Heating-compensated constant-temperature tunneling measurements on stacks of Bi2_2Sr2_2CaCu2_2O8+x_{8+x} intrinsic junctions

In highly anisotropic layered cuprates such as Bi$_2$Sr$_2$CaCu$_2$O$_{8+x}$ tunneling measurements on a stack of intrinsic junctions in a high-bias range are often susceptible to self-heating. In this study we monitored the temperature variation of a stack ("sample stack") of intrinsic junctions by measuring the resistance change of a nearby stack ("thermometer stack") of intrinsic junctions, which was strongly thermal-coupled to the sample stack through a common Au electrode. We then adopted a proportional-integral-derivative scheme incorporated with a substrate-holder heater to compensate the temperature variation. This in-situ temperature monitoring and controlling technique allows one to get rid of spurious tunneling effects arising from the self-heating in a high bias range.Comment: 3 pages, 3 figure

Collective Josephson vortex dynamics in a finite number of intrinsic Josephson junctions

We report the experimental confirmation of the collective transverse plasma modes excited by the Josephson vortex lattice in stacks of intrinsic Josephson junctions in Bi$_{2}$Sr$_{2}$CaCu$_{2}$O$_{8+x}$ single crystals. The excitation was confirmed by analyzing the temperature ($T$) and magnetic field ($H$) dependencies of the multiple sub-branches in the Josephson-vortex-flow region of the current-voltage characteristics of the system. In the near-static Josephson vortex state for a low tunneling bias current, pronounced magnetoresistance oscillations were observed, which represented a triangular-lattice vortex configuration along the c axis. In the dynamic vortex state in a sufficiently high magnetic field and for a high bias current, splitting of a single Josephson vortex-flow branch into multiple sub-branches was observed. Detailed examination of the sub-branches for varying $H$ field reveals that sub-branches represent the different modes of the Josephson-vortex lattice along the c axis, with varied configuration from a triangular to a rectangular lattices. These multiple sub-branches merge to a single curve at a characteristic temperature, above which no dynamical structural transitions of the Josephson vortex lattice is expected

Coarsening model of cavity nucleation and thin film delamination from single-crystal BaTiO3 with proton implantation

The layer splitting mechanism of a proton implanted single crystal ferroelectric BaTiO3 thin film layer from its bulk BaTiO3 substrate has been investigated. The single crystal BaTiO3 thin film layer splits as the hydrogen gas diffuses and the internal cavity pressure increases. Ripening mechanism driven by the pressurized hydrogen in the implantation-induced damage zone makes coarsening of the cavities and causes the delamination of the thin layer during the annealing. A unique criterion relation of blister nucleation and evolution has been derived and a simplified debonding criterion is proposed in terms of dimensionless parameters based on the force equilibrium condition. A numerical simulation of two-bubble evolution and delamination of thin film is performed using a finite element method

Ductile Fracture Simulation of Full-scale Circumferential Cracked Pipes: (II) Stainless Steel

AbstractThis paper reports ductile fracture simulation of full-scale circumferentially cracked pipes using finite element (FE) damage analysis. In the structural integrity, without experimental investigations or with few ones, it is not an easy task to properly evaluate the crack initiation and crack propagation of large-scale components with a crack-like defect. Unfortunately, from an economic perspective, performing experiments of large-scale components would be consequently unfavorable. For these reasons, ductile fracture simulation using FE damage analysis to predict crack behavior is one efficient way to replace the test procedures. In order to simulate ductile tearing of large-scale cracked pipes, element-size-dependent critical damage model based on the stress-modified fracture strain model is proposed. To evaluate fracture behavior of full-scale cracked pipes, tensile and C(T) specimens are calibrated by FE analysis technique. Tensile properties and fracture toughness of stainless steel at 288oC are taken from Battelle Pipe Fracture Encyclopedia. After calibrations, simulated results of the full-scale pipes with a circumferential crack are compared with test data to validate the proposed method

Protein kinase CK2 phosphorylates and activates p21-activated kinase 1

Activation of the p21-activated kinase 1 (PAK1) is achieved through a conformational change that converts an inactive PAK1 dimer to an active monomer. In this paper, we show that this change is necessary but not sufficient to activate PAK1 and that it is, rather, required for CK2-dependent PAK1S223 phosphorylation that converts a monomeric PAK1 into a catalytically active form. This phosphorylation appears to be essential for autophosphorylation at specific residues and overall activity of PAK1. A phosphomimetic mutation (S223E) bypasses the requirement for GTPases in PAK1 activation, whereas the constitutive activity of the PAK1 mutant (PAK1H83,86L), postulated to mimic GTPase-induced structural changes, is abolished by inhibition of S223 phosphorylation. Thus, S223 is likely accessible to CK2 upon conformational changes of PAK1 induced by GTPase-dependent and GTPase-independent stimuli, suggesting that S223 phosphorylation may play a key role in the final step of the PAK1 activation process. The physiological significance of this phosphorylation is reinforced by the observations that CK2 is responsible for epidermal growth factor–induced PAK1 activation and that inhibition of S223 phosphorylation abrogates PAK1-mediated malignant transformation of prostate epithelial cells. Taken together, these findings identify CK2 as an upstream activating kinase of PAK1, providing a novel mechanism for PAK1 activation

Josephson-vortex-flow terahertz emission in layered high-TcT_c superconducting single crystals

We report on the successful terahertz emission (0.6$\sim$1 THz) that is continuous and tunable in its frequency and power, by driving Josephson vortices in resonance with the collective standing Josephson plasma modes excited in stacked Bi$_2$Sr$_2$CaCu$_2$O$_{8+x}$ intrinsic Josephson junctions. Shapiro-step detection was employed to confirm the terahertz-wave emission. Our results provide a strong feasibility of developing long-sought solid-state terahertz-wave emission devices

Properties Of Analyst Forecasts And Bond Underwriting Relationship: Evidence From Korea

Previous studies find that analysts forecast earnings more optimistically but inaccurately when they face the conflict of interest (COI). We extend this line of research by examining whether analysts’ forecasting behavior affected by the mere existence of potential COI are related with underwriting contracts.We document that analysts affiliated with security companies that become underwriters ex post issue more optimistic but less accurate forecasts for firms to issue bonds in Korea. We also find that firms to issue bonds are likely to award underwriting contracts to security companies with analysts who issue more optimistic but less accurate forecasts.  

The Role of the Pleckstrin Homology Domain-Containing Protein CKIP-1 in Activation of p21-activated Kinase 1 (PAK1)

Upon growth factor stimulation, PAK1 is recruited to the plasma membrane and activated by a mechanism that requires its phosphorylation at S223 by the protein kinase CK2. However, the upstream signaling molecules that regulate this phosphorylation event are not clearly defined. Here, we demonstrate a major role of the CK2α-interacting protein CKIP-1 in activation of PAK1. CK2α, CKIP-1 and PAK1 are translocated to membrane ruffles in response to the epidermal growth factor (EGF), where CKIP-1 mediates the interaction between CK2α, and PAK1 in a PI3K-dependent manner. Consistently, we observe that PAK1 mediates phosphorylation and modulation of the activity of p41-Arc, one of its plasma membrane substrate, in a fashion that requires PI3K and CKIP-1. Moreover, CKIP-1 knockdown or PI3K inhibition suppresses PAK1-mediated cell migration and invasion, demonstrating the physiological significance of the PI3K-CKIP-1-CK2α-PAK1 signaling pathway. Taken together, these findings identify a novel mechanism for the activation of PAK1 at the plasma membrane, which is critical for cell migration and invasion