MgO (100) textured films can be prepared by reactive facing targets sputtering at room temperature without postdeposition annealing process when they were deposited on (100) oriented Fe buffer layers. This method allows fabrication of perpendicular magnetic tunnel junction (p-MTJ) with MgO (100) tunneling barrier layer and rare-earth transition metal (RE-TM) alloy thin films as perpendicularly magnetized free and pinned layers. The 3-nm-thick MgO tunneling barrier layer in p-MTJ multilayer prepared on glass substrate revealed (100) crystalline orientation. Extraordinary Hall effect measurement clarified that the perpendicular magnetic components of 3-nm-thick Fe buffer layers on the two ends of MgO tunneling barrier layer were increased by exchange coupling with RE-TM alloy layers. The RA of 35kΩμm2 and tunneling magnetoresistance ratio of 64% was observed in the multilayered p-MTJ element by current-in-plane-tunneling.

Fluctuation field and time dependence of magnetization in TbFeCo amorphous rare earth-transition metal thin films for perpendicular magnetic recording Magnetic properties of ion beam sputter-deposited TbFeCo and GdFeCo thin films with their compensation point were studied using ferromagnetic Hall effect measurement. Gd x ͑Fe 90 Co 10 ͒ 1−x thin films sputter deposited using Kr exhibited high squareness ratio and sharp magnetization reversal compared with those prepared using Ar as sputtering gas. Lower kinetic energy of sputtering ions was effective to attain higher squareness ratio. Ferromagnetic Hall effect clarifies the magnetization reversal process of a FeCo͑x nm͒ layer contacted to a TbFeCo͑50 nm͒ layer. FeCo layer with thickness less than 2 nm is magnetized together with TbFeCo layer. Ferromagnetic Hall measurement is a powerful tool to determine the magnetization process of very thin films and magnetically coupled layers.

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Secreted protein acidic and rich in cysteine (SPARC), also called basement-membrane protein 40 or osteonectin, is a matricellular protein that is abundant not only in bone tissue as a non-collagenous protein but is also ubiquitously expressed in non-calcified tissue. SPARC is located intracellularly and disruption of the Sparc gene has been reported to reduce bone formation and increase fat tissue; however, the mechanism by which SPARC inhibits adipogenesis remains unclear. The present study evaluated the intracellular function of SPARC in adipogenesis using the bone marrow stromal cell line ST2. When ST2 cells with low SPARC production were cloned, intrinsic activator protein-1 (AP-1) activity was markedly higher, mineralized nodule formation was significantly lower and lipid accumulation was significantly increased compared with in the parental ST2 cells. Forced expression of secreted SPARC with the signal peptide-coding sequences of wild-type Sparc or preprotrypsin in SPARC-low ST2 cells significantly reduced AP-1 transcription activity; however, these reductions were not observed in the absence of signal peptide sequences. Recombinant SPARC, produced using Brevibacillus brevis, specifically bound to c-Fos but not c-Jun and inhibited the binding of c-Fos/c-Jun to a TPA-response element sequence. These data suggested that SPARC was incorporated into the cells from the extracellular spaces and serves an intracellular role as a decoy counterpart for c-Fos, as well as being associated with osteoblastogenesis through the inhibition of adipogenesis. These findings may provide new insights into regenerative medicine.

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