Measuring velocity of sound with nuclear resonant inelastic x-ray scattering

Nuclear resonant inelastic x-ray scattering is used to measure the projected partial phonon density of states of materials. A relationship is derived between the low-energy part of this frequency distribution function and the sound velocity of materials. Our derivation is valid for harmonic solids with Debye-like low-frequency dynamics. This method of sound velocity determination is applied to elemental, composite, and impurity samples which are representative of a wide variety of both crystalline and noncrystalline materials. Advantages and limitations of this method are elucidated

Dihydropyridine-induced Ca2+ release from ryanodine-sensitive Ca2+ pools in human skeletal muscle cells

Dihydropyridines (DHPs) are widely used antihypertensive drugs and inhibit excitation-contraction (E–C) coupling in vascular smooth muscle and in myocardial cells by antagonizing L-type Ca2+ channels (DHP receptors). However, contradictory reports exist about the interaction of the DHP with the skeletal muscle isoform of the DHP receptor and E–C coupling in skeletal muscle cells.Using the intracellular fluorescent Ca2+ indicator fura-2, an increase in [Ca2+]i was observed after extracellular application of nifedipine to cultured human skeletal muscle cells. The rise in [Ca2+]i was dose dependent with a calculated EC50 of 614 ± 96 nm nifedipine and a maximum increment in [Ca2+]i of 80 ± 3.2 nm. Similar values were obtained with nitrendipine.This effect of DHPs was restricted to differentiated skeletal muscle cells and was not seen in non-differentiated cells or in PC12 cells. In spite of the observed increase in [Ca2+]i, whole-cell patch clamp experiments revealed that 10 μm nifedipine abolished inward Ba2+ currents through L-type Ca2+ channels completely.Similar to nifedipine, (±)Bay K 8644, an agonist of the L-type Ca2+ channel, also increased [Ca2+]i. This effect could not be enhanced by further addition of nifedipine, suggesting that both DHPs act via a common signalling pathway.Based on the specific mechanism of the skeletal muscle E-C coupling, we propose the stabilization of a conformational state of the DHP receptor by DHPs, which is sufficient to activate the ryanodine receptor