3-Arylamino-quinoxaline-2-carboxamides inhibit the PI3K/Akt/mTOR signaling pathways to activate P53 and induce apoptosis.

Thirty-eight new 3-arylaminoquinoxaline-2-carboxamide derivatives were in silico designed, synthesized and their cytotoxicity against five human cancer cell lines and one normal cells WI-38 were evaluated. Molecular mechanism studies indicated that N-(3-Aminopropyl)-3-(4-chlorophenyl) amino-quinoxaline-2-carboxamide (6be), the compound with the most potent anti-proliferation can inhibit the PI3K-Akt-mTOR pathway via down regulating the levels of PI3K, Akt, p-Akt, p-mTOR and simultaneously inhibit the phosphorylation of Thr308 and Ser473 residues in Akt kinase to servers as a dual inhibitor. Further investigation revealed that 6be activate the P53 signal pathway, modulated the downstream target gene of Akt kinase such p21, p27, Bax and Bcl-2, caused the fluctuation of intracellular ROS, Ca and mitochondrial membrane potential to induce cell cycle arrest and apoptosis in MGC-803 cells.

Analysis of Rayleigh-Brillouin spectral profiles and Brillouin shifts in nitrogen gas and air.

On the basis of experimental Rayleigh-Brillouin scattering data in gaseous nitrogen and air, simulations are performed to describe the observed frequency profiles in analytical form. The experimental data pertain to a λ = 366 nm scattering wavelength, a 90° scattering angle, pressures of 1 and 3 bar, and temperatures in the range 250 - 340 K. Two different models are used to represent the RB-profiles, to distinguish the RB-peaks, and to obtain the Brillouin shift associated with the acoustic waves generated in a gaseous medium.