Thin films of ZnO:Al have been deposited on glass substrates by a pulsed laser deposition technique employing an ArF laser ( λ=193 nm). For all experiments, a repetition rate of 10 Hz, an energy density of 1 J/cm2, and an irradiation time of 20–30 min (12000–18000 shots) were assumed. Optical transmittance of around 90% was observed in the visible region of the spectrum for the 150–200 nm thick film. Resistivities of 1.43×10-4 Ω·cm and 5.62×10-4 Ω·cm were obtained at substrate temperatures of 300°C and room temperature, respectively.

Sorption / Desorption / Reduction / Neptunium / Magnetite / HematiteSummary. Sorption and desorption experiments of Np on magnetite and hematite under aerobic and anaerobic conditions were carried out to investigate the possibility of reduction of Np(V) to Np(IV) at pH 4 to 8 within 7 days. The amount of sorbed Np on magnetite under anaerobic conditions was about 2 or 3 times greater than that under aerobic conditions. Furthermore, the results of desorption experiments indicated that the dominant sorption behavior of Np on magnetite under anaerobic conditions was quite different from that under aerobic conditions. The oxidation state of Np sorbed on the iron oxides was determined by extraction technique using 0.5 M TTA in xylene and 2.0 M HNO 3 solution from the solid phase after sorption experiment. 90% and 10% of extracted Np was Np(IV) for magnetite system under anaerobic and aerobic conditions, respectively. On the other hand, almost 100% of extracted Np was Np(V) for hematite system under both aerobic and anaerobic conditions. These results indicated that Np(V) was reduced to Np(IV) by Fe(II) in magnetite.Redox reaction between Np(V) and Fe(II) was also studied in homogeneous solution without solid to decide if Fe(II) ions released from magnetite into silution or Fe(II) on the solid cause the reduction. Only 6% of Np(V) was reduced by Fe(II) at pH = 4 and 6 even after 7 days. According to this result, it was conjectured that the reduction of Np(V) to Np(IV) takes place not in the liquid phase by Fe(II) ion but on the surface of magnetite.

Solubility of Pu(IV) was measured over a total carbonate concentration range of 10" 4 to 10"' Μ at room temperature (20-25 °C) and I = 0.1. Since carbonate was not detected in the solid phase, the solubility controlling solid was assumed to be a hydrous oxide, Pu0 2 · *H 2 0. A limit of the equilibrium constant of the exchange reaction between Pu0 2 · xH 2 0 and a carbonate solid phase, Pu0C0 3 · xH 2 0, was estimated as: Pu0 2 · *H 2 0 + COT + H 2 0 = Pu0C0 3 · XH 2 0 + 20H~ K < 10" 6 7 .The measured solubility was proportional to the square of the bicarbonate concentration at the pH range of 9.4-10.1. This result was interpreted by Pu0 2 · XH 2 0 + 2HC03" = PU(0H)2(C03)1" + xH 2 0 Κ = At pHs 12 and 13 where carbonate ion is dominant, Pu0 2 · JCH20 + 2COR = PU(0H)4(C03)2" + (x-2)H 2 0 Κ = 10-498±0 ' 31 is the predominant reaction.

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Recently, three marfanoid patients with congenital lipodystrophy and a neonatal progeroid appearance were reported. Although their phenotype was distinct from that of classic Marfan syndrome, they all had a truncating mutation in the penultimate exon, i.e., exon 64, of FBN1, the causative gene for Marfan syndrome. These patients might represent a new entity, but the exact phenotypic and genotypic spectrum remains unknown. Here, we report on a girl born prematurely who exhibited severe congenital lipodystrophy and a neonatal progeroid appearance. The patient exhibited a characteristic growth pattern consisting of an accelerated growth in height with a discrepant poor weight gain. She had a characteristic facial appearance with craniosynostosis. A mutation analysis identified c.8175_8182del8bp, p.Arg2726Glufs*9 in exon 64 of the FBN1 gene. A review of similar, recently reported patients revealed that the cardinal features of these patients include (1) congenital lipodystrophy, (2) premature birth with an accelerated linear growth disproportionate to the weight gain, and (3) a progeroid appearance with distinct facial features. Lines of molecular evidence suggested that this new progeroid syndrome represents a neomorphic phenotype caused by truncated transcripts with an extremely charged protein motif that escapes from nonsense-mediated mRNA decay, altering FBN1-TGF beta signaling, rather than representing the severe end of the hypomorphic phenotype of the FBN1-TGF beta disorder spectrum. We propose that this marfanoid entity comprised of congenital lipodystrophy, a neonatal progeroid appearance, and a peculiar growth profile and caused by rare mutations in the penultimate exon of FBN1, be newly referred to as marfanoid-progeroid syndrome.