Porous polyimide (PI) networks with surface area up to 660 m(2) g(-1) were synthesized by planar structure monomers without detrimental catalysts.

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At present, thiol ligands are generally used whenever the classical Brust-Schiffrin two-phase method is employed to prepare metal nanoparticles. In general, the previous research was mainly focused on utilizing small molecular thiol compounds or thiol polymers as the stabilizers in organic phase to obtain small sized and uniform gold nanoparticles (Au NPs). Such preparations are usually associated with the problems of ligand exchange on the nanoparticle's surface due to strong Au-thiol interaction. Herein, we report an approach to produce fairly uniform Au NPs with diameters about 2-6 nm using thioether end-functional polymer ligands (DDT-PVAc and PTMP-PVAc) as the capping agents. These nanoparticles are thoroughly characterized using DLS, TEM, UV-Vis spectroscopy and other complementary techniques. The results indicate that multidentate thioether polymeric ligands (PTMP-PVAc) lead to formation of smaller but special 'multimer' morphology in organic phase; whereas fairly uniform nanoparticles are produced using monodentate thioether functionalized ligands (DDT-PVAc). Further modification of such polymer ligands to introduce the hydrophilic functionalities realizes the phase transfer of Au NPs from organic to aqueous media.

Amphiphilic block copolymers poly(ethylene glycol)-block-oligo(vinyl acetate) (PEG-b-OVAc) and OVAc-b-PEG-b-OVAc have been demonstrated to be effective surfactants for CO 2 -in-water (C/W) emulsions. However, the high cost and difficulty of synthesis process can render the economics of CO 2 process unfavorable. In this work, by reversible addition-fragmentation chain transfer (RAFT) polymerization, a series of well-defined CO 2 -philic triblock copolymers X-OVAc-b-PEG-b-OVAc-X (where X stands for xanthate group) were synthesized. The structures and molecular weights of these copolymers were characterized by 1 H NMR and GPC. The results of GPC analysis exhibited relatively narrow polydispersity (PDI < 1.35). The process of preparation of X-OVAc-based surfactants was much more simple, inexpensive and also easy to control, which could promote industrial-scale applications. The X-OVAc-based surfactants were found effectively to produce highly concentrated stable C/W emulsions. Porous emulsion-templated materials were prepared by the polymerization of the continuous phase of C/W emulsions. The open-cell morphology of the emulsion-templated materials was evidenced by scanning electron microscope. To tune the morphology of the porous structures, the influence of the surfactant concentration and molecular weight of OVAc block were also investigated. It was shown that X-OVAc-based surfactants can outperform perfluorinated surfactants and approach OVAc-based surfactants for such applications.

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K-ras (Kirsten ras GTPase) mutations are oncogenic events frequently observed in many cancer types especially in pancreatic cancer. Although mitochondrial dysfunction has been associated with K-ras mutation, the molecular mechanisms by which K-ras impacts mitochondria and maintains metabolic homeostasis are not fully understood. In this study, we used two K-ras inducible cell systems, human pancreatic epithelial/ K-rasG12D (HPNE/K-rasG12D) and human embryonic kidney cells with tetracycline repressorT-Rex/K-rasG12V, to evaluate the role of oncogenic K-ras in regulating mitochondrial function. Among a panel of genes known to affect mitochondria, only the expression of OPA3 (optic atrophy protein 3) was consistently up-regulated by K-ras activation in both cell lines. Importantly, high expression of OPA3 was also observed in clinical pancreatic cancer tissues. Genetic knockdown of OPA3 caused a significant decrease of energy metabolism, manifested by a suppression of oxygen consumption rate (OCR) and a decrease in cellular ATP content, leading to inhibition of cell proliferation capacity and reduced expression of epithelial–mesenchymal transition (EMT) markers. Our study suggests that OPA3 may promote cellular energy metabolism and its up-regulation in K-ras-driven cancer is likely a mechanism to offset the negative impact of K-ras on mitochondria to maintain energy homeostasis. As such, OPA3 could be a potential target to kill cancer cells with K-ras mutations.