Thermally flexible epoxy/cellulose blends mediated by an ionic liquid

Blends between the widely used thermoset resin, epoxy, and the most abundant organic material, natural cellulose are demonstrated for the first time. The blending modification induced by charge transfer complexes using a room temperature ionic liquid, leads to the formation of thermally flexible thermoset materials. The blend materials containing low concentrations of cellulose were optically transparent which indicates the miscibility at these compositions. We observed the existence of intermolecular hydrogen bonding between epoxy and cellulose in the presence of the ionic liquid, leading to partial miscibility between these two polymers. The addition of cellulose improves the tensile mechanical properties of epoxy. This study reveals the use of ionic liquids as a compatible processing medium to prepare epoxy thermosets modified with natural polymers.

Antiangiogenic VEGF-Ax: A New Participant in Tumor Angiogenesis

The transcript of the angiogenic factor vascular endothelial growth factor A (VEGF-A) is subject to a multitude of stimulus-dependent, posttranscriptional regulatory events, consistent with its unusually long 30 untranslated region. We have recently reported translational readthrough of VEGFA mRNA whereby translating ribosomes traverse the canonical stop codon to a conserved, downstream stop codon, generating VEGF-Ax (''x'' for extended), a novel, extended isoform with an additional 22 amino acids appended at the C-terminus. This event is the first vertebrate example of protein-regulated, programmed translational readthrough that generates a protein with a known function. Remarkably, VEGF-Ax exhibits potent antiangiogenic activity, both in vitro and in vivo, thus raising profound clinical implications, particularly with respect to cancer treatment. In this review, we discuss the potential of VEGF-Ax as a therapeutic agent and drug target, as well as its possible role in the failure of, or resistance to, conventional anti-VEGF therapies in many types of cancers. (C) 2015 AACR.

Disorder, oscillatory dynamics and state switching: the role of c-Myc

In this paper, using the intrinsically disordered oncoprotein Myc as an example, we present a mathematical model to help explain how protein oscillatory dynamics can influence state switching. Earlier studies have demonstrated that, while Myc overexpression can facilitate state switching and transform a normal cell into a cancer phenotype, its downregulation can reverse state-switching. A fundamental aspect of the model is that a Myc threshold determines cell fate in cells expressing p53. We demonstrate that a non-cooperative positive feedback loop coupled with Myc sequestration at multiple binding sites can generate bistable Myc levels. Normal quiescent cells with Myc levels below the threshold can respond to mitogenic signals to activate the cyclin/cdk oscillator for limited cell divisions but the p53/Mdm2 oscillator remains nonfunctional. In response to stress, the p53/Mdm2 oscillator is activated in pulses that are critical to DNA repair. But if stress causes Myc levels to cross the threshold, Myc inactivates the p53/Mdm2 oscillator, abrogates p53 pulses, and pushes the cyclin/cdk oscillator into overdrive sustaining unchecked proliferation seen in cancer. However, if Myc is downregulated, the cyclin/cdk oscillator is inactivated and the p53/Mdm2 oscillator is reset and the cancer phenotype is reversed. (C) 2015 Elsevier Ltd. All rights reserved.