A primer on sulfur for the planetary geologist

Sulfur has been proposed as the dominant composition for the volcanic material on Io. Sulfur is a complex element which forms many intramolecular and intermolecular allotropes exhibiting a variety of physical properties. Cyclo-S8 sulfur is the most abundant and stable molecular form. The important molecular species within liquid sulfur change in concentration with temperature. Concentrations of the allotropes control the physical properties of the melt. Discontinuities in density, viscosity, and thermal properties reflect the polymerization process within liquid sulfur. Variations in the melting point are related to autodissociation of the liquid. Many solids forms of sulfur have been identified but only orthorhombic alpha and monoclinic beta sulfur, both composed of cyclo-S8 sulfur, are stable under terrestrial conditions. Physical properties of solid sulfur are dependent on the allotrope and, in some cases, the thermal history. Three natural terrestrial sulfur flows are described: (1) Siretoko-Iosan, Japan; (2) Volcan Azufre, Galapagos Islands; and (3) Mauna Loa, Hawaii. All of the flows are associated with fumarolic areas and are considered to have formed by the melting and mobilization of sulfur deposits. Surface textures of the flows indicate a behavior of molten sulfur similar to that of silicate lava. Channels, rivulets, and lobate edges were described for the flows. The solidification of man-made sulfur flows formed as part of the Frasch mining process by which sulfur is removed from the subsurface in a liquid state is described

Spaceborne radar observations: A guide for Magellan radar-image analysis

Geologic analyses of spaceborne radar images of Earth are reviewed and summarized with respect to detecting, mapping, and interpreting impact craters, volcanic landforms, eolian and subsurface features, and tectonic landforms. Interpretations are illustrated mostly with Seasat synthetic aperture radar and shuttle-imaging-radar images. Analogies are drawn for the potential interpretation of radar images of Venus, with emphasis on the effects of variation in Magellan look angle with Venusian latitude. In each landform category, differences in feature perception and interpretive capability are related to variations in imaging geometry, spatial resolution, and wavelength of the imaging radar systems. Impact craters and other radially symmetrical features may show apparent bilateral symmetry parallel to the illumination vector at low look angles. The styles of eruption and the emplacement of major and minor volcanic constructs can be interpreted from morphological features observed in images. Radar responses that are governed by small-scale surface roughness may serve to distinguish flow types, but do not provide unambiguous information. Imaging of sand dunes is rigorously constrained by specific angular relations between the illumination vector and the orientation and angle of repose of the dune faces, but is independent of radar wavelength. With a single look angle, conditions that enable shallow subsurface imaging to occur do not provide the information necessary to determine whether the radar has recorded surface or subsurface features. The topographic linearity of many tectonic landforms is enhanced on images at regional and local scales, but the detection of structural detail is a strong function of illumination direction. Nontopographic tectonic lineaments may appear in response to contrasts in small-surface roughness or dielectric constant. The breakpoint for rough surfaces will vary by about 25 percent through the Magellan viewing geometries from low to high Venusian latitudes. Examples of anomalies and system artifacts that can affect image interpretation are described

Renal tubular HIF-2α expression requires VHL inactivation and causes fibrosis and cysts.

The Hypoxia-inducible transcription Factor (HIF) represents an important adaptive mechanism under hypoxia, whereas sustained activation may also have deleterious effects. HIF activity is determined by the oxygen regulated α-subunits HIF-1α or HIF-2α. Both are regulated by oxygen dependent degradation, which is controlled by the tumor suppressor "von Hippel-Lindau" (VHL), the gatekeeper of renal tubular growth control. HIF appears to play a particular role for the kidney, where renal EPO production, organ preservation from ischemia-reperfusion injury and renal tumorigenesis are prominent examples. Whereas HIF-1α is inducible in physiological renal mouse, rat and human tubular epithelia, HIF-2α is never detected in these cells, in any species. In contrast, distinct early lesions of biallelic VHL inactivation in kidneys of the hereditary VHL syndrome show strong HIF-2α expression. Furthermore, knockout of VHL in the mouse tubular apparatus enables HIF-2α expression. Continuous transgenic expression of HIF-2α by the Ksp-Cadherin promotor leads to renal fibrosis and insufficiency, next to multiple renal cysts. In conclusion, VHL appears to specifically repress HIF-2α in renal epithelia. Unphysiological expression of HIF-2α in tubular epithelia has deleterious effects. Our data are compatible with dedifferentiation of renal epithelial cells by sustained HIF-2α expression. However, HIF-2α overexpression alone is insufficient to induce tumors. Thus, our data bear implications for renal tumorigenesis, epithelial differentiation and renal repair mechanisms

