Thermal Shock Resistances of High Thermal Conductivity C/C-Composite as Plasma Facing Materials for Fusion Reactor Devices

The thermal shock resistances, mechanical and fracture mechanics properties of one directionally oriented carbon fiber reinforced carbon composite HUD-1S, which was recently developed as a plasma facing material for fusion reactor devices, are presented. These results are compared with the cases of a fine grain isotropic graphite PD-600S. HUD-1S has extremely high anisotropies, such as the thermal conductivity in the direction along the fiber orientation is extremely high in excess of the conductivity of copper or silver. But the conductivitics of normal directions are below a half of the case of graphite. The characteristic isotropies on the thermal shock resistances and fracture toughnesses of this composite are given quantitatively

Tensor polarization of 12^{12}C[ 21+^+_1] in the 16^{16}O(13^{13}C,12^{12}C)17^{17}O reaction at 50 MeV

The $^{16}$O($^{13}$C,$^{12}$C)$^{17}$O reaction at 50 MeV has been investigated using the kinematical coincidence method. Polarization tensors $t_{20}$ and $t_{40}$ of $^{12}$C[ 2$^+_1$] for the quantization axis taken along the direction of propagation have been measured by analyzing the energy spectrum of $^{12}$C[ 2$^+_1$] , modulated by the effect of $\gamma$ ray emission. The deduced $t_{40}$ values significantly deviate from zero, contrary to the prediction of the distorted-wave Born approximation theory based on one-step $p$ shell neutron stripping without spin-dependent interactions. The phenomenological spin–orbit interaction necessary to reproduce the magnitude of measured $t_{40}$ is found to be much larger than the folding model prediction. It is shown that the experimental polarization tensors as well as the cross sections can be reproduced by introducing multi-step processes involving excitations in $^{12}$C and $^{13}$C without introducing spin-dependent interactions

Trpm4 Ion Channels in pre-Bo¨tzinger Complex Interneurons Are Essential for Breathing Motor Pattern But Not Rhythm

Inspiratory breathing movements depend on pre-Bötzinger complex (preBötC) interneurons that express calcium (Ca2+)-activated nonselective cationic current (ICAN) to generate robust neural bursts. Hypothesized to be rhythmogenic, reducing ICAN is predicted to slow down or stop breathing; its contributions to motor pattern would be reflected in the magnitude of movements (output). We tested the role(s) of ICAN using reverse genetic techniques to diminish its putative ion channels Trpm4 or Trpc3 in preBötC neurons in vivo. Adult mice transduced with Trpm4-targeted short hairpin RNA (shRNA) progressively decreased the tidal volume of breaths yet surprisingly increased breathing frequency, often followed by gasping and fatal respiratory failure. Mice transduced with Trpc3-targeted shRNA survived with no changes in breathing. Patch-clamp and field recordings from the preBötC in mouse slices also showed an increase in the frequency and a decrease in the magnitude of preBötC neural bursts in the presence of Trpm4 antagonist 9-phenanthrol, whereas the Trpc3 antagonist pyrazole-3 (pyr-3) showed inconsistent effects on magnitude and no effect on frequency. These data suggest that Trpm4 mediates ICAN, whose influence on frequency contradicts a direct role in rhythm generation. We conclude that Trpm4-mediated ICAN is indispensable for motor output but not the rhythmogenic core mechanism of the breathing central pattern generator

Trpm4 ion channels in pre-Bötzinger complex interneurons are essential for breathing motor pattern but not rhythm.

Inspiratory breathing movements depend on pre-Bötzinger complex (preBötC) interneurons that express calcium (Ca2+)-activated nonselective cationic current (ICAN) to generate robust neural bursts. Hypothesized to be rhythmogenic, reducing ICAN is predicted to slow down or stop breathing; its contributions to motor pattern would be reflected in the magnitude of movements (output). We tested the role(s) of ICAN using reverse genetic techniques to diminish its putative ion channels Trpm4 or Trpc3 in preBötC neurons in vivo. Adult mice transduced with Trpm4-targeted short hairpin RNA (shRNA) progressively decreased the tidal volume of breaths yet surprisingly increased breathing frequency, often followed by gasping and fatal respiratory failure. Mice transduced with Trpc3-targeted shRNA survived with no changes in breathing. Patch-clamp and field recordings from the preBötC in mouse slices also showed an increase in the frequency and a decrease in the magnitude of preBötC neural bursts in the presence of Trpm4 antagonist 9-phenanthrol, whereas the Trpc3 antagonist pyrazole-3 (pyr-3) showed inconsistent effects on magnitude and no effect on frequency. These data suggest that Trpm4 mediates ICAN, whose influence on frequency contradicts a direct role in rhythm generation. We conclude that Trpm4-mediated ICAN is indispensable for motor output but not the rhythmogenic core mechanism of the breathing central pattern generator