RESUMEN
Membranes with catalytic function can provide an effective approach for simultaneously transforming reactants to industrial chemicals and separation. However, rational design of stable and high-quality catalytic membranes with controlled structure remains a big challenge. We report a strategy for in situ confined encapsulation of ultrafine Fe2O3 nanoclusters in nitrogen and sulfur co-doped graphene-based membranes for continuous chemical conversion. By manipulation of the active ferric catalytic center and surrounding coordination atoms in doped rGO nanosheets, multiple coordination structures were provided to achieve improved catalytic properties. Angstrom-level confined interlayer structure (â¼8 Å) was constructed by external pressurization of Fe/NS-rGO nanosheets on membrane substrate, and the adsorption energy of 4-nitrophenol (4-NP) molecule between Fe/NS-rGO layers was much stronger than that in traditional nanometer-level confined space due to extra interactions, achieving the catalytic efficiency with a high Turnover Frequency (TOF) value (1596.0 h-1). The prepared ultrathin Fe/NS-rGO catalytic membrane also exhibited excellent water flux and rejection rate for small dye molecules, as well as long-term separation activity toward naphthol green B (NgB) for at least 130 h. The progress offers a viable route to the rational design of high-quality catalytic membranes with tailored structures and properties for wide applications.
RESUMEN
At high cytotoxic concentrations, actinomycin D (ActD) blocks transcription, decreasing levels of MDM2 and thus causing p53 stabilization. At low cytostatic concentrations, ActD causes ribosomal stress, which decreases MDM2 activity, resulting in p53 stabilization and activation. ActD can thus be used for p53-based cyclotherapy. We analyzed pathways mediating ActD-induced p53 expression. Inhibitors (LY294002, wortmannin, and deguelin) of phosphatidylinositol 3-kinases (PI3K) and AKT, but not inhibitors of MEK1/2, JNK, and p38-MAPK abolished the ActD-induced p53 expression in diverse cell types. RNA interference further supported these results. When AKT was downregulated by small hairpin RNA-AKTs, ActD-induced p53 expression was significantly decreased. ActD caused AKT phosphorylation at Ser473, indicating full activation of AKT. The potential for cancer therapy is discussed.