Previous studies of the yeast Saccharomyces cerevisiae indicated that the vacuole is a major site of zinc storage in the cell. However, these studies did not address the absolute level of zinc that was stored in the vacuole nor did they examine the abundances of stored zinc in other compartments of the cell. In this report, we describe an analysis of the cellular distribution of zinc by use of both an organellar fractionation method and an electron probe X-ray microanalysis. With these methods, we determined that zinc levels in the vacuole vary with zinc status and can rise to almost 100 mM zinc (i.e., 7 ؋ 10 8 atoms of vacuolar zinc per cell). Moreover, this zinc can be mobilized effectively to supply the needs of as many as eight generations of progeny cells under zinc starvation conditions. While the Zrc1 and Cot1 zinc transporters are essential for zinc uptake into the vacuole under steady-state growth conditions, additional transporters help mediate zinc uptake into the vacuole during "zinc shock," when zinc-limited cells are resupplied with zinc. In addition, we found that other compartments of the cell do not provide significant stores of zinc. In particular, zinc accumulation in mitochondria is low and is homeostatically regulated independently of vacuolar zinc storage. Finally, we observed a strong correlation between zinc status and the levels of magnesium and phosphorus accumulated in cells. Our results implicate zinc as a major determinant of the ability of the cell to store these other important nutrients.

Two cases of pulmonary alveolar proteinosis, including one death, occurred in workers at a facility producing indium-tin oxide (ITO), a compound used in recent years to make flat panel displays. Both workers were exposed to airborne ITO dust and had indium in lung tissue specimens. One worker was tested for autoantibodies to granulocytemacrophage-colonystimulating factor (GM-CSF) and found to have an elevated level. These cases suggest that inhalational exposure to ITO causes pulmonary alveolar proteinosis, which may occur via an autoimmune mechanism.

Trifunctional hydroxy‐terminated oligomeric polyesters, Mn 500, 1000, and 2000, were prepared by initiating ring‐opening copolymerization of δ‐valerolactone and ε‐caprolactone with glycerol. The prepolymers were converted to crosslinked polyester‐urethanes by their reaction with hexane‐1,6‐diisocyanate in proportions corresponding to 70, 80, 90, and 100% of the hydroxyl content. The moduli of the resulting elastomers varied between 0.12 MPa and 3.83 MPa, and the elongation at break between 60 and 2000%. The residual hydroxyl groups were derivatized by heterogeneous reaction with chloroacetic anhydride or excess hexane‐1,6‐diisocyanate, and these and further transformations of the functional groups were verified by infrared spectroscopy and electron probe x‐ray microanalysis. A second series of hydroxy‐substituted elastomers was synthesized by copolymerization of δ‐valerolactone, ε‐caprolactone, and 4‐(t‐butyldimethylsilyloxy)‐ε‐caprolactone, using different amounts of 2,2‐bis(caprolacton‐4‐yl)propane as the crosslinking agent; removal of the t‐butyldimethylsilyl group to liberate pendant hydroxyl groups was achieved with acetic acid but not fluoride ion. The hydroxylated polyester (but not the polyesterurethanes) was shown to undergo enzymatic surface erosion in rabbit. The biodegradation data were compared with results previously obtained with low‐modulus elastomeric polyesters.

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