A Molecular Signature of Proteinuria in Glomerulonephritis

Proteinuria is the most important predictor of outcome in glomerulonephritis and experimental data suggest that the tubular cell response to proteinuria is an important determinant of progressive fibrosis in the kidney. However, it is unclear whether proteinuria is a marker of disease severity or has a direct effect on tubular cells in the kidneys of patients with glomerulonephritis. Accordingly we studied an in vitro model of proteinuria, and identified 231 “albumin-regulated genes” differentially expressed by primary human kidney tubular epithelial cells exposed to albumin. We translated these findings to human disease by studying mRNA levels of these genes in the tubulo-interstitial compartment of kidney biopsies from patients with IgA nephropathy using microarrays. Biopsies from patients with IgAN (n = 25) could be distinguished from those of control subjects (n = 6) based solely upon the expression of these 231 “albumin-regulated genes.” The expression of an 11-transcript subset related to the degree of proteinuria, and this 11-mRNA subset was also sufficient to distinguish biopsies of subjects with IgAN from control biopsies. We tested if these findings could be extrapolated to other proteinuric diseases beyond IgAN and found that all forms of primary glomerulonephritis (n = 33) can be distinguished from controls (n = 21) based solely on the expression levels of these 11 genes derived from our in vitro proteinuria model. Pathway analysis suggests common regulatory elements shared by these 11 transcripts. In conclusion, we have identified an albumin-regulated 11-gene signature shared between all forms of primary glomerulonephritis. Our findings support the hypothesis that albuminuria may directly promote injury in the tubulo-interstitial compartment of the kidney in patients with glomerulonephritis

Identification of a novel A-kinase anchoring protein 18 isoform and evidence for its role in the vasopressin-induced aquaporin-2 shuttle in renal principal cells

Arginine vasopressin (AVP) increases the water permeability of renal collecting duct principal cells by inducing the fusion of vesicles containing the water channel aquaporin-2 (AQP2) with the plasma membrane (AQP2 shuttle). This event is initiated by activation of vasopressin V2 receptors, followed by an elevation of cAMP and the activation of protein kinase A (PKA). The tethering of PKA to subcellular compartments by protein kinase A anchoring proteins (AKAPs) is a prerequisite for the AQP2 shuttle. During the search for AKAP(s) involved in the shuttle, a new splice variant of AKAP18, AKAP18delta, was identified. AKAP18delta functions as an AKAP in vitro and in vivo. In the kidney, it is mainly expressed in principal cells of the inner medullary collecting duct, closely resembling the distribution of AQP2. It is present in both the soluble and particulate fractions derived from renal inner medullary tissue. Within the particulate fraction, AKAP18delta was identified on the same intracellular vesicles as AQP2 and PKA. AVP not only recruited AQP2, but also AKAP18delta to the plasma membrane. The elevation of cAMP caused the dissociation of AKAP18delta and PKA. The data suggest that AKAP18delta is involved in the AQP2 shuttle

Identification of a novel A-kinase anchoring protein 18 isoform and evidence for its role in the vasopressin-induced aquaporin-2 shuttle in renal principal cells

Arginine vasopressin (AVP) increases the water permeability of renal collecting duct principal cells by inducing the fusion of vesicles containing the water channel aquaporin-2 (AQP2) with the plasma membrane AQP2 shuttle). This event is initiated by activation of vasopressin V2 receptors, followed by an elevation of cAMP and the activation of protein kinase A (PKA). The tethering of PKA to subcellular compartments by protein kinase A anchoring proteins (AKAPs) is a prerequisite for the AQP2 shuttle. During the search for AKAP(s) involved in the shuttle, a new splice variant of AKAP18, AKAP18delta, was identified. AKAP18delta functions as an AKAP in vitro and in vivo. In the kidney, it is mainly expressed in principal cells of the inner medullary collecting duct, closely resembling the distribution of AQP2. It is present in both the soluble and particulate fractions derived from renal inner medullary tissue. Within the particulate fraction, AKAP18delta was identified on the same intracellular vesicles as AQP2 and PKA. AVP not only recruited AQP2, but also AKAP18delta to the plasma membrane. The elevation of cAMP caused the dissociation of AKAP18delta and PKA. The data suggest that AKAP18delta is involved in the AQP2 shuttle