Recovery of chaotic tunneling due to destruction of dynamical localization by external noise

Quantum tunneling in the presence of chaos is analyzed, focusing especially on the interplay between quantum tunneling and dynamical localization. We observed flooding of potentially existing tunneling amplitude by adding noise to the chaotic sea to attenuate the destructive interference generating dynamical localization. This phenomenon is related to the nature of complex orbits describing tunneling between torus and chaotic regions. The tunneling rate is found to obey a perturbative scaling with noise intensity when the noise intensity is sufficiently small and then saturate in a large noise intensity regime. A relation between the tunneling rate and the localization length of the chaotic states is also demonstrated. It is shown that due to the competition between dynamical tunneling and dynamical localization, the tunneling rate is not a monotonically increasing function of Planck's constant. The above results are obtained for a system with a sharp border between torus and chaotic regions. The validity of the results for a system with a smoothed border is also explained.Comment: 14 pages, 15 figure

TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice

Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.Fil: Oda, Sayaka. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; JapónFil: Numaga Tomita, Takuro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; JapónFil: Kitajima, Naoyuki. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; JapónFil: Tomizaki, Takashi. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; Japón. University of Tsukuba; JapónFil: Harada, Eri. Ajinomoto Co.; Japón. EA Pharma Co.; JapónFil: Shimauchi, Tsukasa. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; JapónFil: Nishimura, Akiyuki. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Ajinomoto Co.; JapónFil: Ishikawa, Tatsuya. Kyushu University; Japón. Ajinomoto Co.; Japón. EA Pharma Co.; JapónFil: Kumagai, Yoshito. University of Tsukuba; JapónFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Nishida, Motohiro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Kyushu University; Japón. PRESTO; Japó

Physical properties of a new cuprate superconductor Pr_2Ba_4Cu_7O_{15-\delta}

We present studies of the thermal, magnetic and electrical transport properties of reduced polycrystalline Pr_2Ba_4Cu_7O_{15-\delta} (Pr247) showing a superconducting transition at Tc = 10 - 16 K and compare them with those of as-sintered non-superconducting Pr247. The electrical resistivity in the normal state exhibited T2 dependence up to approximately 150 K. A clear specific heat anomaly was observed at Tc for Pr247 reduced in a vacuum for 24 hrs, proving the bulk nature of the superconducting state. By the reduction treatment, the magnetic ordering temperature TN of Pr moments decreased from 16 to 11 K, and the entropy associated with the ordering increased, while the effective paramagnetic moments obtained from the DC magnetic susceptibility varied from 2.72 to 3.13 mB. The sign of Hall coefficient changed from positive to negative with decreasing temperature in the normal state of a superconducting Pr247, while that of as-sintered one was positive down to 5 K. The electrical resistivity under high magnetic fields was found to exhibit T^a dependence (a = 0.08 - 0.4) at low temperatures. A possibility of superconductivity in the so-called CuO double chains is discussed.Comment: Science and Technology of Advanced Materials (in press

TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice

Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6

Variety of the Wave Change in Compound Muscle Action Potential in an Animal Model

Study DesignAnimal study.PurposeTo review the present warning point criteria of the compound muscle action potential (CMAP) and investigate new criteria for spinal surgery safety using an animal model.Overview of LiteratureLittle is known about correlation palesis and amplitude of spinal cord monitoring.MethodsAfter laminectomy of the tenth thoracic spinal lamina, 2-140 g force was delivered to the spinal cord with a tension gage to create a bilateral contusion injury. The study morphology change of the CMAP wave and locomotor scale were evaluated for one month.ResultsFour different types of wave morphology changes were observed: no change, amplitude decrease only, morphology change only, and amplitude and morphology change. Amplitude and morphology changed simultaneously and significantly as the injury force increased (p<0.05) Locomotor scale in the amplitude and morphology group worsened more than the other groups.ConclusionsAmplitude and morphology change of the CMAP wave exists and could be the key of the alarm point in CMAP

Viscoplastic Deformation of Lead Free Solder Alloy- Experiments and Simulations

In this paper, viscoplastic deformations of Sn-3.5Ag-0.75Cu solder alloy are discussed. First, the following experiments are conducted: (1) Pure tension at several strain rates. (2) Cyclic tension-compression loading with several strain amplitudes at several strain rates. (3) Creep tests at several stress levels. The test results show that the Sn-3.5Ag-0.75Cu solder alloy has large strain rate and temperature effects, and that there is a noticeable transient creep region in the creep curves. A viscoplastic constitutive model for the solder alloy is also discussed. The model is constructed based on the dislocation density based constitutive model proposed by Estrin [6]. The constitutive model well simulates both the time and temperature dependences on the deformation of the lead free solder alloy. Finally, the constitutive model is incorporated into a general purpose FEM program (Marc) to clarify the applicability of the model to the structural analysis.Key Engineering Materials, Volume 233-23

統計教育ツールとしての jamovi / Introducing jamovi as a tool for education in statistics.

オープンソースの統計ソフトウェアである jamovi が有償ソフトウェアに比べて，統計教育のためのツールとして何がどのように優れているかを論じ，jamovi による統計分析の例を解説した。/ We proposed that open-source statistical software “jamovi” is a successful candidate of educational tool in statistics, because it has a user-friendly GUI and is based on powerful statistical programming language R. In this paper, we argued the potential benefits of “jamovi” and introduced how it works with typical statistical testing