Vortex Fluid State below an Onset Temperature T_0 of Solid 4He

Detailed studies of AC velocity Vac and temperature dependence of torsional oscillator responses of solid 4He are reported. A characteristic onset temperature T0 about 0.5 K is found, below which a significant Vac dependent change occurs in the energy dissipation for the sample at 32 bar. A Vac dependence of the non-classical rotational inertia fraction, NCRIF also appears below about T0. This value of T0 excludes the possible explanation of supersolid by liquid superfluidity in grain boundaries or other liquid related origins. The log(Vac) linear dependence was found in NCRIF. Furthermore, this linear slope changes in proportion to 1/T 2 for 40 < Vac < 400 micro-m/s, then crosses over to about 1/T for larger Vac. We discuss properties of the vortex fluid state proposed by Anderson above Tc, below T0.Comment: 4pages,4 figure

Annealing Effect for Supersolid Fraction in 4^4He

We report on experimental confirmation of the non-classical rotational inertia (NCRI) in solid helium samples originally reported by Kim and Chan. The onset of NCRI was observed at temperatures below ~400 mK. The ac velocity for initiation of the NCRI suppression is estimated to be ~10 $\mu$m/sec. After an additional annealing of the sample at $T= 1.8$ K for 12 hours, ~ 10% relative increase of NCRI fraction was observed. Then after repeated annealing with the same conditions, the NCRI fraction was saturated. It differs from Reppy's observation on a low pressure solid sample.Comment: to be published in J. of Low Temp. Phys. (QFS2006 proceedings

Spin-Torque Diode Measurements of MgO-Based Magnetic Tunnel Junctions with Asymmetric Electrodes

We present a detailed study of the spin-torque diode effect in CoFeB/MgO/CoFe/NiFe magnetic tunnel junctions. From the evolution of the resonance frequency with magnetic field at different angles, we clearly identify the free-layer mode and find an excellent agreement with simulations by taking into account several terms for magnetic anisotropy. Moreover, we demonstrate the large contribution of the out-of-plane torque in our junctions with asymmetric electrodes compared to the in-plane torque. Consequently, we provide a way to enhance the sensitivity of these devices for the detection of microwave frequency

Regulation of Epithelial Sodium Transport via Epithelial Na+ Channel

Renal epithelial Na+ transport plays an important role in homeostasis of our body fluid content and blood pressure. Further, the Na+ transport in alveolar epithelial cells essentially controls the amount of alveolar fluid that should be kept at an appropriate level for normal gas exchange. The epithelial Na+ transport is generally mediated through two steps: (1) the entry step of Na+ via epithelial Na+ channel (ENaC) at the apical membrane and (2) the extrusion step of Na+ via the Na+, K+-ATPase at the basolateral membrane. In general, the Na+ entry via ENaC is the rate-limiting step. Therefore, the regulation of ENaC plays an essential role in control of blood pressure and normal gas exchange. In this paper, we discuss two major factors in ENaC regulation: (1) activity of individual ENaC and (2) number of ENaC located at the apical membrane

Attenuated response to liver injury in moesin-deficient mice: Impaired stellate cell migration and decreased fibrosis

AbstractHepatic stellate cells (HSCs) respond to injury with a coordinated set of events (termed activation), which includes migration and upregulation of matrix protein production. Cell migration requires an intact actin cytoskeleton that is linked to the plasma membrane by ezrin–radixin–moesin (ERM) proteins. We have previously found that the linker protein in HSCs is exclusively moesin. Here, we describe HSC migration and fibrogenesis in moesin-deficient mice. We developed an acute liver injury model that involved focal thermal denaturation and common bile duct ligation. HSC migration and collagen deposition were assessed by immunohistology and quantitative real-time PCR. Activated HSCs were isolated from wild-type or moesin-deficient mice for direct examination of migration. Activated HSCs from wild-type mice were positive for moesin. Migration of moesin-deficient HSCs was significantly reduced. In a culture assay, 22.1% of normal HSCs migrated across a filter in 36h. In contrast, only 1.3% of activated moesin-deficient HSCs migrated. Collagen deposition around the injury area similarly was reduced in moesin-deficient liver. The linker protein moesin is essential for HSC activation and migration in response to injury. Fibrogenesis is coupled to migration and reduced in moesin-deficient mice. Agents that target moesin may be beneficial for chronic progressive fibrosis