For 2%<=epsilon <= 6%, biaxial strain relaxation is dominated by emission and propagation of dislocations (plastic flow) from the surface of the void accompanied by ductile void growth. For 6%<epsilon<10%, the biaxial strain in the thin film is relaxed by both ductile void growth and emission of dislocations
from the surfaces of the thin film. For epsilon >= 10%, strain relaxation is dominated by dislocation emission from the surfaces of the thin PHA-848125 cost film, leading to a structural transformation from the face-centered cubic to a hexagonal close-packed phase. The defect nucleation mechanisms and the high-strain response of the thin films are found to be significantly different
from those observed in < 111 >-oriented Cu thin films [M. R. Gungor and D. Maroudas, J. Appl. Phys. 97, 113527 (2005); M. R. Gungor and D. Maroudas, Appl. Phys. Lett. 87, 171913 (2005)]. (C) 2009 American Institute of Physics. [doi:10.1063/1.3240326]“
“Background: Mal de Meleda (MDM) (MIM #248300) is an autosomal recessive palmoplantar keratoderma (PPK). It is characterized clinically by erythematous hyperkeratotic plaques over palms and soles that start early in life and progress later in life in a transgradiens form associated Mocetinostat ic50 with pain, macerations, foul odor, pseudoainhum, brachydactyly, onychodystrophy and perioral erythema.
Objective: To look for SLURP-1 gene mutations in patients with MDM.
Methods: We collected
peripheral blood samples from Pakistani family members affected with MDM and 100 population-matched unrelated healthy control individuals in EDTA-containing tubes. All exons of the SLURP-1 gene with adjacent sequences at exon-intron borders were amplified. The amplified PCR products were directly sequenced in an ABI Prism 310 Automated Sequencer. Screening selleck compound assay, using the restriction enzyme Hph1 was performed.
Results: We determined three mutations in the SLURP-1 gene: one novel mutation, c.Ivs1 + 1G > A, and two recurrent mutations, p.R96X and p.G86R. Screening assays for the novel mutation excluded the possibility of polymorphism. In vivo transcription assays showed that the mutation c.Ivs1 + 1 G > A leads to aberrant splicing events.
Conclusion: Our results expand the spectrum of mutations in SLURP-1 gene. (C) 2009 Published by Elsevier Ireland Ltd on behalf of Japanese Society for Investigative Dermatology.”
“We present a systematic study on the magnetization reversal in square arrays of magnetic nanostructures. To account for the unavoidable inhomogeneities of the magnetic properties due to, i.e., template preparation, a distribution of magnetic anisotropy values was taken into account.