Taking account of elastic gg→gg and bremsstrahlung gg↔ggg processes, as well as quark elastic scattering, we calculated the shear viscous coefficient of a chemically equilibrating quark-gluon plasma at finite baryon density. We found that the inelastic bremsstrahlung processes make the shear viscosity remarkably lower, and the ratio of shear viscosity to entropy density η/s increases with increasing initial quark chemical potential. Considering the effect of shear viscosity the evolution of the QGP system was investigated. We found that the evolution of the system becomes slower owing to viscosity compared to the one in the ideal case, and the inelastic bremsstrahlung processes make the slower rate of the system not as much as in our previous calculations.
We have studied the evolution and dilepton production of a chemically equilibrating quark-gluon system at finite baryon density. We found that due to the increase of the quark phase lifetime with increasing initial quark chemical potential and other factors, such as, higher initial temperature, larger gluon density, and gluon fusion or quark annihilation cross section, thermal charmed quarks provide a dominant contribution to the dilepton yield. This results in a significant enhancement of intermediate mass dilepton production.
By considering the effect of shear viscosity we have investigated the evolution of a chemically equilibrating quark-gluon plasma at finite baryon density. Based on the evolution of the system we have performed a complete calculation for the dilepton production from the following processes: qq→ll, qq→gll, Compton-like scattering (qg→qll,qg→qll), gluon fusion gḡ→cc, annihilation qq→cc as well as the multiple scattering of quarks. We have found that quark-antiquark annihilation, Compton-like scatterring, gluon fusion, and multiple scattering of quarks give important contributions. Moreover, we have also found that the dilepton yield is an increasing function of the initial quark chemical potential, and the increase of the quark phase lifetime because of the viscosity also obviously raises the dilepton yield.
Hashimoto’s thyroiditis (TH) is a risk factor for the occurrence of papillary thyroid carcinoma (PTC), which is considered to be the most common type of thyroid cancer. In recent years, the prevalence of PTC with TH has been increasing, but little is known about the genetic alteration in PTC with TH. This study analyzed the mutation spectrum and mutation signature of somatic single nucleotide variants (SNV) for 10 non-tumor and tumor pair tissues of PTC with TH using whole-exome sequencing. The ANK3 protein expression was evaluated by immunohistochemistry in PTC with TH and PTC samples. Moreover, the functional role of ANK3 in PTC cells was determined by CCK-8 proliferation assay, colony formation assays, cell cycle analysis, cell invasion and migration and in vivo study through overexpression assay. Our results showed three distinct mutational signatures and the C>T/G>A substitution was the most common type of SNV. Gene-set enrichment analysis showed that most of the significantly mutated genes were enriched in the regulation of actin cytoskeleton signaling. Moreover, NCOR2, BPTF, ANK3, and PCSK5 were identified as the significantly mutated genes in PTC with TH, most of which have not been previously characterized. Unexpectedly, it was found that ANK3 was overexpressed in cytoplasm close to the membrane of PTC cells with TH and in almost all PTC cases, suggesting its role as a diagnostic marker of PTC. Ectopic expression of ANK3 suppressed invasion and migration, increased apoptosis of B-CPAP and TPC-1 cells. Moreover, our findings revealed that enhanced ANK3 expression inhibits growth of PTC cells both in vitro and in vivo. Ectopic expression of ANK3 significantly enhanced E-cadherin protein expression and inhibited PTC progression, at least in part, by suppression of epithelial-mesenchymal transition (EMT). Our study shows that ANK3 exerts an anti-oncogenic role in the development of PTC and might be an indolent maintainer of PTC.
Laboratory environments (A) are typically two-dimensional, small, with or without objects and restrained conspecifics; while natural environments (B) are large, dynamic, and rich in complex landforms and heterogeneous surfaces.
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