Solid-state refrigeration technology based on caloric effects are promising to replace the currently used vapor compression cycles. However, their application is restricted due to limited performances of caloric materials. Here, we have identified colossal barocaloric effects (CBCEs) in a class of disordered solids called plastic crystals. The obtained entropy changes are about 380 J kg -1 K -1 in the representative neopentylglycol around room temperature. Inelastic neutron scattering reveals that the CBCEs in plastic crystals are attributed to the combination of the vast molecular orientational disorder, giant compressibility and high anharmonic lattice dynamics. Our study establishes the microscopic scenario for CBCEs in plastic crystals and paves a new route to the next-generation solid-state refrigeration technology.

Perovskite CH3NH3PbI3 exhibits outstanding photovoltaic performances, but the understanding of the atomic motions remains inadequate even though they take a fundamental role in transport properties. Here, we present a complete atomic dynamic picture consisting of molecular jumping rotational modes and phonons, which is established by carrying out high-resolution time-of-flight quasi-elastic and inelastic neutron scattering measurements in a wide energy window ranging from 0.0036 to 54 meV on a large single crystal sample, respectively. The ultrafast orientational disorder of molecular dipoles, activated at ∼165 K, acts as an additional scattering source for optical phonons as well as for charge carriers. It is revealed that acoustic phonons dominate the thermal transport, rather than optical phonons due to sub-picosecond lifetimes. These microscopic insights provide a solid standing point, on which perovskite solar cells can be understood more accurately and their performances are perhaps further optimized.

As a generic property, all substances transfer heat through microscopic collisions of constituent particles . A solid conducts heat through both transverse and longitudinal acoustic phonons, but a liquid employs only longitudinal vibrations. As a result, a solid is usually thermally more conductive than a liquid. In canonical viewpoints, such a difference also serves as the dynamic signature distinguishing a solid from a liquid. Here, we report liquid-like thermal conduction observed in the crystalline AgCrSe. The transverse acoustic phonons are completely suppressed by the ultrafast dynamic disorder while the longitudinal acoustic phonons are strongly scattered but survive, and are thus responsible for the intrinsically ultralow thermal conductivity. This scenario is applicable to a wide variety of layered compounds with heavy intercalants in the van der Waals gaps, manifesting a broad implication on suppressing thermal conduction. These microscopic insights might reshape the fundamental understanding on thermal transport properties of matter and open up a general opportunity to optimize performances of thermoelectrics.

Objective-To determine whether the administration of an active form of vitamin D 3 (calcitriol) could prevent atherosclerosis through anti-inflammatory actions. Methods and Results-Recent clinical studies have shown that lack of vitamin D 3 is a risk factor for cardiovascular events.Oral calcitriol administration decreased atherosclerotic lesions, macrophage accumulation, and CD4 ϩ T-cell infiltration at the aortic sinus, when compared with the corresponding observations in control mice. We observed a significant increase in Foxp3 ϩ regulatory T cells and a decrease in CD80 ϩ CD86 ϩ dendritic cells (DCs) in the mesenteric lymph nodes, spleen, and atherosclerotic lesions in oral calcitriol-treated mice in association with increased interleukin 10 and decreased interleukin 12 mRNA expression. CD11cϩ DCs from the calcitriol group showed reduced proliferative activity of T lymphocytes, suggesting the suppression of DC maturation. Neutralization of CD25 in vivo revealed that calcitriol inhibited atherosclerosis mainly in a regulatory T cell-dependent manner but also partly because of a decrease in DC maturation. , is a secosteroid hormone that not only plays a central role in bone and calcium metabolism but also modulates the immune response. Recent epidemiological studies have shown a relationship between low plasma levels of vitamin D 3 and a predisposition to cardiovascular events. [1][2][3] This finding is supported by a meta-analysis showing that oral vitamin D 3 treatment contributes to the improvement of mortality from all causes, in part by decreasing cardiovascular deaths. 4 Transgenic rats constitutively expressing vitamin D-24-hydroxylase, a model of vitamin D 3 deficiency, showed aggravated atherosclerosis under a high-fat and high-cholesterol diet, when compared with control rats. 5 However, there are no reports about the direct effects of an orally administered active form of vitamin D 3 on atherosclerosis. Conclusion-Oral See accompanying article on page 2317It is widely recognized that atherosclerosis is a complex inflammatory disease of the arterial wall, 6,7 in which the T-lymphocyte-mediated pathogenic immune response plays a critical role. Clinical strategies developed to modulate the immune response have been insufficient for preventing atherosclerosis. Cumulative data based on experimental animal models suggest that CD4 ϩ T cells are present within plaques from the initial stages of the disease in mice, and adaptive transfer of these cells is potentially proatherogenic. 8 Accumulating evidence has revealed novel functions of several subsets of regulatory T cells (Tregs), which maintain immunologic tolerance to self-antigens and inhibit atherosclerosis development by suppressing the inflammatory response of effector T cells. 9 -12 These studies have provided new insights into the immunopathogenesis of atherosclerosis and imply that promotion of regulatory immune responses may have therapeutic potential for suppression of atherosclerotic diseases.In addition to Tregs, dendritic cells (DCs) are al...

