No abstract

The short-chain n-alcohol-induced changes in phase behaviors of aqueous mixed 1,3-propanediyl bis(dodecyl dimethylammonium bromide) (12-3-12) and sodium dodecyl sulfonate (AS) system have been investigated. For the 12-3-12/AS/HO mixed system, there are two kinds of aqueous two-phase systems with excess cationic surfactant (ATPS-C). The molar ratio of 12-3-12 to AS (MR) and the total surfactant concentration ( m) in the top phase are smaller than those in the bottom phase of ATPS-C. It is worth noting that the addition of ethanol or n-propanol leads to different influences on the ATPS-C. Molecular dynamics (MD) simulation results illustrate that the different influences ascribe to the difference in the cosurfactant effect of ethanol and n-propanol. When ethanol is used as additive, the difference in m leads to the difference in interactions between surfactants and ethanol for the two coexisting phases of ATPS-C, determining the difference in their combination ability with the mixed solvent. It is the main reason for the ethanol-induced phase inversion of the first kind of ATPS-C. When n-propanol is added, in addition to m, MR is also a key factor influencing the interactions between 12-3-12 and AS and between surfactants and n-propanol due to the stronger cosurfactant effect of n-propanol. MD simulations indicate that vesicles with smaller MR are easier and faster to form. These vesicles spontaneously accumulate at the top phase accompanied by certain amount of mixed solvent transferred from the bottom phase of ATPS-C. Meanwhile, the competition for the mixed solvent arising from the surfactant-rich bottom phase prevents the transferring. The two factors work together to cause the increase of m in the top phase of ATPS-C with the addition of n-propanol, leading to n-propanol-induced phase concentration inversion rather than phase inversion of ATPS-C. On the basis of the experimental results and MD simulations, ethanol-induced phase inversion mechanism or n-propanol-induced phase concentration inversion mechanism of ATPS-C has been proposed.

The production of functional activated carbon (AC) prepared from cheap agricultural biomass combustion residue rice husk ash (RHA) has been utilized as the adsorbent for the removal of Methylene Blue from an aqueous solution was examined in this study. The RHA was subjected to a chemical pretreatment by ZnCl2, followed by carbonization in a muffle. The experimental data were analyzed by the Freundlich models of adsorption. Equilibrium data fitted well with the Freundlich model. The rates of adsorption were found to conform to the pseudo-second-order kinetics with good correlation.

To explore the role of matching water affinities between the oppositely charged headgroups, the micellization of cetyltrimethylammonium bromide (CTA+Br–)/sodium dodecanoate (Na+L–) mixed system and the CTA+Br–/sodium dodecylsulfonate (Na+AS–) mixed system has been investigated by the surface tension method and molecular dynamic (MD) simulation. In comparison with the CTA+Br–/Na+L– system, the CTA+Br–/Na+AS– system shows stronger micelle formation ability, smaller critical micelle concentration (cmc), and stronger synergistic effect arising from the higher degree of matching water affinities between the headgroups CTA+ and AS–. To explore the role of matching water affinities between the oppositely charged constituent counterions, the micellization of CTA+X–/Y+L– mixed systems with various counterions has been investigated. The higher degree of matching water affinities between counterions X– and Y+ and the higher degree of mismatching water affinities between headgroups and counterions are unfavorable to the screening effect of counterions on the electrostatic attraction between headgroups CTA+ and L–, leading to stronger micelle formation ability and smaller cmc and vice versa. MD simulation results also indicate that, for the mixed micellization of cationic/anionic surfactants, the role of matching water affinities between oppositely charged headgroups is more important than that between oppositely charged constituent counterions.

Cancer cells are characterized as the uncontrolled proliferation, which demands high levels of nucleotides that are the building blocks for DNA replication. CAD is a trifunctional enzyme that initiates the de novo pyrimidine synthesis, which is normally enhanced in cancer cells to preserve the pyrimidine pool for cell division. Glioma, representing the majority of brain cancers, is highly addicted to nucleotides like pyrimidine to sustain the abnormal growth and proliferation of cells. CAD is previously reported to by dysregulated in glioma, but the underlying mechanism remains unclear. Here, we showed that the expression of CAD was upregulated in glioma, which was positively correlated with tumor grade and the survival of glioma patients. Knockdown of CAD robustly inhibited the cell proliferation and colony formation of glioblastoma (GBM) cells, indicating the essential role of CAD in the pathogenesis of GBM. Mechanistically, we firstly identified that CAD was modified by the K29-linked polyubiquitination, and subsequently subjected to degradation. CHIP interacted and ubiquitinated CAD, which accounted for the anti-proliferative role of CHIP in GBM. Specifically, the ectopic expression of CAD dramatically enhanced the colony formation of GBM cells, which was subsequently abolished by CHIP overexpression. To sustain the expression of CAD, CHIP is significantly downregulated, which is correlated with the poor prognosis and survival of GBM patients. Notably, low level of CHIP and high level of CAD predict the short overall survival of GBM patients. These results illustrated the essential role of CAD in glioma and reveal novel therapeutic targets for CAD-positive and CHIP-negative cancer.