22 research outputs found

    Mathematical relation predicts achievable densities of compacted particles

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    Series of mathematical relationships predicts compact densities of spherical shapes in a cylinder as a function of particle dimension, and compact density of angular shapes as a function of particle shape and absolute size

    Environmentally assisted cracking in light water reactors. Semiannual report, July 1998-December 1998.

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    This report summarizes work performed by Argonne National Laboratory on fatigue and environmentally assisted cracking (EAC) in light water reactors from July 1998 to December 1998. Topics that have been investigated include (a) environmental effects on fatigue S-N behavior of primary pressure boundary materials, (b) irradiation-assisted stress corrosion cracking of austenitic stainless steels (SSs), and (c) EAC of Alloys 600 and 690. Fatigue tests have been conducted to determine the crack initiation and crack growth characteristics of austenitic SSs in LWR environments. Procedures are presented for incorporating the effects of reactor coolant environments on the fatigue life of pressure vessel and piping steels. Slow-strain-rate tensile tests and posttest fractographic analyses were conducted on several model SS alloys irradiated to {approx}0.3 and 0.9 x 10{sup 21} n {center_dot} cm{sup -2} (E > 1 MeV) in helium at 289 C in the Halden reactor. The results have been used to determine the influence of alloying and impurity elements on the susceptibility of these steels to irradiation-assisted stress corrosion cracking. Fracture toughness J-R curve tests were also conducted on two heats of Type 304 SS that were irradiated to {approx}0.3 x 10{sup 21} n {center_dot} cm{sup -2} in the Halden reactor. Crack-growth-rate tests have been conducted on compact-tension specimens of Alloys 600 and 690 under constant load to evaluate the resistance of these alloys to stress corrosion cracking in LWR environments

    The binding epitopes of neurotrophin-3 to its receptors trkC and gp75 and the design of a multifunctional human neurotrophin.

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    Survival and maintenance of vertebrate neurons are influenced by neurotrophic factors which mediate their signal by binding to specific cell surface receptors. We determined the binding sites of human neurotrophin-3 (NT-3) to its receptors trkC and gp75 by mutational analysis and compared them to the analogous interactions of nerve growth factor (NGF) with trkA and gp75. The trkC binding site extends around the central beta-strand bundle and in contrast to NGF does not make use of non-conserved loops and the six N-terminal residues. The gp75 epitope is dominated by loop residues and the C-terminus of NT-3. A novel rapid biological screening procedure allowed the identification of NT-3 mutants that are able to signal efficiently through the non-preferred receptors trkA and trkB, which are specific for NGF and BDNF respectively. Mutation of only seven residues in NT-3 resulted in a human neurotrophin variant which bound to all receptors of the trk family with high affinity and efficiently supported the survival of NGF-, BDNF- and NT-3-dependent neurons. Our results suggest that the specificity among neurotrophic factors is not solely encoded in sequence diversity, but rather in the way each neurotrophin interacts with its preferred receptor
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