The Unusual Superconducting State at 49 K in Electron-Doped CaFe2As2 at Ambient

We report the detection of unusual superconductivity up to 49 K in single crystalline CaFe2As2 via electron-doping by partial replacement of Ca by rare-earth. The superconducting transition observed suggests the possible existence of two phases: one starting at ~ 49 K, which has a low critical field ~ 4 Oe, and the other at ~ 21 K, with a much higher critical field > 5 T. Our observations are in strong contrast to previous reports of doping or pressurizing layered compounds AeFe2As2 (or Ae122), where Ae = Ca, Sr or Ba. In Ae122, hole-doping has been previously observed to generate superconductivity with a transition temperature (Tc) only up to 38 K and pressurization has been reported to produce superconductivity with a Tc up to 30 K. The unusual 49 K phase detected will be discussed.Comment: 11 pages, 8 figure

Doping dependent evolution of magnetism and superconductivity in Eu1-xKxFe2As2 (x = 0-1) and temperature dependence of lower critical field Hc1

We have synthesized the polycrystalline samples of Eu1-xKxFe2As2 (x = 0-1) and carried out systematic characterization using x-ray diffraction, ac & dc magnetic susceptibility, and electrical resistivity measurements. We have seen a clear signature of the coexistence of superconducting transition (Tc = 5.5 K) with SDW ordering in our under doped sample viz. x = 0.15. The spin density wave transition observed in EuFe2As2 get completely suppressed at x = 0.3 and superconductivity arises below 20 K. Superconducting transition temperature Tc increases with increase in K content and a maximum Tc = 33 K is reached for x = 0.5, beyond which it decreases again. The doping dependent T(x) phase diagram is extracted from the magnetic and electrical transport data. It is found that magnetic ordering of Eu-moments coexists with superconductivity up to x = 0.6. The isothermal magnetization data taken at 2 K for the doped samples suggest 2+ valence states of Eu ions. We also present the temperature dependence of the lower critical field Hc1 of superconducting polycrystalline samples. The value of Hc1(0) obtained for x = 0.3, 0.5, and 0.7 after taking the demagnetization factor into account is 248, 385, and 250 Oe, respectively. The London penetration depth {\lambda}(T) calculated from the lower critical field does not show exponential behaviour at low temperature, as would be expected for a fully gapped clean s-wave superconductor. In contrast, it shows a T2 power-law feature down to T = 0.4 Tc, as observed in Ba1-xKxFe2As2 and BaFe2-xCoxAs2.Comment: 17 pages, 10 figure

HMGB1: a novel protein that induced platelets active and aggregation via Toll-like receptor-4, NF-kappaB and cGMP dependent mechanisms

BACKGROUND: Thrombotic diseases are a group of prevalent and life-threatening diseases. Selective inhibition of pathological thrombosis holds the key to treat variety of thrombotic diseases. The pathological thrombosis can be induced by either tissue necrosis and deregulated inflammation. HMGB1, as an important proinflammatory cytokine and a late mediator, also involves on thrombosis disease. However, the underlying mechanisms are not fully understood. METHODS: Immunofluorescence, ELISA assay, Platelet Aggregation, Thromboelastogram (TEG) analyzes. Flow cytometric analysis and Western blot analysis were used to investigated the role of HMGB1 in platelet aggregation and obtained following observations. RESULTS: By doing so, we obtained the following observations: i) Highly purified HMGB1 recombinant protein induces platelet aggregation and secretion in a dose-dependent manner in the presence of serum. ii) Low concentration of extracellular HMGB1 could synergistically promote subthreshold concentration of collagen or thrombin induced platelet aggregation. iii) Extracellular HMGB1 promoted platelet aggregation in a platelet-expressed GPIIb/IIIa-dependent manner. iv) We proposed that extracellular HMGB1 seems to promote the phosphorylation of GPIIb/IIIa and subsequent platelet aggregation via TLR4/NF-kappaB and cGMP pathway. CONCLUSIONS: In this study, we provide evidence for the hypothesis that HMGB1 interact with platelet might play an important role in the haemostasis and thrombotic diseases. Our research might be provide an interesting avenue for the treatment of thrombotic diseases in the future