Search

In this study, we consider the initial boundary value problem of the planar magnetohydrodynamics (MHD) system when the viscous coefficients and heat conductivity depend on the temperature, which are assumed to be proportional to θα{\theta }^{\alpha }, α≥0\alpha \ge 0, and θβ{\theta }^{\beta }, β≥0\beta \ge 0, respectively, and magnetic diffusivity coefficient depends on the specific volume. We prove the existence and uniqueness of the global-in-time classical solution with general large initial data provided that α\alpha is sufficiently small and there is no restriction on the parameter β\beta . Moreover, the nonlinearly exponential stability of the solution is obtained. As a result, we extend the works given by Sun et al. for the full compressible Navier-Stokes equations and by Li and Shang for the full compressible MHD equations.

In this paper, we first provide a derivation of compressible nonisentropic Hall-magnetohydrodynamic (Hall-MHD) system from generalized Ohm's law. Then, we prove the global existence of strong solutions for the compressible nonisentropic Hall-MHD model based on the standard energy method in H 2 -framework. Finally, optimal decay rates of strong solutions in L 2 -norm are obtained if the initial data belong to L 1 additionally. [ABSTRACT FROM AUTHOR]

Inhibiting the protein neddylation pathway using the NEDD8-activating enzyme inhibitor MLN4924 represents an attractive anticancer strategy having been demonstrated to exhibit promising anticancer efficacy and with tolerable levels of toxicity; however, the mechanism by which MLN4924 inhibits cell proliferation in human esophageal squamous cell carcinoma (ESCC) cells requires further investigation. The present study revealed that MLN4924 treatment led to G2 cell cycle arrest and enhanced the protein stability of Wee1-like protein kinase and cyclin dependent protein kinase inhibitor 1A and B and p27. Furthermore, MLN4924 induced DNA damage and sensitized esophageal cancer cells to cisplatin by enhancing apoptosis. These findings extend the understanding of the function and mechanism of MLN4924 in ESCC and provide further evidence for the future development of neddylation inhibitors in clinical trials of esophageal cancer therapy, either alone or in combination. [ABSTRACT FROM AUTHOR]

Inhibiting the protein neddylation pathway using the NEDD8-activating enzyme inhibitor MLN4924 represents an attractive anticancer strategy having been demonstrated to exhibit promising anticancer efficacy and with tolerable levels of toxicity; however, the mechanism by which MLN4924 inhibits cell proliferation in human esophageal squamous cell carcinoma (ESCC) cells requires further investigation. The present study revealed that MLN4924 treatment led to G 2 cell cycle arrest and enhanced the protein stability of Wee1-like protein kinase and cyclin dependent protein kinase inhibitor 1A and B and p27. Furthermore, MLN4924 induced DNA damage and sensitized esophageal cancer cells to cisplatin by enhancing apoptosis. These findings extend the understanding of the function and mechanism of MLN4924 in ESCC and provide further evidence for the future development of neddylation inhibitors in clinical trials of esophageal cancer therapy, either alone or in combination.