Enhancement of the electronic contribution to the low temperature specific heat of Fe/Cr magnetic multilayer

We measured the low temperature specific heat of a sputtered $(Fe_{23\AA}/Cr_{12\AA})_{33}$ magnetic multilayer, as well as separate $1000\AA$ thick Fe and Cr films. Magnetoresistance and magnetization measurements on the multilayer demonstrated antiparallel coupling between the Fe layers. Using microcalorimeters made in our group, we measured the specific heat for $4<T<30 K$ and in magnetic fields up to $8 T$ for the multilayer. The low temperature electronic specific heat coefficient of the multilayer in the temperature range $4<T<14 K$ is $\gamma_{ML}=8.4 mJ/K^{2}g-at$. This is significantly larger than that measured for the Fe or Cr films (5.4 and $3.5 mJ/K^{2}mol$ respectively). No magnetic field dependence of $\gamma_{ML}$ was observed up to $8 T$. These results can be explained by a softening of the phonon modes observed in the same data and the presence of an Fe-Cr alloy phase at the interfaces.Comment: 20 pages, 5 figure

Transcriptional silencing of the Dickkopfs-3 (Dkk-3) gene by CpG hypermethylation in acute lymphoblastic leukaemia

Dkk-3 is a newly characterised mortalisation-related gene and an antagonist of the Wnt oncogenic signalling pathway whose expression is decreased in a variety of cancer cell lines, suggesting that the Dkk-3 gene, located at chromosome 11p15.1, functions as a tumour suppressor gene. Although 11p15 is a ‘hot spot’ for methylation in acute lymphoblastic leukaemia (ALL), the role of Dkk-3 abnormalities has never been evaluated in this disease. We analysed CpG island methylation of the Dkk-3 promoter in six ALL cell lines and 183 ALL patients. We observed Dkk-3 hypermethylation in all cell lines and in cells from 33% (60/183) of ALL patients. Moreover, Dkk-3 methylation was associated with decreased Dkk-3 mRNA expression and this expression was restored after exposure to the demethylating agent 5-AzaC. Clinical features did not differ between hypermethylated and unmethylated patients. Estimated disease-free survival (DFS) and overall survival at 10 and 11 years, respectively, were 49.8 and 45.6% for normal patients and 10.5 and 15.1% for hypermethylated patients (P¼0.001 and 0.09). Multivariate analysis demonstrated that Dkk-3 methylation was an independent prognostic factor predicting DFS (P¼0.0009). Our data suggest that Dkk-3 methylation occurs at an early stage in ALL pathogenesis and probably influences the clinical behaviour of the disease