134 research outputs found

    Nonperturbative photon qqˉq\bar{q} light front wave functions from a contact interaction model

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    We propose a method to calculate the qqˉq\bar{q} light front wave functions (LFWFs) of photon at low-virtuality, i.e., the light front amplitude of γ∗→qqˉ\gamma^*\rightarrow q\bar{q} at low Q2Q^2, based on a light front projection approach. We exemplify this method using a contact interaction model within Dyson-Schwinger equations formalism and obtain the nonperturbative photon qqˉq\bar{q} LFWFs. In this case, we find the nonperturbative effects are encoded in the enhanced quark mass and a dressing function of covariant quark-photon vertex, as compared to the leading order quantum electrodynamics photon qqˉq\bar{q} LFWFs. We then use nonperturbative-effect modified photon qqˉq\bar{q} LFWFs to study the inclusive deep inelastic scattering HERA data in the framework of the color dipole model. The results demonstrate that the theoretical description of data at low Q2Q^2 can be significantly improved once the nonperturbative corrections are included in the photon LFWFs.Comment: 11 pages, 4 figure

    Alkali burn induced corneal spontaneous pain and activated neuropathic pain matrix in the central nerve system in mice

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    Purpose: To explore whether alkali burn causes corneal neuropathic pain and activates neuropathic pain matrix in the central nerve system in mice. Methods: A corneal alkali burn mouse model (grade II) was used. Mechanical threshold in the cauterized area was tested using Von Frey hairs. Spontaneous pain behavior was investigated with conditioned place preference (CPP). Phosphor extracellular signal-regulated kinase (ERK), which is a marker for neuronal activation in chronic pain processing, was investigated in several representative areas of the neuropathic pain matrix: the two regions of the spinal trigeminal nucleus (subnucleus interpolaris/caudalis ,Vi/Vc; subnucleus caudalis/upper cervical cord , Vc/C1), insular cortex, anterior cingulated cortex (ACC), and the rostroventral medulla (RVM). Further, pharmacologically blocking pERK activation in ACC of alkali burn mice was performed in a separate study. Results: Corneal alkali burn caused long lasting damage to the corneal subbasal nerve fibers and mice exhibited spontaneous pain behavior. By testing in several representative areas of neuropathic pain matrix in the higher nerve system, phosphor extracellular signal-regulated kinase (ERK) was significantly activated in Vc/C1, but not in Vi/Vc. Also, ERK was activated in the insular cortex, ACC, and RVM. Furthermore, pharmacologically blocking ERK activation in ACC abolished alkali burn induced corneal spontaneous pain. Conclusion: Alkali burn could cause corneal spontaneous pain and activate neuropathic pain matrix in the central nerve system. Furthermore, activation of ERK in ACC is required for alkali burn induced corneal spontaneous pain
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