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

Physiological and Molecular Responses to Altered Sodium Intake in Rat Pregnancy

In pregnancy, a high plasma volume maintains uteroplacental perfusion and prevents placental ischemia, a condition linked to elevated maternal blood pressure (BP). Reducing BP by increasing Na+ intake via plasma volume expansion appears contra‐ intuitive. We hypothesize that an appropriate Na+ intake in pregnancy reduces maternal BP and adapts the renin‐angiotensin system in a pregnancy‐specific manner.Methods and Results: BP was measured by implanted telemetry in Sprague‐ Dawley rats before and throughout pregnancy. Pregnant and nonpregnant animals received either a normal‐salt (0.4%; NS), high‐salt (8%; HS), or low‐salt (0.01%; LS) diet, or HS (days 1–14) followed by LS (days 14–20) diet (HS/LS). Before delivery (day 20), animals were euthanized and organs collected. Food, water, and Na+ intake were monitored in metabolic cages, and urinary creatinine and Na+ were analyzed. Na+ intake and retention increased in pregnancy (NS, LS), leading to a positive Na+ balance (NS, LS). BP was stable during LS, but reduced in HS conditions in pregnancy. The renin‐angiotensin system was adapted as expected. Activating cleavage of α‐ and γ‐subunits of the renal epithelial Na+ channel and expression of‐ full length medullary β‐subunits, accentuated further in all LS conditions, were upregulated in pregnancy.Conclusions: Pregnancy led to Na+ retention adapted to dietary changes. HS exposure paradoxically reduced BP. Na+ uptake while only modestly linked to the renin‐angiotensin system is enhanced in the presence of posttranslational renal epithelial Na+ channel modifications. This suggests (1) storage of Na+ in pregnancy upon HS exposure, bridging periods of LS availability; and (2) that potentially non–renin‐angiotensin–related mechanisms participate in ENaC activation and consecutive Na+ retention

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

The renal cortical interstitium: morphological and functional aspects

The renal interstitial compartment, situated between basement membranes of epithelia and vessels, contains two contiguous cellular networks. One network is formed by interstitial fibroblasts, the second one by dendritic cells. Both are in intimate contact with each other. Fibroblasts are interconnected by junctions and connected to basement membranes of vessels and tubules by focal adhesions. Fibroblasts constitute the “skeleton” of the kidney. In the renal cortex, fibroblasts produce erythropoietin and are distinguished from other interstitial cells by their prominent F-actin cytoskeleton, abundance of rough endoplasmic reticulum, and by ecto-5′-nucleotidase expression in their plasma membrane. The resident dendritic cells belong to the mononuclear phagocyte system and fulfil a sentinel function. They are characterized by their expression of MHC class II and CD11c. The central situation of fibroblasts suggests that signals from tubules, vessels, and inflammatory cells converge in fibroblasts and elicit an integrated response. Following tubular damage and inflammatory signals fibroblasts proliferate, change to the myofibroblast phenotype and increase their collagen production, potentially resulting in renal fibrosis. The acquisition of a profibrotic phenotype by fibroblasts in renal diseases is generally considered a main causal event in the progression of chronic renal failure. However, it might also be seen as a repair process