We report on the epitaxial growth of a group-IV ferromagnetic semiconductor, Mn(x)Ge(1-x), in which the Curie temperature is found to increase linearly with manganese (Mn) concentration from 25 to 116 kelvin. The p-type semiconducting character and hole-mediated exchange permit control of ferromagnetic order through application of a +/-0.5-volt gate voltage, a value compatible with present microelectronic technology. Total-energy calculations within density-functional theory show that the magnetically ordered phase arises from a long-range ferromagnetic interaction that dominates a short-range antiferromagnetic interaction. Calculated spin interactions and percolation theory predict transition temperatures larger than measured, consistent with the observed suppression of magnetically active Mn atoms and hole concentration.

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In 1996 three cruises were conducted to simultaneously quantify the fine-scale optical and physical structure of the water column. Data from 120 profiles were used to investigate the temporal occurrence and spatial distribution of thin layers of phytoplankton as they relate to variations in physical processes. Thin layers ranged in thickness from a few centimeters to a few meters. They may extend horizontally for kilometers and persist for days. Thin layers are a recurring feature in the marine environment; they were observed and measured in 54% of our profiles. Physical processes are important in the temporal and spatial distribution of thin layers. Thin layer depth was closely associated with depth and strength of the pycnocline. Over 71% of all thin layers were located at the base of, or within, the pycnocline. The strong statistical relationships between thin layers and physical structure indicate that we cannot understand thin layer dynamics without understanding both local circulation patterns and regional physical forcing.

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The temperature and salt dependencies of absorption by liquid water (H2O) and heavy water (D2O) were determined using a hyperspectral absorption and attenuation meter (WET Labs, AC-S). Sodium chloride (NaCl) was used as a proxy for seawater salts. There was no significant temperature (PsiT) or salt (PsiS) dependency of absorption at wavelengths <550 nm. At wavelengths >550 nm, PsiT exhibited peaks at approximately 604, 662, and 740 nm. A small negative trough in PsiS occurred at approximately 590 nm, followed by a small positive peak approximately 620 nm, a larger negative trough at approximately 720 nm, and a strong positive peak at approximately 755 nm. The salt dependency of absorption by heavy water, Psis(H), exhibited a negative power-law shape with very low Psis(H), at wavelengths >550 nm. Our experiments with NaCl, clean open ocean seawater, and artificial seawater support the hypothesis that salts modify the absorption spectra of seawater by modifying the molecular matrix and vibrations of pure water.

The particulate scattering characteristics of coastal waters were examined at nine locations around the United States, including near-shore sites in the Gulf of Mexico and the Atlantic and Pacific oceans. The scattering measurements were used in conjunction with inversion models to estimate particle size distributions and bulk refractive indices of the suspended particles. The relationships between various scattering properties and chlorophyll concentration were also investigated and compared with previous relationships described for case I waters. Although the general patterns of scattering and particle characteristics in coastal waters were fairly consistent, fine-scale variability within the water column was substantial. Combining optical measurements with inversion techniques provided a more informative view of the environment and a better understanding of the nature of particle populations in the coastal ocean.

SUMMARY. Increased permeability of the pulmonary microvasculature is felt to cause acute noncardiogenic lung edema, and histological studies of edematous lungs show gaps between apparently healthy endothelial cells. To determine whether alterations in endothelial cell cytoskeletons would alter endothelial permeability, we exposed monolayers of pulmonary artery endothelial cells grown on micropore filters to cytochalasin B or D. Cytochalasin exposed monolayers demonstrated a 2-to 3-fold increase in endothelial permeability that was readily reversible by washing the monolayers free of cytochalasins. Parallel phase contrast and fluorescence microscopy demonstrated retraction of cell cytoplasm and disruption of bundles of microfilaments in cytochalasin exposed cells. These changes also were readily reversed after washing the cells free of cytochalasins. To test the relevance of these findings to an in situ microvasculature, we added cytochalasin B to the perfusate of isolated rabbit lungs and observed that cytochalasin B caused a high permeability lung edema. These studies suggest that endothelial cell cytoskeletons may be important determinants of endothelial permeability. (Circ Res 51: 657-661, 1982) ACUTE noncardiogenic lung edema is believed to result from increased permeability of the pulmonary microvasculature (Staub, 1978). Although many animal and ex vivo models of noncardiogenic lung edema have been studied, the mechanism of increased endothelial permeability remains unknown. Several studies of the systemic circulation have suggested that increased endothelial permeability induced by histamine is associated with endothelial cells pulling apart and gaps forming between cells (Majno and Palade, 1961;Majno et al., 1967). Hurley (1982) has provided evidence that similar gaps in the continuity of the endothelium may be important in high permeability lung edema.The permeability of epithelial surfaces has been studied more thoroughly than that of endothelial surfaces, and several studies have suggested a role of microfilaments of the cytoskeleton in regulating epithelial permeability (Meza et al., 1980;Bentzel et al., 1980;Duffey et al., 1981). We hypothesized that the cytoskeleton might also contribute to regulation of endothelial permeability. To test this, we added the microfilament disrupting agents, cytochalasin B and D, to monolayers of endothelial cells grown on micropore filters, and we observed that cytochalasins caused a readily reversible increase in endothelial permeability. The increased permeability was associated with disruption of the microfilament apparatus and formation of gaps between adjacent endothelial cells, whereas the recovery was associated initially with the localization of actin to the junction of adjacent cells and later reorganization into the normal pattern of microfilaments for endothelial cells. To support the relevance of these in vitro findings to an intact microvasculature, we added cytochalasin B to the perfusate of isolated lungs, and we found that cytochalasin B increased ...

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