Superplastic behavior in a powder-metallurgy TiAl alloy with a metastable microstructure

Superplasticity in a powder-metallurgy TiAl alloy (Ti-47Al-2Cr-2Nb) with a metastable microstructure has been studied. Samples were tested at temperatures ranging from 650 to 1100{degrees}C, and at strain rate ranging from 10{sup -6} to 10{sup -4} s{sup -1}. An elongation value of over 300 obtained at a strain rate of 2 x 10{sup -5} s{sup -1} and at a temperature as lo as 800{degrees}C, which is close to the ductile-to-brittle-transition temperature. This is in contrast to the prior major observations of superplastic behaviors in TiAl in which typical temperatures of 1000{degrees}C have usually been required for superplasticity. It is proposed that the occurrence of superplasticity at 8000{degrees}C in the present alloy is caused by the presence of a B2 phase. During superplastic deformation (grain boundary sliding), the soft P grains accommodate sliding strains to reduce the propensity for cavitation at grain triple junctions and, thus, delays the fracture process. The final microstructure consists of stable, equiaxed y+a{sub 2} grains

Investigation of the Δn = 0 selection rule in Gamow-Teller transitions : The β-decay of 207 Hg

Gamow-Teller β decay is forbidden if the number of nodes in the radial wave functions of the initial and final states is different. This Δn=0 requirement plays a major role in the β decay of heavy neutron-rich nuclei, affecting the nucleosynthesis through the increased half-lives of nuclei on the astrophysical r-process pathway below both Z=50 (for N>82) and Z=82 (for N>126). The level of forbiddenness of the Δn=1ν1g 9/2 →π0g 7/2 transition has been investigated from the β − decay of the ground state of 207 Hg into the single-proton-hole nucleus 207 Tl in an experiment at the ISOLDE Decay Station. From statistical observational limits on possible γ-ray transitions depopulating the π0g 7/2 −1 state in 207 Tl, an upper limit of 3.9×10 −3 % was obtained for the probability of this decay, corresponding to log⁡ft>8.8 within a 95% confidence limit. This is the most stringent test of the Δn=0 selection rule to date

Short-term local delivery of an inhibitor of ras farnesyltransferase prevents neointima formation in vivo after porcine coronary balloon angioplasty

Background- Mitogenic stimuli present at the site of coronary arterial balloon injury contribute to the progression and development of a restenotic lesion, many signaling through a common pathway involving the small G protein p21ras. Our aim was to demonstrate in biochemical studies that farnesyl protein transferase inhibitor III (FPTIII) is an inhibitor of p21ras processing and that when it is given locally in vivo at the site of coronary balloon injury in a porcine model, it can inhibit neointima formation. Methods and Results- FPTIII (1 to 25 µmol/L) concentration-dependently reduced p21ras levels in porcine coronary artery smooth muscle cell membranes. FPTIII also prevented p42/p44 MAPK activation and DNA synthesis in response to platelet-derived growth factor in these cells at a concentration of 25 µmol/L. Application of 25 µmol/L FPTIII locally for 15 minutes to balloon-injured porcine coronary arteries in vivo prevented neointima formation assessed at 4 weeks, reduced proteoglycan deposition, and inhibited adventitial hypertrophy. Coronary arteries from FPTIII-treated pigs had no deterioration in contraction or in endothelium-dependent relaxation. Conclusions- The study demonstrates in the pig that short-term local delivery of inhibitors of p21ras-dependent mitogenic signal transduction prevents restenosis after balloon angioplasty

Diversity and natural history of a Lithothamnion muelleri-Sargassum horridum community in the Gulf of California

We quantitatively assessed the relative contribution of the rhodolith form of Lithothamnion muelleri, a likely foundation species, to macroorganism diversity in a community also inhabited by the large fucalean Sargassum horridum at a site near Cabo Los Machos at the mouth of Bahía Concepción, Baja California Sur, Mexico. The composition and abundance of seaweeds, epibenthic invertebrates, and fish were estimated in March and October 2003, and invertebrates within rhodoliths (cryptofauna) in March 2003. Rhodoliths and Sargassum horridum had the highest cover of all organisms within the 0.5-km2, 2-8-m-deep cobble-sand site. A total of 29 species of seaweeds, 40 taxa of benthic invertebrates, and 33 species of fish were sampled in transects and quadrats. Macroalgal and fish diversity were similar between sampling times as a result of loss and replacement of taxa, but benthic invertebrate diversity declined without replacement from March to October. Rhodolith cover was similar at both sampling times. The cover and density of S. horridum were highly seasonal, and the non-rhodolith flora changed from abundant S. horridum (35% cover) in March to abundant red algal turf in October (22% cover). The sea urchin Arbacia incisa, tunicates, and polychaetes were the most abundant epibenthic invertebrates in March, but declined by October, the former to zero. Grunts (Haemulon maculicauda) and porgies (Calamus brachysomus) were the most abundant fish at both sampling times, but there were large temporal changes in some other species, especially schooling fishes. Rhodolith density in March was 24 ind m2, with numerous individuals >8 cm diameter. Fifteen rhodoliths from a range of size classes contained 114 cryptofaunal taxa with an average of 40 taxa/individual in the largest rhodoliths. These results show the importance of rhodolith habitat to diversity, the large temporal changes in some assemblages, and the exceptionally high diversity of this subtropical community

A new transcriptional role for matrix metalloproteinase-12 in antiviral immunity

Interferon-α (IFN-α) is essential for antiviral immunity, but in the absence of matrix metalloproteinase-12 (MMP-12) or IκBα (encoded by NFKBIA) we show that IFN-α is retained in the cytosol of virus-infected cells and is not secreted. Our findings suggest that activated IκBα mediates the export of IFN-α from virus-infected cells and that the inability of cells in Mmp12−/− but not wild-type mice to express IκBα and thus export IFN-α makes coxsackievirus type B3 infection lethal and renders respiratory syncytial virus more pathogenic. We show here that after macrophage secretion, MMP-12 is transported into virus-infected cells. In HeLa cells MMP-12 is also translocated to the nucleus, where it binds to the NFKBIA promoter, driving transcription. We also identified dual-regulated substrates that are repressed both by MMP-12 binding to the substrate's gene exons and by MMP-12–mediated cleavage of the substrate protein itself. Whereas intracellular MMP-12 mediates NFKBIA transcription, leading to IFN-α secretion and host protection, extracellular MMP-12 cleaves off the IFN-α receptor 2 binding site of systemic IFN-α, preventing an unchecked immune response. Consistent with an unexpected role for MMP-12 in clearing systemic IFN-α, treatment of coxsackievirus type B3–infected wild-type mice with a membrane-impermeable MMP-12 inhibitor elevates systemic IFN-α levels and reduces viral replication in pancreas while sparing intracellular MMP-12. These findings suggest that inhibiting extracellular MMP-12 could be a new avenue for the development of antiviral treatments. © 2014, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved