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Measurements of the optical constants of metals at submillimeter wavelengths are sparse. We have used a nonresonant cavity to measure, at room temperature, the angle averaged absorptance spectra P(omega) of aluminum, molybdenum, tantalum, titanium, tungsten, and iron in the 30-300-cm(-1) wavenumber region. The real part of the normalized surface impedance spectrum, z(omega) = r(omega) + ix(omega), was determined from P(omega). Measurements were also made on iron from 400 to 4000 cm(-1) using standard reflectance techniques. The r(omega) spectrum was combined with previous measurements by others at higher frequencies and Kramers-Kronig analyses of the resultant combined r(omega) spectra provided epsilon(omega) = epsilon(1)(omega) + iepsilon(2)(omega) and N(omega) = n(omega) + ik(omega).

Measurements of the optical properties, and thus the optical constants, of metals at submillimeter wavelengths are almost nonexistent. We used a nonresonant cavity to measure at ambient temperature the angle averaged absorptance spectra P(omega) of gold, nickel, and lead in the 30-300-cm(-1) wave-number region. The real part of the normalized surface impedance spectrum z(omega) = r(omega) + ix(omega) was determined from P(omega). The r(omega) spectrum was combined with previous measurements by others at higher frequencies, and Kramers- Kronig analyses of the resultant r(omega) spectra provided (omega) =, (1) (omega) + i(2)(omega) and N(omega) = n(omega) + ik(omega) for gold and nickel in the 35-15,000-cm(-1) region and for lead in the 15-15,000-cm(-1) region. We also derived an exact analytical expression for P(omega) of a metal.

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Macrophage colony-stimulating factor (M-CSF) is a hematopoietic growth factor that is responsible for the survival and proliferation of monocytes and the differentiation of monocytes into macrophages, including Kupffer cells (KCs) in the liver. KCs play an important role in the clearance of several serum enzymes, including aspartate aminotransferase and creatine kinase, that are typically elevated as a result of liver or skeletal muscle injury. We used three distinct animal models to investigate the hypothesis that increases in the levels of serum enzymes can be the result of decreases in KCs in the apparent absence of hepatic or skeletal muscle injury. Specifically, neutralizing M-CSF activity via a novel human monoclonal antibody reduced the CD14 ؉ CD16 ؉ monocyte population, depleted KCs, and increased aspartate aminotransferase and creatine kinase serum enzyme levels in cynomolgus macaques. In addition, the treatment of rats with clodronate liposomes depleted KCs and led to increased serum enzyme levels, again without evidence of tissue injury. Finally, in the osteopetrotic (Csf1 op /Csf1 op ) mice lacking functional M-CSF and having reduced levels of KCs, the levels of serum enzymes are higher than in wild-type littermates. Together, these findings support a mechanism for increases in serum enzyme levels through M-CSF regulation of tissue macrophage homeostasis without concomitant histopathological changes in either the hepatic or skeletal system.