The breakdown of both strange metal and superconducting states at a pressure-induced quantum critical point in iron-pnictide superconductors.

Here we report the first observation of the concurrent breakdown of the strange metal (SM) normal state and superconductivity at a pressure-induced quantum critical point in Ca10(Pt4As8)((Fe0.97Pt0.03)2As2)5 superconductor. We find that, upon suppressing the superconducting state, the power exponent (α) changes from 1 to 2, and the slope of the temperature-linear resistivity per FeAs layer (A□) gradually diminishes. At a critical pressure, A□ and superconducting transition temperature (Tc) go to zero concurrently, where a quantum phase transition from a superconducting state with a SM normal state to a non-superconducting Fermi liquid state occurs. Scaling analysis reveals that the change of A□ with Tc obeys the relation of Tc ~ (A□)0.5, similar to what is seen in other chemically doped unconventional superconductors. These results suggest that there is a simple but powerful organizational principle of connecting the SM normal state with the high-Tc superconductivity.

Inhibition of eukaryotic initiation factor 4E phosphorylation by cercosporamide selectively suppresses angiogenesis, growth and survival of human hepatocellular carcinoma.

Mnk kinase is required for the phosphorylation and activation of the eukaryotic initiation factor 4E (eIF4E), which regulates translation of proteins involve in important aspects of hepatocellular carcinoma (HCC). Here we investigated whether an antifungal agent, cercosporamide, which had been recently identified as a potent Mnk inhibitor, is active against HCC and angiogenesis. We showed that cercosporamide significantly inhibited growth and induced caspase-dependent apoptosis on numerous HCC cell lines, while sparing normal liver cells. In addition, cercosporamide impaired HCC angiogenesis via inhibiting HCC-endothelial cells (HCC-EC) capillary network formation, migration, proliferation and survival. Importantly, cercosporamide sensitized HCC cells to cisplatin in in vitro cell culture and in vivo HCC xenograft mouse model. Cercosporamide blocked the phosphorylation of eIF4E but not Erk or p38 in a dose- and time-dependent manner in HCC and HCC-EC cells, suggesting that suppression of eIF4E phosphorylation was the result of inhibition of Mnk but not Mnk upstream pathways. Overexpression of constitutively active eIF4E (S209D) but not the nonphosphorylatable eIF4E (S209A) abolished the inhibitory effects of cercosporamide in HepG2 cells. Altogether, our work demonstrates that cercosporamide acts as a Mnk inhibitor through blockage of eIF4E phosphorylation and selectively exhibits anti-HCC activities. Our work suggests that targeting MNK-eIF4E pathway represents a therapeutic strategy to overcome chemo-resistance for HCC treatment.

Pressure-induced superconductivity and its scaling with doping-induced superconductivity in the iron pnictide with skutterudite intermediary layers.

Pressure-induced superconductivity is oberserved in Ca10(Pt3As8)(Fe2As2)5 by in situ high-pressure resistance and magnetic susceptibility measurements. Scaling of the pressure-induced and doping-induced superconductivity shows that the electronic phase diagrams of the pressurized and chemically doped 10­3­8 compound are similar in the moderate pressure and doping range but are disparate at higher pressure and heavy doping.

Pressure-induced superconductivity and its scaling with doping-induced superconductivity in the iron pnictide with skutterudite intermediary layers.

Pressure-induced superconductivity is oberserved in Ca10 (Pt3 As8 )(Fe2 As2 )5 by in situ high-pressure resistance and magnetic susceptibility measurements. Scaling of the pressure-induced and doping-induced superconductivity shows that the electronic phase diagrams of the pressurized and chemically doped 10-3-8 compound are similar in the moderate pressure and doping range but are disparate at higher pressure and heavy doping.

Pressure-driven quantum criticality in iron-selenide superconductors.

We report a finding of a pressure-induced quantum critical transition in K0.8Fe(x)Se2 (x = 1.7 and 1.78) superconductors through in situ high-pressure electrical transport and x-ray diffraction measurements in diamond anvil cells. Transitions from metallic Fermi liquid behavior to non-Fermi liquid behavior and from antiferromagnetism to paramagnetism are found in the pressure range of 9.2-10.3 GPa, in which superconductivity tends to disappear. The change around the quantum critical point from the coexisting antiferromagnetism state and the Fermi liquid behavior to the paramagnetism state and the non-Fermi liquid behavior in the iron-selenide superconductors demonstrates a unique mechanism for their quantum critical transition.

Re-emerging superconductivity at 48 kelvin in iron chalcogenides.

Pressure has an essential role in the production and control of superconductivity in iron-based superconductors. Substitution of a large cation by a smaller rare-earth ion to simulate the pressure effect has raised the superconducting transition temperature T(c) to a record high of 55 K in these materials. In the same way as T(c) exhibits a bell-shaped curve of dependence on chemical doping, pressure-tuned T(c) typically drops monotonically after passing the optimal pressure. Here we report that in the superconducting iron chalcogenides, a second superconducting phase suddenly re-emerges above 11.5 GPa, after the T(c) drops from the first maximum of 32 K at 1 GPa. The T(c) of the re-emerging superconducting phase is considerably higher than the first maximum, reaching 48.0-48.7 K for Tl(0.6)Rb(0.4)Fe(1.67)Se(2), K(0.8)Fe(1.7)Se(2) and K(0.8)Fe(1.78)Se(2).