We introduce and propose zircon M257 as a future reference material for the determination of zircon U‐Pb ages by means of secondary ion mass spectrometry. This light brownish, flawless, cut gemstone specimen from Sri Lanka weighed 5.14 g (25.7 carats). Zircon M257 has TIMS‐determined, mean isotopic ratios (2s uncertainties) of 0.09100 ± 0.00003 for 206pb/238U and 0.7392 ± 0.0003 for 207pb/235U. Its 206pb/238U age is 561.3 ± 0.3 Ma (unweighted mean, uncertainty quoted at the 95% confidence level); the U‐Pb system is concordant within uncertainty of decay constants. Zircon M257 contains ∼ 840 μg g−1 U (Th/U ∼ 0.27). The material exhibits remarkably low heterogeneity, with a virtual absence of any internal textures even in cathodoluminescence images. The uniform, moderate degree of radiation damage (estimated from the expansion of unit‐cell parameters, broadening of Raman spectral parameters and density) corresponds well, within the “Sri Lankan trends”, with actinide concentrations, U‐Pb age, and the calculated alpha fluence of 1.66 × 1018 g−1. This, and a (U+Th)/He age of 419 ± 9 Ma (2s), enables us to exclude any unusual thermal history or heat treatment, which could potentially have affected the retention of radiogenic Pb. The oxygen isotope ratio of this zircon is 13.9%o VSMOW suggesting a metamorphic genesis in a marble or calc‐silicate skarn.

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Monocytes/macrophages are prominent in atherosclerotic plaques where the vascular remodeling and plaque rupture may be influenced by the lipids and cytokines at these sites. Therefore, we evaluated the effects of factors found within the vascular wall, such as cytokines, oxidized low-density lipoprotein (ox-LDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL), on monocyte-derived matrix metalloproteinase-1 (MMP-1) and -9 (MMP-9) and tissue inhibitor of metalloproteinases-1 (TIMP-1). ox-LDL, LDL, and HDL alone had no effect on MMP-1, MMP-9, or TIMP-1 production. However, in the presence of tumor necrosis factor (TNF)-α and GM-CSF, ox-LDL enhanced MMP-1 significantly by two- to threefold, increased MMP-9 slightly, and had no effect on TIMP-1 production. In contrast, HDL suppressed the induction of MMP-1 by TNF-α and GM-CSF as well as the ox-LDL-mediated increase in MMP-1 production. The enhancement of MMP-1 production by ox-LDL occurred through, in part, a prostaglandin E2 (PGE2)-dependent pathway as indomethacin suppressed and PGE2 restored MMP-1 production. This conclusion was supported further by ox-LDL-mediated increases in PGE2 and cyclooxygenase-2 (COX-2) production. These data suggest that the interaction of primary monocytes with ox-LDL and proinflammatory cytokines may contribute to vascular remodeling and plaque rupture.