Thermoelectric properties of layered oxyselenides La1–xSrxCuOSe (x = 0 to 0.2)

Thermoelectric properties of layered oxyselenides La1–xSrxCuOSe (x = 0.00 to 0.20) were investigated to evaluate the potential as thermoelectric material. Temperature dependence of the electrical conductivity and Seebeck coefficient measured in a temperature range of 373 to 673 K indicated that nondoped LaCuOSe was a p-type degenerate semiconductor due to Cu vacancies, while Sr-doped materials with x = 0.05 to 0.20 were p-type metals. The electrical conductivity increased and Seebeck coefficient decreased with increasing Sr concentration up to x = 0.10 in La1–xSrxCuOSe, suggesting that the effective hole carriers increase with increasing Sr content up to x = 0.10. Thermoelectric power factors were drastically enhanced by the Sr doping, and the value reached 1.0–1.4×10–4 W m–1 K–2 for La0.95Sr0.05CuOSe. Thermal conductivities measured for the materials with x = 0.00 and 0.05 were 2.1 W m–1 K–1 and 2.3 W m–1 K–1 at room temperature, respectively. These results lead to an estimation of Z value of 4.4×10–5 K–1 for La0.95Sr0.05CuOSe

Thermoelectric properties of delafossite-type layered oxides AgIn1–xSnxO2

The thermoelectric properties of delafossite-type layered oxides AgIn1–xSnxO2 that consist of alternating layers of Ag and In1–xSnxO2 were investigated to elucidate their potential as a thermoelectric material. Polycrystalline materials of the AgIn1–xSnxO2 were prepared by a cation exchange reaction between NaIn1–xSnxO2 and AgCl. The solubility limit of the Sn atoms on the In sites was approximately x=0.05. The electrical conductivity and Seebeck coefficient were measured between 373 and 673 K in air. Undoped AgInO2 was an n-type semiconductor with conductivities of 10–4–10–2 –1 cm–1, and the electron carriers were generated via the formation of oxygen vacancies. AgIn0.95Sn0.05O2 was an n-type degenerate semiconductor with conductivities of 100–101 –1 cm–1 where the Sn atoms acted as electron donors. This drastic increase in the electrical conductivity increased the thermoelectric power factor by approximately two orders of magnitude to 10–6–10–5 W m–1 K–2

SOCS, Inflammation, and Autoimmunity

Cytokines play essential roles in innate and adaptive immunity. However, excess cytokines or dysregulation of cytokine signaling will cause a variety of diseases, including allergies, autoimmune diseases, inflammation, and cancer. Most cytokines utilize the so-called Janus kinase–signal transducers and activators of transcription pathway. This pathway is negatively regulated by various mechanisms including suppressors of cytokine signaling (SOCS) proteins. SOCS proteins bind to JAK or cytokine receptors, thereby suppressing further signaling events. Especially, suppressor of cytokine signaling-1 (SOCS1) and SOCS3 are strong inhibitors of JAKs, because these two contain kinase inhibitory region at the N-terminus. Studies using conditional knockout mice have shown that SOCS proteins are key physiological as well as pathological regulators of immune homeostasis. Recent studies have also demonstrated that SOCS1 and SOCS3 are important regulators of helper T cell differentiation and functions. This review focuses on the roles of SOCS1 and SOCS3 in T cell mediated inflammatory diseases

Thermoelectric properties of delafossite-type layered oxides AgIn1–xSnxO2

The thermoelectric properties of delafossite-type layered oxides AgIn1–xSnxO2 that consist of alternating layers of Ag and In1–xSnxO2 were investigated to elucidate their potential as a thermoelectric material. Polycrystalline materials of the AgIn1–xSnxO2 were prepared by a cation exchange reaction between NaIn1–xSnxO2 and AgCl. The solubility limit of the Sn atoms on the In sites was approximately x=0.05. The electrical conductivity and Seebeck coefficient were measured between 373 and 673 K in air. Undoped AgInO2 was an n-type semiconductor with conductivities of 10–4–10–2 –1 cm–1, and the electron carriers were generated via the formation of oxygen vacancies. AgIn0.95Sn0.05O2 was an n-type degenerate semiconductor with conductivities of 100–101 –1 cm–1 where the Sn atoms acted as electron donors. This drastic increase in the electrical conductivity increased the thermoelectric power factor by approximately two orders of magnitude to 10–6–10–5 W m–1 K–2

