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The frequency of giant arcs - highly distorted and strongly gravitationally lensed background galaxies - is a powerful test for cosmological models. Previous comparisons of arc statistics for the currently favored concordance cosmological model ( lambda cold dark matter [LCDM]) with observations have shown an apparently large discrepancy in underpredicting cluster arcs. We present new ray-shooting results, based on a high-resolution (1024(3) particles in a 320 h(-1) Mpc box) large-scale structure simulation normalized to the Wilkinson Microwave Anisotropy Probe (WMAP) observations. We follow light rays through a pseudo - three-dimensional matter distribution approximated by up to 38 lens planes and evaluate the occurrence of arcs for various source redshifts. We find that the frequency of strongly lensed background galaxies is a steep function of source redshift: the optical depth for giant arcs increases by a factor of 5 when background sources are moved from redshift z(s) = 1.0 to 1.5. This is a consequence of a small decrease of the critical surface mass density for lensing, combined with the very steep cluster mass function at the high-mass end plus a modest contribution from secondary lens planes. Our results are consistent with those of Bartelmann et al. if we - as they did - restrict all sources to be at z(s) = 1. If we allow sources extending to or beyond z(s) greater than or equal to 1.5, the apparent discrepancy vanishes: the frequency of arcs increases by about a factor of 10 as compared to previous estimates, and results in roughly one arc per 20 deg(2) over the sky, in good agreement with the observed frequency of arcs
Energy balance is maintained by controlling both energy intake and energy expenditure. Thyroid hormones play a crucial role in regulating energy expenditure. Their levels are adjusted by a tight feed back-control led regulation of thyroid hormone production/incretion and by their hepatic metabolism. Thyroid hormone degradation has previously been shown to be enhanced by treatment with phenobarbital or other antiepileptic drugs due to a CAR-dependent induction of phase 11 enzymes of xenobiotic metabolism. We have recently shown, that PPAR alpha agonists synergize with phenobarbital to induce another prototypical CAR target gene, CYP2B1. Therefore, it was tested whether a PPAR alpha agonist could enhance the phenobarbital-dependent acceleration of thyroid hormone elimination. In primary cultures of rat hepatocytes the apparent half-life of T3 was reduced after induction with a combination of phenobarbital and the PPARa agonist WY14643 to a larger extent than after induction with either Compound alone. The synergistic reduction of the half-life could be attributed to a synergistic induction of CAR and the CAR target genes that code for enzymes and transporters involved in the hepatic elimination of T3, such as OATP1A1, OATP1A3, UGT1A3 and UCT1A10. The PPAR alpha-dependent CAR induction and the subsequent induction of T3-eliminating enzymes might be of physiological significance for the fasting- incluced reduction in energy expenditure by fatty acids as natural PPARa ligands. The synergism of the PPAR alpha agonist WY14643 and phenobarbital in inducing thyroid hormone breakdown might serve as a paradigm for the synergistic disruption of endocrine control by other combinations of xenobiotics.