Toward a versatile toolbox for cucurbit[n]uril-based supramolecular hydrogel networks through in situ polymerization

The success of exploiting cucurbit[n]uril (CB[n])-based molecular recognition in self-assembled systems has sparked a tremendous interest in polymer and materials chemistry. In this study, polymerization in the presence of host-guest complexes is applied as a modular synthetic approach toward a diverse set of CB[8]-based supramolecular hydrogels with desirable properties, such as mechanical strength, toughness, energy dissipation, self-healing, and shear-thinning. A range of vinyl monomers, including acrylamide-, acrylate-, and imidazolium-based hydrophilic monomers, could be easily incorporated as the polymer backbones, leading to a library of CB[8] hydrogel networks. This versatile strategy explores new horizons for the construction of supramolecular hydrogel networks and materials with emergent properties in wearable and self-healable electronic devices, sensors, and structural biomaterials. © 2017 The Authors. Journal of Polymer Science Part A: Polymer Chemistry Published by Wiley Periodicals, Inc. J. Polym. Sci., Part A: Polym. Chem. 2017 , 55, 3105–3109     

Silibinin Treatment Inhibits the Growth of Hedgehog Inhibitor‐Resistant Basal Cell Carcinoma Cells via Targeting EGFR‐MAPK‐Akt and Hedgehog Signaling

Basal cell carcinoma (BCC) is the most common skin malignancy. Deregulated hedgehog signaling plays a central role in BCC development; therefore, hedgehog inhibitors have been approved to treat locally advanced or metastatic BCC. However, the development of resistance to hedgehog inhibitors is the major challenge in effective treatment of this disease. Herein, we evaluated the efficacy of a natural agent silibinin to overcome resistance with hedgehog inhibitors (Sant‐1 and GDC‐0449) in BCC cells. Silibinin (25–100 μm ) treatment for 48 h strongly inhibited growth and induced death in ASZ001, Sant‐1‐resistant (ASZ001‐Sant‐1) and GDC‐0449‐resistant (ASZ001‐GDC‐0449) BCC cells. Furthermore, colony‐forming ability of ASZ001, ASZ001‐Sant‐1 and ASZ001‐GDC‐0449 cells was completely inhibited by silibinin treatment. Molecular analysis showed that silibinin treatment decreased the level of phosphorylated EGFR (Tyrosine 1173) and total EGFR in ASZ001‐Sant‐1 cells, key signaling molecules responsible for BCC resistance toward hedgehog inhibitors. Further, silibinin treatment decreased the phosphorylated Akt (Serine 473), phosphorylated ERK1/2 (Threonine 202/Tyrosine 204), cyclin D1 and Gli‐1 level but increased the SUFU expression in ASZ001‐Sant‐1‐resistant cells. Silibinin treatment of ASZ001‐Sant‐1‐resistant cells also decreased bcl‐2 but increased cleaved caspase 3 and PARP cleavage, suggesting induction of apoptosis. Together, these results support silibinin use to target hedgehog inhibitor‐resistant BCC cells.     

Immersed Boundaries in Large Eddy Simulation of Compressible Flows

Methods to immerse walls in a structured mesh are examined in the context of fully compressible solutions of the Navier–Stokes equations. The ghost cell approach is tested along with compressible conservative immersed boundaries in canonical flow configurations; the reflexion of pressure waves on walls arbitrarily inclined on a cartesian mesh is studied, and mass conservation issues examined in both a channel flow inclined at various angles and flow past a cylinder. Then, results from Large Eddy Simulation of a flow past a rectangular cylinder and a transonic cavity flow are compared against experiments, using either a multi-block mesh conforming to the wall or immersed boundaries. Different strategies to account for unresolved transport by velocity fluctuations in LES are also compared. It is found that immersed boundaries allow for reproducing most of the coupling between flow instabilities and pressure-signal properties observed in the transonic cavity flow. To conclude, the complex geometry of a trapped vortex combustor, including a cavity, is simulated and results compared against experiments.