Iodine-doped Cu2 Se shows a significantly improved thermoelectric performance during phase transitions by electron and phonon critical scattering, leading to a dramatic increase in zT by a factor of 3-7 times culminating in zT values of 2.3 at 400 K.

CD25+CD4+ T cells are naturally occurring regulatory T cells that are anergic and have suppressive properties. Although they can be isolated from the spleens of normal mice, there are limited studies on how they can be activated or expanded in vivo. We found that oral administration of OVA to OVA TCR transgenic mice resulted in a modification of the ratio of CD25+CD4+ to CD25−CD4+ cells with an increase of CD25+CD4+ T cells accompanied by a decrease of CD25−CD4+ T cells. The relative increase in CD25+CD4+ T cells persisted for as long as 4 wk post feeding. We also found that CTLA-4 was dominantly expressed in CD25+CD4+ T cells and there was an increase in the percentage of CD25+CD4+ T cells expressing CTLA-4 in OVA-fed mice. In contrast to CD25−CD4+ cells, CD25+CD4+ cells from fed mice proliferated only minimally to OVA or anti-CD3 and secreted IL-10 and elevated levels of TGF-β1 following anti-CD3 stimulation. CD25+CD4+ cells from fed mice suppressed the proliferation of CD25−CD4+ T cells in vitro more potently than CD25+CD4+ T cells isolated from unfed mice, and this suppression was partially reversible by IL-10 soluble receptor or TGF-β soluble receptor and high concentration of anti-CTLA-4. With anti-CD3 stimulation, CD25+CD4+ cells from unfed mice secreted IFN-γ, whereas CD25+CD4+ cells from fed mice did not. Adoptive transfer of CD25+CD4+ T cells from fed mice suppressed in vivo delayed-type hypersensitivity responses in BALB/c mice. These results demonstrate an Ag-specific in vivo method to activate CD25+CD4+ regulatory T cells and suggest that they may be involved in oral tolerance.

High-performance lead-free piezoelectric materials are in great demand for next-generation electronic devices to meet the requirement of environmentally sustainable society. Here, ultrahigh piezoelectric properties with piezoelectric coefficients (d ≈700 pC N , d * ≈980 pm V ) and planar electromechanical coupling factor (k ≈76%) are achieved in highly textured (K,Na)NbO (KNN)-based ceramics. The excellent piezoelectric properties can be explained by the strong anisotropic feature, optimized engineered domain configuration in the textured ceramics, and facilitated polarization rotation induced by the intermediate phase. In addition, the nanodomain structures with decreased domain wall energy and increased domain wall mobility also contribute to the ultrahigh piezoelectric properties. This work not only demonstrates the tremendous potential of KNN-based ceramics to replace lead-based piezoelectrics but also provides a good strategy to design high-performance piezoelectrics by controlling appropriate phase and crystallographic orientation.

CD25(+)CD4(+) regulatory T cells inhibit the activation of autoreactive T cells in vitro and in vivo, and suppress organ-specific autoimmune diseases. The mechanism of CD25(+)CD4(+) T cells in the regulation of experimental autoimmune encephalomyelitis (EAE) is poorly understood. To assess the role of CD25(+)CD4(+) T cells in EAE, SJL mice were immunized with myelin proteolipid protein (PLP)(139-151) to develop EAE and were treated with anti-CD25 mAb. Treatment with anti-CD25 antibody following immunization resulted in a significant enhancement of EAE disease severity and mortality. There was increased inflammation in the central nervous system (CNS) of anti-CD25 mAb-treated mice. Anti-CD25 antibody treatment caused a decrease in the percentage of CD25(+)CD4(+) T cells in blood, peripheral lymph node (LN) and spleen associated with increased production of IFN-gamma and a decrease in IL-10 production by LN cells stimulated with PLP(130-151) in vitro. In addition, transfer of CD25(+)CD4(+) regulatory T cells from naive SJL mice decreased the severity of active EAE. In vitro, anti-CD3-stimulated CD25(+)CD4(+) T cells from naive SJL mice secreted IL-10 and IL-10 soluble receptor (sR) partially reversed the in vitro suppressive activity of CD25(+)CD4(+) T cells. CD25(+)CD4(+) T cells from IL-10-deficient mice were unable to suppress active EAE. These findings demonstrate that CD25(+)CD4(+) T cells suppress pathogenic autoreactive T cells in actively induced EAE and suggest they may play an important natural regulatory function in controlling CNS autoimmune disease through a mechanism that involves IL-10.