Method and apparatus for analyzing material properties using ultrasound

Apparatus is disclosed for investigating the mechanical properties of a solid material such as bone, including means for positioning the apparatus in proximity to a surface of the material, at least one emitting ultrasound transducer, at least one receiving ultrasound transducer positioned to received ultrasound waves that have been emitted and have contacted the surface of the material, means for varying the angle of incidence of the emitted ultrasound wave towards the material, means for determining the alignment of the surface of the material with respect to the emitting and receiving ultrasound transdsucers, and signal analyzer means coupled to the receiving transducer for determining at least one characteristic of the received ultrasound wave which is indicative of a mechanical property of the material. A method is also disclosed of using such apparatus. The present invention permits the quick and efficient evaluation of treatment for osteoporosis, and whether that treatment has in fact reduced the tendency of a patient's bones to fracture.Board of Regents, University of Texas Syste

Method and apparatus for analyzing material properties using reflected ultrasound

A method and apparatus which assesses the mechanical properties of a material by launching an ultrasound signal at the material while varying the angle of incidence and analyzing the amplitude of the ultrasound wave reflected by the material. The method and apparatus correlates extrema (maxima or minima inflection points) in the reflected angle with the angle of incidence of the transmitted signal to identify critical angles of incidence. The velocity of the pressure wave in the material has been found to be a function of a first critical angle corresponding to a first maxima as the angle of incidence is increased in the range 0.degree.-90.degree.. The velocity of the shear wave in the material has been found to be a function of a second critical angle corresponding to a second maxima following the first maxima. Young's modulus of elasticity, Poisson's modulus, and density can be approximated using the velocity of the pressure wave and shear wave for isotropic materials. A third critical angle corresponding to a minima after the first critical angle (reflected amplitude approaching o) has been found particularly useful in conjunction with the first and second critical angles in assessing bone density and in determining whether the second critical point is at a maximum or an inflection point. The extension of the method in which the plane of scattering is rotated around the normal to bone while keeping the point of observation fixed has been found particularly useful in assessing the mechanical properties of anisotropic materials such as cortical bone.Board of Regents, University of Texas Syste

Stone-Wales Transformation Paths in Fullerene C60

The mechanisms of formation of a metastable defect isomer of fullerene C60 due to the Stone-Wales transformation are theoretically studied. It is demonstrated that the paths of the "dynamic" Stone-Wales transformation at a high sufficient for overcoming potential barriers) temperature can differ from the two "adiabatic" transformation paths discussed in the literature. This behavior is due to the presence of a great near-flat segment of the potential-energy surface in the neighborhood of metastable states. Besides, the sequence of rupture and formation of interatomic bonds is other than that in the case of the adiabatictransformation.Comment: 10 pages, 6 figure

Instantaneous Normal Mode Analysis of Supercooled Water

We use the instantaneous normal mode approach to provide a description of the local curvature of the potential energy surface of a model for water. We focus on the region of the phase diagram in which the dynamics may be described by the mode-coupling theory. We find, surprisingly, that the diffusion constant depends mainly on the fraction of directions in configuration space connecting different local minima, supporting the conjecture that the dynamics are controlled by the geometric properties of configuration space. Furthermore, we find an unexpected relation between the number of basins accessed in equilibrium and the connectivity between them.Comment: 5 pages, 4 figure

Ischaemic preconditioning improves proteasomal activity and increases the degradation of δPKC during reperfusion

The response of the myocardium to an ischaemic insult is regulated by two highly homologous protein kinase C (PKC) isozymes, delta and epsilon PKC. Here, we determined the spatial and temporal relationships between these two isozymes in the context of ischaemia/reperfusion (I/R) and ischaemic preconditioning (IPC) to better understand their roles in cardioprotection. Using an ex vivo rat model of myocardial infarction, we found that short bouts of ischaemia and reperfusion prior to the prolonged ischaemic event (IPC) diminished delta PKC translocation by 3.8-fold and increased epsilon PKC accumulation at mitochondria by 16-fold during reperfusion. In addition, total cellular levels of delta PKC decreased by 60 +/- 2.7% in response to IPC, whereas the levels of epsilon PKC did not significantly change. Prolonged ischaemia induced a 48 +/- 11% decline in the ATP-dependent proteasomal activity and increased the accumulation of misfolded proteins during reperfusion by 192 +/- 32%; both of these events were completely prevented by IPC. Pharmacological inhibition of the proteasome or selective inhibition of epsilon PKC during IPC restored delta PKC levels at the mitochondria while decreasing epsilon PKC levels, resulting in a loss of IPC-induced protection from I/R. Importantly, increased myocardial injury was the result, in part, of restoring a delta PKC-mediated I/R pro-apoptotic phenotype by decreasing pro-survival signalling and increasing cytochrome c release into the cytosol. Taken together, our findings indicate that IPC prevents I/R injury at reperfusion by protecting ATP-dependent 26S proteasomal function. This decreases the accumulation of the pro-apoptotic kinase, delta PKC, at cardiac mitochondria, resulting in the accumulation of the pro-survival kinase, epsilon PKC.NIH[AA11147]Oklahoma Center for Advancement of Science and Technology[HR05-171S