Inclusive angular distribution of alpha and Li fragments produced in the Fe-C and Fe-Pb collisions at 1.88 GeV/u

The LS (laboratory system) emission angles theta for 2188 and 298 Li fragments, produced inclusively in relativistic Fe-C and Fe-Pb collisions, have been measured in reference to incident Fe-ion beam tracks nearby in nuclear emulsion. An empirical differential frequency formula, dN(cot theta) = exp (a + b cot theta)d(cot theta) is obtained with the constant b approx. = -0.026 at 1.88 GeV/u, which seems to be independent on the kinds of target nucleus as well as on the kinds of projectile fragments

Silibinin induces apoptosis via calpain-dependent AIF nuclear translocation in U87MG human glioma cell death

<p>Abstract</p> <p>Background</p> <p>Silibinin, a natural polyphenolic flavonoid, has been reported to induce cell death in various cancer cell types. However, the molecular mechanism is not clearly defined. Our previous study showed that silibinin induces glioma cell death and its effect was effectively prevented by calpain inhibitor. The present study was therefore undertaken to examine the role of calpain in the silibinin-induced glioma cell death.</p> <p>Methods</p> <p>U87MG cells were grown on well tissue culture plates and cell viability was measured by MTT assay. ROS generation and △ψ_mwere estimated using the fluorescence dyes. PKC activation and Bax expression were measured by Western blot analysis. AIF nuclear translocation was determined by Western blot and immunocytochemistry.</p> <p>Results</p> <p>Silibinin induced activation of calpain, which was blocked by EGTA and the calpain inhibitor Z-Leu-Leu-CHO. Silibinin caused ROS generation and its effect was inhibited by calpain inhibitor, the general PKC inhibitor GF 109203X, the specific PKC_δinhibitor rottlerin, and catalase. Silibinin-induce cell death was blocked by calpain inhibitor and PKC inhibitors. Silibinin-induced PKC_δactivation and disruption of △ψ_mwere prevented by the calpain inhibitor. Silibinin induced AIF nuclear translocation and its effect was prevented by calpain inhibitor. Transfection of vector expressing microRNA of AIF prevented the silibinin-induced cell death.</p> <p>Conclusions</p> <p>Silibinin induces apoptotic cell death through a calpain-dependent mechanism involving PKC, ROS, and AIF nuclear translocation in U87MG human glioma cells.</p

Electrodynamics of the vanadium oxides VO2 and V2O3

The optical/infrared properties of films of vanadium dioxide (VO2) and vanadium sesquioxide (V2O3) have been investigated via ellipsometry and near-normal incidence reflectance measurements from far infrared to ultraviolet frequencies. Significant changes occur in the optical conductivity of both VO2 and V2O3 across the metal-insulator transitions at least up to (and possibly beyond) 6 eV. We argue that such changes in optical conductivity and electronic spectral weight over a broad frequency range is evidence of the important role of electronic correlations to the metal-insulator transitions in both of these vanadium oxides. We observe a sharp optical transition with possible final state (exciton) effects in the insulating phase of VO2. This sharp optical transition occurs between narrow a1g bands that arise from the quasi-one-dimensional chains of vanadium dimers. Electronic correlations in the metallic phases of both VO2 and V2O3 lead to reduction of the kinetic energy of the charge carriers compared to band theory values, with paramagnetic metallic V2O3 showing evidence of stronger correlations compared to rutile metallic VO2.Comment: 11 pages, 7 figure

Monoclinic and Correlated Metal Phase in VO_2 as Evidence of the Mott Transition: Coherent Phonon Analysis

In femtosecond pump-probe measurements, the appearance of coherent phonon oscillations at 4.5 THz and 6.0 THz indicating the rutile metal phase of VO_2 does not occur simultaneously with the first-order metal-insulator transition (MIT) near 68^oC. The monoclinic and correlated metal(MCM) phase between the MIT and the structural phase transition (SPT) is generated by a photo-assisted hole excitation which is evidence of the Mott transition. The SPT between the MCM phase and the rutile metal phase occurs due to subsequent Joule heating. The MCM phase can be regarded as an intermediate non-equilibrium state.Comment: 4 pages, 2 figure