The crosslinker contents of the hydrogel have a significant effect on the mineralization outcome, including crystallinity, content, and morphology of the mineral growth within the 3d gelatin methacrylate scaffold.

We report that the finite thickness of three-dimensional topological insulator (TI) thin films produces an observable magnetoresistance (MR) in phase coherent transport in parallel magnetic fields. The MR data of Bi2Se3 and (Bi,Sb)2Te3 thin films are compared with existing theoretical models of parallel field magnetotransport. We conclude that the TI thin films bring parallel field transport into a unique regime in which the coupling of surface states to bulk and to opposite surfaces is indispensable for understanding the observed MR. The {\beta} parameter extracted from parallel field MR can in principle provide a figure of merit for searching TI compounds with more insulating bulk than existing materials.Comment: 6 pages, 4 figure

During viral infection, extracellular dsRNA is a potent signaling molecule that activates many innate immune cells including macrophages. TLR3 is a well-known receptor for extracellular dsRNA, and internalization of extracellular dsRNA is required for endosomal TLR3 activation. Preserved inflammatory responses of TLR3-deficient macrophages to extracellular dsRNA strongly support a TLR3-independent mechanism in dsRNA-mediated immune responses. The present study demonstrated that CD11b/CD18 (Mac-1), a surface integrin receptor, recognized extracellular dsRNA and induced macrophage immune responses. CD11b deficiency reduced inflammatory cytokine induction elicited by polyinosinic:polycytidylic acid (poly I:C, a synthetic dsRNA) in mouse sera and livers and in cultured peritoneal macrophages. DsRNA-binding assay and confocal immunofluorescence showed that Mac-1, especially the CD11b subunit, interacted and colocalized with poly I:C on the surface of macrophages. Further mechanistic studies revealed two distinct signaling events following dsRNA recognition by Mac-1. Firstly, Mac-1 facilitated poly I:C internalization through the activation of PI3K signaling and enhanced TLR3-dependent activation of interferon regulatory factor 3 (IRF3) in macrophages. Secondly, poly I:C induced activation of phagocyte NADPH oxidase (NOX2) in a TLR3-independent, but Mac-1 dependent manner. Subsequently, NOX2-derived intracellular reactive oxygen species activated MAPK and NFκB pathways. Our results indicate that extracellular dsRNA activates Mac-1 to enhance TLR3-dependent signaling and to trigger TLR3-independent, but Mac-1-dependent inflammatory oxidative signaling, identifying a novel mechanistic basis for macrophages to recognize extracellular dsRNA to regulate innate immune responses. This study identifies Mac-1 as a novel surface receptor for extracellular dsRNA and implicates Mac-1 as a potential therapeutic target for virus-related inflammatory diseases.

To effectively repair or replace damaged tissues, it is necessary to design three dimensional (3D) extracellular matrix (ECM) mimicking scaffolds with tunable biomechanical properties close to the desired tissue application. In the present work, gelatin methacrylate (GelMA) and dextran glycidyl methacrylate (DexMA) with tunable mechanical and biological properties were utilized to prepared novel bicomponent polymeric hydrogels by cross-linking polymerization using photoinitiation. We controlled the degree of substitution (DS) of glycidyl methacrylate in DexMA so that they could obtain relevant mechanical properties. The results indicated that copolymer hydrogels demonstrated a lower swelling ratio and higher compressive modulus as compared to the GelMA. Moreover, all of the hydrogels exhibited a honeycomb-like architecture, the pore sizes decreased as DS increased, and NIH-3T3 fibroblasts encapsulated in these hydrogels all exhibited excellent viability. These characteristics suggest a class of photocrosslinkable, tunable mechanically copolymer hydrogels that may find potential application in tissue engineering and regenerative medicine applications.

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