Specific Heat of a Three Dimensional Metal Near a T=0 Magnetic Transition with Dynamic Exponent z=2,3,4

We derive expressions for the universal contribution to the specific heat of a three-dimensional metal near a zero-temperature phase transition with dynamic exponent $z=2,3$, or 4. The results allow a quantitative comparison of theory to data. We illustrate the application of our results by analyzing data for Ce$_{1-x}$Lu$_x$Cu$_2$Si$_2$, which has been claimed to be near a quantum critical point.Comment: 23 pages, revtex. For figures, send mail to [email protected]

DELETIONS OF THE SURVIVAL MOTOR-NEURON GENE IN UNAFFECTED SIBLINGS OF PATIENTS WITH SPINAL MUSCULAR-ATROPHY

DNA studies in 103 spinal muscular atrophy (SMA) patients from The Netherlands revealed homozygosity for a survival motor neuron (SMN) deletion in 96 (93%) of 103. Neuronal apoptosis inhibitory protein deletions were found in 38 (37%) of 103 and occurred most frequently in SMA type I. SMN deletions have not yet been described to occur in healthy subjects. In this study, however, four unaffected sibs from two SMA families showed homozygosity for SMN deletions. Homozygosity for an SMN deletion in unaffected persons seems to be very rare. Therefore, demonstration of a homozygous SMN deletion in a clinically presumed SMA patient should be considered as a confirmation of the diagnosis, whether or not SMN is in fact the causal gene for SMA.</p

DELETIONS OF THE SURVIVAL MOTOR-NEURON GENE IN UNAFFECTED SIBLINGS OF PATIENTS WITH SPINAL MUSCULAR-ATROPHY

DNA studies in 103 spinal muscular atrophy (SMA) patients from The Netherlands revealed homozygosity for a survival motor neuron (SMN) deletion in 96 (93%) of 103. Neuronal apoptosis inhibitory protein deletions were found in 38 (37%) of 103 and occurred most frequently in SMA type I. SMN deletions have not yet been described to occur in healthy subjects. In this study, however, four unaffected sibs from two SMA families showed homozygosity for SMN deletions. Homozygosity for an SMN deletion in unaffected persons seems to be very rare. Therefore, demonstration of a homozygous SMN deletion in a clinically presumed SMA patient should be considered as a confirmation of the diagnosis, whether or not SMN is in fact the causal gene for SMA