Rayleigh's principle is combined with Backus' harmonic tensor decomposition to investigate the effect of a small anisotropy on the propagation of Love and Rayleigh surface waves in an arbitrarily stratified half‐space. A slight elastic anisotropy gives rise to an azimuthal dependence of the phase velocities of both Love and Rayleigh waves of the form c(ω, θ) = A1(ω) + A2(ω) cos 2θ + A3(ω) sin 2θ + A4(ω) cos 4θ + A5(ω) sin 4θ where ω is the angular frequency and θ is the azimuth of the wave‐number vector. This azimuthal dependence of the Love and Rayleigh wave phase velocities produces, in turn, a similar azimuthal dependence of the Love and Rayleigh wave group velocities. In view of the accumulating evidence from seismic refraction surveys of upper mantle anisotropy under oceans, the theory may be applicable to Love and Rayleigh wave propagation along oceanic paths.

Human cells lacking functional p53 exhibit a partial deficiency in nucleotide excision repair (NER), the pathway for repair of UV-induced DNA damage. The global genomic repair (GGR) subpathway of NER, but not transcription-coupled repair (TCR), is mainly affected by p53 loss or inactivation. We have utilized mouse embryo fibroblasts (MEFs) lacking p53 genes or downstream effector genes of the p53 pathway, gadd45 (Gadd45a) or p21 (Cdkn1a), as well as MEFs lacking both gadd45 and p21 genes to address the potential contribution of these downstream effectors to p53-associated DNA repair. Loss of p53 or gadd45 had a pronounced effect on GGR, while p21 loss had only a marginal effect, determined by measurements of repair synthesis (unscheduled DNA synthesis), by immunoassays to detect removal of UV photoproducts from genomic DNA, and by assays determining strand-specific removal of CPDs from the mouse dhfr gene. Taken together, the evidence suggests a role for Gadd45, but relatively little role for p21, in DNA repair responses to UV radiation. Recent evidence suggests that Gadd45 binds to UV-damaged chromatin and may affect lesion accessibility. MEFs lacking p53 or gadd45 genes exhibited decreased colony-forming ability after UV radiation and cisplatin compared to wildtype MEFs, indicating their sensitivity to DNA damage. We provide evidence that Gadd45 affects chromatin remodelling of templates concurrent with DNA repair, thus indicating that Gadd45 may participate in the coupling between chromatin assembly and DNA repair.

Summary. We have extended our calculation of the theoretical period of the Chandler wobble to account for the non‐hydrostatic portion of the Earth's equatorial bulge and the effect of the fluid core upon the lengthening of the period due to the pole tide. We find the theoretical period of a realistic perfectly elastic Earth with an equilibrium pole tide to be 426.7 sidereal days, which is 8.5 day shorter than the observed period of 435.2 day. Using Rayleigh's principle for a rotating Earth, we exploit this discrepancy together with the observed Chandler Q to place constraints on the frequency dependence of mantle anelasticity. If Qμ in the mantle varies with frequency σ as σα between 30 s and 14 months and if Qμ in the lower mantle is of order 225 at 30 s, we find that 0.04 ρα≤ 0.11; if instead Qμ in the lower mantle is of order 350 near 200 s, we find that 0.11 ≤α≤ 0.19. In all cases these limits arise from exceeding the 68 per cent confidence limits of ± 2.6 day in the observed period. Since slight departures from an equilibrium pole tide affect the Q much more strongly than the period we believe these limits to be robust.

The cancer chemopreventive properties of selenium compounds are well documented, yet little is known of the mechanism(s) by which these agents inhibit carcinogenesis. We show that selenium in the form of selenomethionine (SeMet) can activate the p53 tumor suppressor protein by a redox mechanism that requires the redox factor Ref1. Assays to measure direct reduction͞oxidation of p53 showed a SeMet-dependent response that was blocked by a dominant-negative Ref1. By using a peptide containing only p53 cysteine residues 275 and 277, we demonstrate the importance of these residues in the SeMet-induced response. SeMet induced sequence-specific DNA binding and transactivation by p53. Finally, cellular responses to SeMet were determined in mouse embryo fibroblasts wild-type or null for p53 genes. The evidence suggests that the DNA repair branch of the p53 pathway was activated. The central relevance of DNA repair to cancer prevention is discussed.cancer chemoprevention ͉ selenium ͉ APE͞Ref1 ͉ p53 tumor suppressor gene ͉ DNA repair S elenium compounds in various forms are cancer-preventive. They have a 20-year history of mammary (1) and colon (2) cancer prevention in rodent models and are in phase II and III clinical trials for prostate cancer prevention (3). Several chemical forms of selenium have been used in laboratory studies. The prototype forms are sodium selenite, which causes single-and double-strand-break DNA damage, and selenomethionine (SeMet), which is relatively nontoxic and non-DNA-damaging (4-6). The mechanism(s) by which selenium compounds exert their anticancer properties is not known, although proposed mechanisms include cytosine methyltransferase inhibition (7