Mast cells mediate both IgE-dependent allergic reactions and protective responses against acute infections, possibly through the activation of Toll-like receptors (TLRs). We find that antigen interacts synergistically with TLR2 and TLR4 ligands to markedly enhance production of cytokines in murine mast cell lines. However, the TLR ligands neither stimulated degranulation and release of arachidonic acid nor influenced such responses to antigen, probably because these ligands failed to generate a necessary calcium signal. The enhanced cytokine production could be attributed to synergistic activation of mitogen-activated protein kinases in addition to the engagement of a more effective repertoire of IntroductionImmunoglobulin E (IgE)-dependent atopic diseases such as allergic rhinitis, asthma, and anaphylactic reactions affect, respectively, 20%, 7%, and 2% of the population in the United States. 1,2 The respiratory manifestations of these diseases may be exacerbated by acute respiratory infections from influenza, rhino-and syncytial viruses in humans 3,4 and animals, 5,6 as well as by lipopolysaccharide (LPS), which is a ubiquitous environmental contaminant from Gram-negative bacteria. 7,8 These pathogens may act through Tolllike receptors (TLRs). 9,10 TLR4 appears to play an essential role in the immune response to respiratory syncytial virus in the human lung, 11,12 and ligands for TLR2 and TLR4 augment inflammatory responses to inhaled antigen in the mouse lung. 13,14 Thirteen TLRs have been described to date, each of which recognize specific pathogen-associated molecular patterns. 15,16 Cooperative interactions between TLRs allow further discrimination. For example, a widely used synthetic ligand, tripalmitoyl Cys-Ser-(Lys) 4 (P3C), 17 has preference for TLR2/TLR1 heterodimers, while bacterial peptidoglycans (PGN) and macrophage-activating lipopeptide from Mycoplasma fermentans (MALP2) have preference for TLR2/ TLR6 heterodimers.TLRs interact with ligands as homodimers or, as noted for TLR2, heterodimers, and thus recruit cytosolic adaptor molecules that include myeloid differentiation protein 88 (MyD88), MyD88-adaptor like/TIR-associated protein (MAL/TIRAP), Toll-receptorassociated activator of interferon (TRIF), and Toll-receptorassociated molecule (TRAM). 16,18,19 The recruitment of MyD88 by TLR2 and TLR4, the focus of the present study, results in sequential activation of protein kinase interleukin-1 (IL-1) receptorassociated kinases (IRAKs) and transforming growth factor-␤-activated kinase (TAK1). TAK1, in turn, regulates activation of mitogen-activated protein (MAP) kinases and the transcription factor, nuclear factor B (NF-B), with ensuing production of inflammatory cytokines. TLR4 also activates a MyD88-independent pathway through TRAM and TRIF that uses interferon (IFN)-regulatory factor (IRF3) and NF-B to induce production of IFN-␤. In addition, TLRs engage signaling molecules that are commonly used by other types of receptors, such as phosphatidylinositol 3-kinase (PI3K), AKT, and possibly Src kina...

Flexible thermoelectric generators (TEGs) can provide uninterrupted, green energy from body-heat, overcoming bulky battery configurations that limit the wearable-technologies market today. High-throughput production of flexible TEGs is currently dominated by printing techniques, limiting material choices and performance. This work investigates the compatibility of physical vapour deposition (PVD) techniques with a flexible commercial process, roll-to-roll (R2R), for thermoelectric applications. We demonstrate, on a flexible polyimide substrate, a sputtered Bi2Te3/GeTe TEG with Seebeck coefficient (S) of 140 μV/K per pair and output power (P) of 0.4 nW per pair for a 20 °C temperature difference. For the first time, thermoelectric properties of R2R sputtered Bi2Te3 films are reported and we demonstrate the ability to tune the power factor by lowering run times, lending itself to a high-speed low-cost process. To further illustrate this high-rate PVD/R2R compatibility, we fabricate a TEG using Virtual Cathode Deposition (VCD), a novel high deposition rate PVD tool, for the first time. This Bi2Te3/Bi0.5Sb1.5Te3 TEG exhibits S = 250 μV/K per pair and P = 0.2 nW per pair for a 20 °C temperature difference.

A controllable transformation from interfacial to filamentary switching mode is presented on a ZrO2/ZrO2 − x/ZrO2 tri-layer resistive memory. The two switching modes are investigated with possible switching and transformation mechanisms proposed. Resistivity modulation of the ZrO2 − x layer is proposed to be responsible for the switching in the interfacial switching mode through injecting/retracting of oxygen ions. The switching is compliance-free due to the intrinsic series resistor by the filaments formed in the ZrO2 layers. By tuning the RESET voltages, controllable and stable multistate memory can be achieved which clearly points towards the capability of developing the next-generation multistate high-performance memory.Electronic supplementary materialThe online version of this article (doi:10.1186/s11671-017-2155-0) contains supplementary material, which is available to authorized users.

Cu/a-SiC/Au resistive memory cells are measured using voltage pulses and exhibit the highest ROFF/RON ratio recorded for any resistive memory. The switching kinetics are investigated and fitted to a numerical model, using thermal conductivity and resistivity properties of the dielectric. The SET mechanism of the Cu/a-SiC/Au memory cells is found to be due to ionic motion without joule heating contributions, whereas the RESET mechanism is found to be due to thermally assisted ionic motion. The conductive filament diameter is extracted to be around 4nm. The high thermal conductivity and resistivity for the Cu/a-SiC/Au memory cells result in slow switching but with high thermal reliability and stability, showing potential for use in harsh environments. Radiation properties of SiC memory cells are investigated. No change was seen in DC sweep or pulsed switching nor in conductive mechanisms, up to 2Mrad(Si) using 60Co gamma irradiation.