SOCS3 Is Essential in the Regulation of Fetal Liver Erythropoiesis

AbstractSOCS3 (CIS3/JAB2) is an SH2-containing protein that binds to the activation loop of Janus kinases, inhibiting kinase activity, and thereby suppressing cytokine signaling. During embryonic development, SOCS3 is highly expressed in erythroid lineage cells and is Epo independent. Transgene-mediated expression blocks fetal erythropoiesis, resulting in embryonic lethality. SOCS3 deletion results in an embryonic lethality at 12–16 days associated with marked erythrocytosis. Moreover, the in vitro proliferative capacity of progenitors is greatly increased. SOCS3-deficient fetal liver stem cells can reconstitute hematopoiesis in lethally irradiated adults, indicating that its absence does not disturb bone marrow erythropoiesis. Reconstitution of lymphoid lineages in JAK3-deficient mice also occurs normally. The results demonstrate that SOCS3 is critical in negatively regulating fetal liver hematopoiesis

Omentin Prevents Myocardial Ischemic Injury Through AMP-Activated Protein Kinase- and Akt-Dependent Mechanisms

ObjectivesThis study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms.BackgroundObesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity.MethodsIn patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion.ResultsThis study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt.ConclusionsOur data indicate that omentin functions as an adipokine that ameliorates acute ischemic injury in the heart by suppressing myocyte apoptosis through both AMPK- and Akt-dependent mechanisms

Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis

Atherosclerosis is an inflammatory vascular disease responsible for the first cause of mortality worldwide. Recent studies have clearly highlighted the critical role of the immunoinflammatory balance in the modulation of disease development and progression. However, the immunoregulatory pathways that control atherosclerosis remain largely unknown. We show that loss of suppressor of cytokine signaling (SOCS) 3 in T cells increases both interleukin (IL)-17 and IL-10 production, induces an antiinflammatory macrophage phenotype, and leads to unexpected IL-17–dependent reduction in lesion development and vascular inflammation. In vivo administration of IL-17 reduces endothelial vascular cell adhesion molecule–1 expression and vascular T cell infiltration, and significantly limits atherosclerotic lesion development. In contrast, overexpression of SOCS3 in T cells reduces IL-17 and accelerates atherosclerosis. We also show that in human lesions, increased levels of signal transducer and activator of transcription (STAT) 3 phosphorylation and IL-17 are associated with a stable plaque phenotype. These results identify novel SOCS3-controlled IL-17 regulatory pathways in atherosclerosis and may have important implications for the understanding of the increased susceptibility to vascular inflammation in patients with dominant-negative STAT3 mutations and defective Th17 cell differentiation

Virus-Infection or 5′ppp-RNA Activates Antiviral Signal through Redistribution of IPS-1 Mediated by MFN1

In virus-infected cells, RIG-I-like receptor (RLR) recognizes cytoplasmic viral RNA and triggers innate immune responses including production of type I and III interferon (IFN) and the subsequent expression of IFN-inducible genes. Interferon-β promoter stimulator 1 (IPS-1, also known as MAVS, VISA and Cardif) is a downstream molecule of RLR and is expressed on the outer membrane of mitochondria. While it is known that the location of IPS-1 is essential to its function, its underlying mechanism is unknown. Our aim in this study was to delineate the function of mitochondria so as to identify more precisely its role in innate immunity. In doing so we discovered that viral infection as well as transfection with 5′ppp-RNA resulted in the redistribution of IPS-1 to form speckle-like aggregates in cells. We further found that Mitofusin 1 (MFN1), a key regulator of mitochondrial fusion and a protein associated with IPS-1 on the outer membrane of mitochondria, positively regulates RLR-mediated innate antiviral responses. Conversely, specific knockdown of MFN1 abrogates both the virus-induced redistribution of IPS-1 and IFN production. Our study suggests that mitochondria participate in the segregation of IPS-1 through their fusion processes

Suppression of Sproutys Has a Therapeutic Effect for a Mouse Model of Ischemia by Enhancing Angiogenesis

Sprouty proteins (Sproutys) inhibit receptor tyrosine kinase signaling and control various aspects of branching morphogenesis. In this study, we examined the physiological function of Sproutys in angiogenesis, using gene targeting and short-hairpin RNA (shRNA) knockdown strategies. Sprouty2 and Sprouty4 double knockout (KO) (DKO) mice were embryonic-lethal around E12.5 due to cardiovascular defects. The number of peripheral blood vessels, but not that of lymphatic vessels, was increased in Sprouty4 KO mice compared with wild-type (WT) mice. Sprouty4 KO mice were more resistant to hind limb ischemia and soft tissue ischemia than WT mice were, because Sprouty4 deficiency causes accelerated neovascularization. Moreover, suppression of Sprouty2 and Sprouty4 expression in vivo by shRNA targeting accelerated angiogenesis and has a therapeutic effect in a mouse model of hind limb ischemia. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases