTp_T spectra and constituent quark degree of freedom in pp-Pb collisions at sNN=5.02\sqrt{s_{NN}}=5.02 TeV

We show that the experimental data of $p_T$ spectra of identified hadrons released recently by ALICE collaboration for $p$-Pb collisions at $\sqrt{s_{NN}}=5.02$ TeV exhibit a distinct universal behavior --- the quark number scaling. We further show that the scaling is a direct consequence of quark (re-)combination mechanism of hadronization and can be regarded as a strong indication of the existence of the underlying source with constituent quark degree of freedom for the production of hadrons in $p$-Pb collisions at such high energies. We make also predictions for production of other hadrons.Comment: 5 pages, 3 figure

A local structural descriptor for image matching via normalized graph laplacian embedding

This paper investigates graph spectral approaches to the problem of point pattern matching. Specifically, we concentrate on the issue of how to effectively use graph spectral properties to characterize point patterns in the presence of positional jitter and outliers. A novel local spectral descriptor is proposed to represent the attribute domain of feature points. For a point in a given point-set, weight graphs are constructed on its neighboring points and then their normalized Laplacian matrices are computed. According to the known spectral radius of the normalized Laplacian matrix, the distribution of the eigenvalues of these normalized Laplacian matrices is summarized as a histogram to form a descriptor. The proposed spectral descriptor is finally combined with the approximate distance order for recovering correspondences between point-sets. Extensive experiments demonstrate the effectiveness of the proposed approach and its superiority to the existing methods

A rapamycin-sensitive signaling pathway contributes to long-term synaptic plasticity in the hippocampus

Many forms of long-lasting behavioral and synaptic plasticity require the synthesis of new proteins. For example, long-term potentiation (LTIP) that endures for more than an hour requires both transcription and translation. The signal-transduction mechanisms that couple synaptic events to protein translational machinery during long-lasting synaptic plasticity, however, are not well understood. One signaling pathway that is stimulated by growth factors and results in the translation of specific mRNAs includes the rapamycin-sensitive kinase mammalian target of rapamycin (mTOR, also known as FRAP and RAFT-1). Several components of this translational signaling pathway, including mTOR, eukaryotic initiation factor-4E-binding proteins 1 and 2, and eukaryotic initiation factor-4E, are present in the rat hippocampus as shown by Western blot analysis, and these proteins are detected in the cell bodies and dendrites in the hippocampal slices by immunostaining studies. In cultured hippocampal neurons, these proteins are present in dendrites and are often found near the presynaptic protein, synapsin I. At synaptic sites, their distribution completely overlaps with a postsynaptic protein, PSD-95. These observations suggest the postsynaptic localization of these proteins. Disruption of mTOR signaling by rapamycin results in a reduction of late-phase LTP expression induced by high-frequency stimulation; the early phase of LTIP is unaffected. Rapamycin also blocks the synaptic potentiation induced by brain-derived neurotrophic factor in hippocampal slices. These results demonstrate an essential role for rapamycin-sensitive signaling in the expression of two forms of synaptic plasticity that require new protein synthesis. The localization of this translational signaling pathway at postsynaptic sites may provide a mechanism that controls local protein synthesis at potentiated synapses

The entropy puzzle and the quark combination model

We use two available methods, the Duhem-Gibbs relation and the entropy formula in terms of particle phase space distributions, to calculate the entropy in a quark combination model. The entropy of the system extracted from the Duhem-Gibbs relation is found to increase in hadronization if the average temperature of the hadronic phase is lower than that of the quark phase. The increase of the entropy can also be confirmed from the entropy formula if the volume of the hadronic phase is larger than 2.5-3.0 times that of the quark phase. So whether the entropy increases or decreases during combination depends on the temperature before and after combination and on how much expansion the system undergoes during combination. The current study provides an example to shed light on the entropy issue in the quark combination model.Comment: RevTex 4, 4 pages, 2 tables, 4 figures, discussions and references added, to appear in PR

WNT5A Signaling Contributes to Aβ-Induced Neuroinflammation and Neurotoxicity

Neurodegenration is a pathological hallmark of Alzheimer's disease (AD), but the underlying molecular mechanism remains elusive. Here, we present evidence that reveals a crucial role of Wnt5a signaling in this process. We showed that Wnt5a and its receptor Frizzled-5 (Fz5) were up-regulated in the AD mouse brain, and that beta-amyloid peptide (Aβ), a major constituent of amyloid plaques, stimulated Wnt5a and Fz5 expression in primary cortical cultures; these observations indicate that Wnt5a signaling could be aberrantly activated during AD pathogenesis. In support of such a possibility, we observed that inhibition of Wnt5a signaling attenuated while activation of Wnt5a signaling enhanced Aβ-evoked neurotoxicity, suggesting a role of Wnt5a signaling in AD-related neurodegeneration. Furthermore, we also demonstrated that Aβ-induced neurotoxicity depends on inflammatory processes, and that activation of Wnt5a signaling elicited the expression of proinflammatory cytokines IL-1β and TNF-α whereas inhibition of Wnt5a signaling attenuated the Aβ-induced expression of the cytokines in cortical cultures. Our findings collectively suggest that aberrantly up-regulated Wnt5a signaling is a crucial pathological step that contributes to AD-related neurodegeneration by regulating neuroinflammation