We have plated polycrystalline CoxFe3−xO4 (x=0 and 0.43) films on PET and glass substrates at 80–90 °C in an aqueous solution by new three methods: (1) spraying, (2) spin coating, and (3) thin liquid-film methods. The reaction solution is (1) sprayed, (2) spin coated, and (3) flowed through a gap between the substrate and a glass plate, respectively, making a thin (5–400 μm) coating of the solution on the substrate. Since the solution flows off, the composition of the solution on the substrate does not significantly change during the plating, and the ferrite particles formed in the solution are washed away. This improves the film quality compared to previous methods. We have further improved the film quality by introducing CH3COO− buffer ions into the solution, and also by filtering the solution. By the thin liquid-film method, we have obtained maximum deposition rates of ∼160 and ∼300 Å/min by the spraying and the thin liquid-film methods, respectively. The films of Fe3O4 and CoxFe3–xO4 (x=0.43) plated by the thin liquid-film method exhibited a preferential texture of (100) and (111) planes, respectively, parallel to the surface. Both films had a columnar structure normal to the surface, but the magnetization lies in the surface plane.
Signaling through activin type IIB receptor (ActRIIB) has been shown to regulate the axial formation and the development of foregut-derived organs such as the pancreas in mice. Here, we provide genetic evidence that ActRIIB and Smad2 genes cooperatively regulated asymmetrical patterning of the thoracic organs and pancreas development in mice. The loss of one allele of Smad2 on ActRIIB ؊/؊ background resulted in the increased severity of ActRIIB ؊/؊ phenotypes, including right pulmonary isomerism and complex cardiac malformations, and resulted in 100% frequency of death soon after birth. Of interest, 14% of compound heterozygous ActRIIB ؉/؊ Smad2 ؉/؊ mice exhibited the ActRIIB ؊/؊ phenotypes and died soon after birth. In the pancreas, hypoplastic islets were found not only in ActRIIB ؊/؊ but also in Smad2 ؉/؊ mice. A more severe phenotype was also found in ActRIIB ؉/؊ Smad2 ؉/؊ mice. As well, these mutant mice exhibited impaired glucose tolerance in a gene dosage-sensitive manner. This genetic evidence strongly suggested that ActRIIB and Smad2 function in the same signaling pathway to regulate axial patterning and pancreas islet formation by means of a threshold mechanism. Developmental Dynamics 236:2865-2874, 2007.
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