A spin-1/2 triangular-lattice Heisenberg antiferromagnet (TLHAF) is a prototypical frustrated quantum magnet, which exhibits remarkable quantum many-body effects that arise from the synergy between spin frustration and quantum fluctuation. The ground-state properties of a spin-1/2 TLHAF are theoretically well understood. However, the theoretical consensus regarding the magnetic excitations is limited. The experimental study of the magnetic excitations in spin-1/2 TLHAFs has also been limited. Here we show the structure of magnetic excitations in the spin-1/2 TLHAF Ba3CoSb2O9 investigated by inelastic neutron scattering. Significantly different from theoretical expectations, the excitation spectrum has a three-stage energy structure. The lowest-energy first stage is composed of dispersion branches of single-magnon excitations. The second and third stages are dispersive continua accompanied by a columnar continuum extending above 10 meV, which is six times larger than the exchange interaction J = 1.67 meV. Our results indicate the shortcomings of the current theoretical framework.

Using inelastic neutron scattering technique, we measured the spin wave dispersion over the entire Brillouin zone of room temperature multiferroic BiFeO 3 single crystals with magnetic excitations extending to as high as 72.5 meV. The full spin waves can be explained by a simple Heisenberg Hamiltonian with a nearest neighbor exchange interaction (J=4.38 meV), a next nearest neighbor exchange interaction (J'=0.15 meV), and a Dzyaloshinskii-Moriyalike term (D=0.107 meV). This simple Hamiltonian determined, for the first time, for BiFeO 3 provides a fundamental ingredient for understanding of the novel magnetic properties of BiFeO 3 .

Background-Accumulating evidence suggests that several subsets of regulatory T cells that actively mediate immunologic tolerance play crucial roles in atherogenesis. Recently, orally administered anti-CD3 monoclonal antibody has been shown as an inducer of novel regulatory T cells expressing latency-associated peptide (LAP) on their surface, which potently prevents systemic autoimmunity. In the present study, we hypothesized that oral anti-CD3 antibody treatment may inhibit atherosclerosis in mice. Methods and Results-Six-week-old apolipoprotein E-deficient mice on a standard diet were orally given anti-CD3 antibody or control immunoglobulin G on 5 consecutive days, and atherosclerosis was assessed at age 16 weeks. Oral administration of anti-CD3 antibody significantly reduced atherosclerotic lesion formation and accumulations of macrophages and CD4 ϩ T cells in the plaques compared with controls. We observed a significant increase in LAP ϩ cells and CD25ϩ Foxp3 ϩ cells in the CD4 ϩ T-cell population in anti-CD3-treated mice, in association with increased production of the antiinflammatory cytokine transforming growth factor-␤ and suppressed T-helper type 1 and type 2 immune responses. Neutralization of transforming growth factor-␤ in vivo abrogated the preventive effect of oral anti-CD3 antibody. Key Words: atherosclerosis Ⅲ immune system Ⅲ inflammation Ⅲ lymphocytes A therosclerosis is an inflammatory condition of the arterial wall involving cells of innate and adaptive immunity. 1,2 It leads to severe clinical events caused by the rupture of plaques and thrombotic occlusion of the artery and is the main cause of acute coronary syndrome and stroke, which account for approximately half of the deaths in Western countries. It is now widely recognized that chronic inflammation via T-cell-mediated pathogenic immune responses plays an important role in atherogenesis. 2 Accumulating evidence suggests that several subsets of regulatory T cells (Tregs), which have been shown to maintain immunologic unresponsiveness to self-antigens, 3 inhibit atherosclerosis development through the downregulation of activated T-cell responses. 4 -6 These studies imply that promotion of an endogenous regulatory immune response has a therapeutic potential to suppress atherosclerotic diseases. Conclusions-Our Clinical Perspective on p 2005Anti-CD3-specific antibodies strongly suppress immune responses by antigenic modulation of the T-cell receptor/CD3 complex. 7 In 1985, parenteral anti-CD3 antibody was available for use in acute transplant rejection in humans. However, its long-term use is limited because of severe side effects such as mitogenicity and antiglobulin responses. 7 The mitogenicity of anti-CD3 antibody with Fc portion is caused by interacting with Fc receptors (FcRs) on monocytes or macrophages. Therefore, humanized Fc-mutated antibodies were designed and demonstrated to be effective in human autoimmune diabetes for a long period, although they still induce low levels of cytokine release because of some degree of T-cell a...

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