Reducing nonideal to ideal coupling in random matrix description of chaotic scattering: Application to the time-delay problem

We write explicitly a transformation of the scattering phases reducing the problem of quantum chaotic scattering for systems with M statistically equivalent channels at nonideal coupling to that for ideal coupling. Unfolding the phases by their local density leads to universality of their local fluctuations for large M. A relation between the partial time delays and diagonal matrix elements of the Wigner-Smith matrix is revealed for ideal coupling. This helped us in deriving the joint probability distribution of partial time delays and the distribution of the Wigner time delay.Comment: 4 pages, revtex, no figures; published versio

AC resistivity of d-wave ceramic superconductors

We model d-wave ceramic superconductors with a three-dimensional lattice of randomly distributed $\pi$ Josephson junctions with finite self-inductance. The linear and nonlinear ac resistivity of the d-wave ceramic superconductors is obtained as function of temperature by solving the corresponding Langevin dynamical equations. We find that the linear ac resistivity remains finite at the temperature $T_p$ where the third harmonics of resistivity has a peak. The current amplitude dependence of the nonlinear resistivity at the peak position is found to be a power law. These results agree qualitatively with experiments. We also show that the peak of the nonlinear resistivity is related to the onset of the paramagnetic Meissner effect which occurs at the crossover temperature $T_p$, which is above the chiral glass transition temperature $T_{cg}$.Comment: 7 eps figures, Phys. Rev. B (in press

Dual-FRET imaging of IP3 and Ca2+ revealed Ca2+-induced IP3 production maintains long lasting Ca2+ oscillations in fertilized mouse eggs

In most species, fertilization induces Ca(2+) transients in the egg. In mammals, the Ca(2+) rises are triggered by phospholipase Czeta (PLCzeta) released from the sperm; IP3 generated by PLCzeta induces Ca(2+) release from the intracellular Ca(2+) store through IP3 receptor, termed IP3-induced Ca(2+) release. Here, we developed new fluorescent IP3 sensors (IRIS-2s) with the wider dynamic range and higher sensitivity (Kd = 0.047-1.7 muM) than that we developed previously. IRIS-2s employed green fluorescent protein and Halo-protein conjugated with the tetramethylrhodamine ligand as fluorescence resonance energy transfer (FRET) donor and acceptor, respectively. For simultaneous imaging of Ca(2+) and IP3, using IRIS-2s as the IP3 sensor, we developed a new single fluorophore Ca(2+) sensor protein, DYC3.60. With IRIS-2s and DYC3.60, we found that, right after fertilization, IP3 concentration ([IP3]) starts to increase before the onset of the first Ca(2+) wave. [IP3] stayed at the elevated level with small peaks followed after Ca(2+) spikes through Ca(2+) oscillations. We detected delays in the peak of [IP3] compared to the peak of each Ca(2+) spike, suggesting that Ca(2+)-induced regenerative IP3 production through PLC produces small [IP3] rises to maintain [IP3] over the basal level, which results in long lasting Ca(2+) oscillations in fertilized eggs

Astrodynamics Science About Itokawa, Gravity and Ephemeris

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76347/1/AIAA-2006-6658-569.pd

Intravenous Administration of Human Amniotic Mesenchymal Stem Cells in the Subacute Phase of Cerebral Infarction in a Mouse Model Ameliorates Neurological Disturbance by Suppressing Blood Brain Barrier Disruption and Apoptosis via Immunomodulation

Neuro-inflammation plays a key role in the pathophysiology of brain infarction. Cell therapy offers a novel therapeutic option due to its effect on immunomodulatory effects. Amniotic stem cells, in particular, show promise owing to their low immunogenicity, tumorigenicity, and easy availability from amniotic membranes discarded following birth. We have successfully isolated and expanded human amniotic mesenchymal stem cells (hAMSCs). Herein, we evaluated the therapeutic effect of hAMSCs on neurological deficits after brain infarction as well as their immunomodulatory effects in a mouse model in order to understand their mechanisms of action. One day after permanent occlusion of the middle cerebral artery (MCAO), hAMSCs were intravenously administered. RT-qPCR for TNFα, iNOS, MMP2, and MMP9, immunofluorescence staining for iNOS and CD11b/c, and a TUNEL assay were performed 8 days following MCAO. An Evans Blue assay and behavioral tests were performed 2 days and several months following MCAO, respectively. The results suggest that the neurological deficits caused by cerebral infarction are improved in dose-dependent manner by the administration of hAMSCs. The mechanism appears to be through a reduction in disruption of the blood brain barrier and apoptosis in the peri-infarct region through the suppression of pro-inflammatory cytokines and the M2-to-M1 phenotype shift