Quantitative assessment of fatigue damage accumulation in wavy slip metals from acoustic harmonic generation

A comprehensive, analytical treatment is presented of the microelastic–plastic nonlinearities resulting from the interaction of a stress perturbation with dislocation substructures and cracks that evolve during cyclic fatigue of wavy slip metals. The interaction is quantified by a material nonlinearity parameter β extracted from acoustic harmonic generation measurements. The contribution to β from the substructures is obtained from the Cantrell model. The contribution to β from cracks is obtained by applying the Paris law to the Nazarov–Sutin crack nonlinearity equation. The nonlinearity parameter resulting from the two contributions is predicted to increase monotonically by hundreds of percent during fatigue from the virgin state to fracture. The increase in β during the first 80–90% fatigue life is dominated by the evolution of dislocation substructures, while the last 10–20% is dominated by crack growth. Application of the model to aluminium alloy 2024-T4 in stress-controlled loading at 276?MPa yields excellent agreement between theory and experiment.     

Nonperturbative quantum calculation of the index of refraction of multilevel systems

We calculate the index of refraction (n) nonperturbatively for a multilevel ladder of states, and show that the dependence of n on the strength of an applied laser field departs qualitatively from that expected for a two-level system and employed in previous phenomenological models of self-focusing.     

Cytotoxicity and photocytotoxicity of a dendritic C(60) mono-adduct and a malonic acid C(60) tris-adduct on Jurkat cells

The cytotoxic and photocytotoxic effects of two water-soluble fullerene derivatives, a dendritic C(60) mono-adduct and the malonic acid C(60) tris-adduct were tested on Jurkat cells. Cell growth and vitality were determined by a cell counting and staining technique. After 2 weeks cultivation in the presence of the fullerene derivatives, it was found that only the dendritic mono-adduct inhibits cell growth (within 2 weeks the cell number decreased to 19%), whereas the tris-malonic acid adduct has little effect. The growth inhibition is reversible; cultivating the same cells further in the absence of fullerene, the cell number increased to 106.4%. Other experiments showed that these fullerene derivatives become toxic when irradiated with UVA or UVB light. The cell death is mainly caused by membrane damage and it is UV dose-dependent. Tris-malonic acid fullerene was found to be more phototoxic than the dendritic derivative. This result is in contrast to the singlet oxygen quantum yields determined for the two compounds. We propose that the two fullerene derivatives may interact with the cell membrane in different ways thus causing the observed effects. Further experiments will be done to determine the location and concentration of the two compounds in and on the cells.     

Reactions of cyclononatetraenyl dianion with electrophiles: geometry and conformation of 1,3,6-cyclononatrienes

Carbonation of the parent cyclononatetraene dianion gives a mixture of (a) the minor products, 1,3,6-cyclononatriene-5,9- and 5,8-dicarboxylic acids, and (b) the major product, bis(5-carboxy-1,3,6-cyclononatrien-9-yl). In contrast, the 9,9-dimethyl dianion affords almost entirely a mixture of the two monocyclic diacids. Similar results are obtained on trimethylsilylation. Conformations of the products are discussed.     

DNA EXCISION REPAIR IN LYMPHOCYTES FOLLOWING PHOTOAFFINITY LABELING WITH ETHIDIUM MONOAZIDE

Irradiation of ethidium monoazide by fluorescent light promotes a chemical decomposition of the azide into a highly reactive nitrene intermediate. Covalent bonding of this electrophile to the DNA in the cell provokes repair of damage which can be monitored by incorporation of [³H]-thymidine. Human lymphocytes were labeled with [¹⁴C]-ethidium azide and then allowed to undergo DNA repair. Repair incorporation of [³H]-thymidine showed saturation at 5 µM ethidium azide, but excision of the labeled drug failed to saturate at 20 µM, suggesting that excision and resynthesis are two separate events. Cells were also labeled with the photosensitive drug and/or exposed to UV radiation, and then allowed to undergo a period of DNA repair. The tritium incorporation for the combined insults was less than the sum of the two insults. Quinacrine, progesterone and chloroquine inhibited repair incorporation of [³H]-thymidine, but had no effect on the excision of the drug from the DNA. After damage by ethidium azide, chromatin was isolated from lymphocytes which had been allowed to repair label with [³H]-thymidine. Partial digestion of the chromatin with micrococcal nuclease released 80% of the tritium when approximately 40% of the DNA had been hydrolyzed by the enzyme.     

Multiple Reversals of Competitive Dominance in Ecological Reserves via External Habitat Degradation

In this article we continue an examination of the consequences of habitat degradation on species interactions begun by Cantrell, Cosner and Fagan in Cantrell et al., J. Math. Biol. 37, 491–533 (1998). In Cantrell et al., J. Math. Biol. 37, 491–533 (1998), two competing species were thought to inhabit a pristine patch of habitat surrounded by matrix habitat whose level of degradation is variable. The dynamics of the species interactions was modeled by diffusive Lotka–Volterra competition equations in the patch supplemented by Robin boundary conditions on the interface between the pristine patch and the matrix habitat. Habitat degradation was incorporated into the model via a tunable hostility parameter in the boundary conditions. Analysis of the model showed that it is possible for a species to be competitively dominant in the pristine patch when the surrounding environs are only mildly unfavorable but to lose this advantage and be competitively inferior in the patch when matrix hostility is severe. In this article we address the question of just how delicately competitive advantage within the pristine patch depends on the level of degradation in the environs surrounding the pristine patch. We show that it is indeed possible for competitive advantage to reverse more than once as the level of degradation in the matrix habitat increases and also examine the effects thereof on the number and nature of equilibria through a detailed bifurcation analysis.Dedicated to Professor Shui-Nee Chow on the occasion of his 60th birthday.