Shadowing in the nuclear photoabsorption above the resonance region

A model based on the hadronic fluctuations of the real photon is developed to describe the total photonucleon and photonuclear cross sections in the energy region above the nucleon resonances. The hadronic spectral function of the photon is derived including the finite width of vector-meson resonances and the quark-antiquark continuum. The shadowing effect is evaluated considering the effective interaction of the hadronic component with the bound nucleons within a Glauber-Gribov multiple scattering theory. The low energy onset of the shadowing effect is interpreted as a possible signature of a modification of the hadronic spectral function in the nuclear medium. A decrease of the $\rho$-meson mass in nuclei is suggested for a better explanation of the experimental data.Comment: 8 pages, 7 figure

Rethinking naive realism

Perceptions are externally-directed - they present us with a mind-independent reality, and thus contribute to our abilities to think about this reality, and to know what is objectively the case. But perceptions are also internally-dependent - their phenomenal characters depend on the neuro-computational properties of the subject. A good theory of perception must account for both these facts. But Naive realism has been criticized for failing to accommodate the latter one. This paper evaluates and responds to this criticism. It first argues that a certain version of naive realism, often called “selectionism”, does indeed struggle with the internal-dependence of perceptions. It then develops an alternate version of naive realism which does not. This alternate version, inspired by an idea of Martin's, accommodates the internal-dependence of perceptions by recognizing the role that the subject's neuro-computational properties play in shaping perceptual phenomenology. At the same time, it retains the distinctive naive realist account of the external-directedness of perceptions

ω(→π+π−π0) \omega (\to \pi^+\pi^-\pi^0) meson photoproduction on proton

The cross section is estimated for the $\pi^+\pi^-\pi^0$ invariant mass distribution in the $\gamma p$ reaction in the GeV region. This reaction is assumed to proceed through the formation of the $\omega$ meson in the intermediate state, since the production cross section for this meson in the $\gamma p$ reaction in GeV region is significant and it has large branching ratio (88.8%) in the $\pi^+\pi^-\pi^0$ channel. The cross sections for this reaction have been calculated using the energy dependent reaction amplitude, i.e., $f_{\gamma p \to \omega p}(0)$, extracted from the latest $\omega$ meson photoproduction data. We use established procedure to calculate other factors, like width and propagator of the $\omega$ meson, so that our calculation can provide reliable cross section. The calculated results reproduce the measured $\pi^+\pi^-\pi^0$ invariant mass distribution spectra in the $\gamma p$ reaction.Comment: 13 pages, 5 figure

Up-regulation of human inducible nitric oxide synthase by p300 transcriptional complex

p300, a ubiquitous transcription coactivator, plays an important role in gene activation. Our previous work demonstrated that human inducible nitric oxide synthase (hiNOS) expression can be highly induced with the cytokine mixture (CM) of TNF-α + IL-1β + IFN-γ. In this study, we investigated the functional role of p300 in the regulation of hiNOS gene expression. Our initial data showed that overexpression of p300 significantly increased the basal and cytokine-induced hiNOS promoter activities in A549 cells. Interestingly, p300 activated cytokine-induced hiNOS transcriptional activity was completely abrogated by deleting the upstream hiNOS enhancer at -5 kb to -6 kb in the promoter. Furthermore, p300 over-expression increased cytokine-induced transcriptional activity on a heterologous minimal TK promoter with the same hiNOS enhancer. Site-directed mutagenesis of the hiNOS AP-1 motifs revealed that an intact upstream (-5.3kb) AP-1 binding site was critical for p300 mediated cytokine-induced hiNOS transcription. Furthermore, our ChIP analysis demonstrated that p300 was binding to Jun D and Fra-2 proteins at -5.3 kb AP-1 binding site in vivo. Lastly, our 3C assay was able to detect a long DNA loop between the hiNOS enhancer and core promoter site, and ChIP loop assay confirmed that p300 binds to AP-1 and RNA pol II proteins. Overall, our results suggest that coactivator p300 mediates cytokine-induced hiNOS transactivation by forming a distant DNA loop between its enhancer and core promoter region