Characterization of ETBE + Cl and Isooctane + Cl Combustion Products using Synchrotron Photoionization

The low temperature (298 – 700 K) oxidation characterizations of a series of fuel additives (ETBE and isooctane) were studied at advanced light source in Lawrence Berkley National lab, using a multiplexed chemical kinetics photoionization mass spectrometer with tunable synchrotron radiation. Using Cl atoms as initiators in presence of oxygen, photoionization data were collected. Data analysis was performed via characterization of the reaction species photoionization spectra and kinetic traces, from which the products and also the intermediates were identified. Relevant reaction dynamics on potential energy surfaces were calculated, reaction enthalpies of each individual step were presented using the CBS-QB3 composite model, and reaction pathways were proposed

Pyrimidine-thioindole inhibits gastric cancer cell proliferation via up-regulation of expression of tumor suppressor miR-145

Purpose: To investigate the effect of pyrimidine-thioindole on gastric cancer proliferation and the underlying mechanism of action. Methods: Cell viability and apoptosis were determined using MTT assay and Annexin V/PI assay, respectively. Reverse transcription-polymerase chain reaction (RT-PCR) was used for the determination of expression levels of miR-145, while protein expression levels were assayed by western blotting. Results: Pyrimidine-thioindole treatment significantly inhibited the proliferation of AGS and SNU-5 cells (p < 0.05), but had no effect on the viability of GES-1 cells. Exposure to pyrimidine-thioindole at doses of 8 and 10 µM significantly enhanced the apoptosis of AGS and SNU-5 cells (p < 0.05). Pyrimidinethioindole exposure markedly increased the proportions of AGS and SNU-5 cells in G1 phase (p < 0.05). In AGS and SNU-5 cell lines, pyrimidine-thioindole exposure at doses of 8 and 10 µM significantly upregulated the expression of miR-145, with higher enhancement of miR-145 expression in AGS cells than in SNU-5 cells. Moreover, pyrimidine-thioindole downregulated the expressions of MMP-2, MMP-9, c-Myc, p-PI3K and p-AKT in AGS and SNU-5 cells. Pyrimidine-thioindole treatment enhanced the expression of p21 in AGS and SNU-5 cells, relative to untreated cells (p < 0.05). Conclusion: These results suggest that pyrimidine-thioindole activates apoptotic signaling pathway, leading to reduction in cell proliferation and arrest of cell cycle. Moreover, it de-activates PI3K/AKT pathway and promotes miR-145 expression in AGS and SNU-5 cells. Thus, pyrimidine-thioindole has therapeutic significance for the management of gastric cancer