Spectral and orbital survey of medium-sized meteoroids

Aims. We investigate the spectra, material properties, and orbital distribution of millimeter- to decimeter-sized meteoroids. Our study aims to distinguish the characteristics of populations of differently sized meteoroids and reveal the heterogeneity of identified meteoroid streams. We verify the surprisingly large ratio of pure iron meteoroids on asteroidal orbits detected among mm-sized bodies. Methods. Emission spectra and multi-station meteor trajectories were collected within the AMOS network observations. The sample is based on 202 meteors of −1 to −14 magnitude, corresponding to meteoroids of mm to dm sizes. Meteoroid composition is studied by spectral classification based on relative intensity ratios of Na, Mg, and Fe and corresponding monochromatic light curves. Heliocentric orbits, trajectory parameters, and material strengths inferred from empirical KB and PE parameters were determined for 146 meteoroids. Results. An overall increase of Na content compared to the population of mm-sized meteoroids was detected, reflecting weaker effects of space weathering processes on larger meteoroids. The preservation of volatiles in larger meteoroids is directly observed. We report a very low ratio of pure iron meteoroids and the discovery of a new spectral group of Fe-rich meteors. The majority of meteoroids on asteroidal orbits were found to be chondritic. Thermal processes causing Na depletion and physical processes resulting in Na-rich spectra are described and linked to characteristically increased material strengths. Numerous major and minor shower meteors were identified in our sample, revealing various degrees of heterogeneity within Halley-type, ecliptical, and sungrazing meteoroid streams. Our results imply a scattered composition of the fragments of comet 2P/Encke and 109P/Swift-Tuttle. The largest disparities were detected within α-Capricornids of the inactive comet 169P/NEAT and δ-Aquarids of the sungrazing 96P/Machholz. We also find a spectral similarity between κ-Cygnids and Taurids, which could imply a similar composition of the parent objects of the two streams.

Responses of distal nephron Na+ transporters to acute volume depletion and hyperkalemia

We assessed effects of acute volume reductions induced by administration of diuretics in rats. Direct block of Na+ transport produced changes in urinary electrolyte excretion. Adaptations to these effects appeared as alterations in the expression of protein for the distal nephron Na+ transporters NCC and ENaC. Two hours after a single injection of furosemide (6 mg/kg) or hydrochlorothiazide (HCTZ; 30 mg/kg) Na+ and K+ excretion increased but no changes in the content of activated forms of NCC (phosphorylated on residue T53) or ENaC (cleaved γ-subunit) were detected. In contrast, amiloride (0.6 mg/kg) evoked a similar natriuresis that coincided with decreased pT53NCC and increased cleaved γENaC. Alterations in posttranslational membrane protein processing correlated with an increase in plasma K+ of 0.6–0.8 mM. Decreased pT53NCC occurred within 1 h after amiloride injection, whereas changes in γENaC were slower and were blocked by the mineralocorticoid receptor antagonist spironolactone. Increased γENaC cleavage correlated with elevation of the surface expression of the subunit as assessed by in situ biotinylation. Na depletion induced by 2 h of furosemide or HCTZ treatment increases total NCC expression without affecting ENaC protein. However, restriction of Na intake for 10 h (during the day) or 18 h (overnight) increased the abundance of both total NCC and of cleaved α- and γENaC. We conclude that the kidneys respond acutely to hyperkalemic challenges by decreasing the activity of NCC while increasing that of ENaC. They respond to hypovolemia more slowly, increasing Na+ reabsorptive capacities of both of these transporters.

Regulation of ENaC trafficking in rat kidney

The epithelial Na channel (ENaC) forms a pathway for Na+ reabsorption in the distal nephron, and regulation of these channels is essential for salt homeostasis. In the rat kidney, ENaC subunits reached the plasma membrane in both immature and fully processed forms, the latter defined by either endoglycosidase H–insensitive glycosylation or proteolytic cleavage. Animals adapted to a low-salt diet have increased ENaC surface expression that is specific for the mature forms of the subunit proteins and is similar (three- to fourfold) for α, β, and γENaC. Kidney membranes were fractionated using differential centrifugation, sucrose-gradient separation, and immunoabsorption. Endoplasmic reticulum membranes, isolated using an antibody against calnexin, expressed immature γENaC, and the content decreased with Na depletion. Golgi membranes, isolated with an antibody against the cis-Golgi protein GM130, expressed both immature and processed γENaC; Na depletion increased the content of processed γENaC in this fraction by 3.8-fold. An endosomal compartment isolated using an antibody against Rab11 contained both immature and processed γENaC; the content of processed subunit increased 2.4-fold with Na depletion. Finally, we assessed the content of γENaC in the late endocytic compartments indirectly using urinary exosomes. All of the γENaC in these exosomes was in the fully cleaved form, and its content increased by 4.5-fold with Na depletion. These results imply that stimulation of ENaC surface expression results at least in part from increased rates of formation of fully processed subunits in the Golgi and subsequent trafficking to the apical membrane.

K+-induced natriuresis is preserved during Na+ depletion and accompanied by inhibition of the Na+-Cl− cotransporter

During hypovolemia and hyperkalemia, the kidneys defend homeostasis by Na+ retention and K+ secretion, respectively. Aldosterone mediates both effects, but it is unclear how the same hormone can evoke such different responses. To address this, we mimicked hypovolemia and hyperkalemia in four groups of rats with a control diet, low-Na+ diet, high-K+ diet, or combined diet. The low-Na+ and combined diets increased plasma and kidney ANG II. The low-Na+ and high-K+ diets increased plasma aldosterone to a similar degree (3-fold), whereas the combined diet increased aldosterone to a greater extent (10-fold). Despite similar Na+ intake and higher aldosterone, the high-K+ and combined diets caused a greater natriuresis than the control and low-Na+ diets, respectively ( P < 0.001 for both). This K+-induced natriuresis was accompanied by a decreased abundance but not phosphorylation of the Na+-Cl− cotransporter (NCC). In contrast, the epithelial Na+ channel (ENaC) increased in parallel with aldosterone, showing the highest expression with the combined diet. The high-K+ and combined diets also increased WNK4 but decreased Nedd4-2 in the kidney. Total and phosphorylated Ste-20-related kinase were also increased but were retained in the cytoplasm of distal convoluted tubule cells. In summary, high dietary K+ overrides the effects of ANG II and aldosterone on NCC to deliver sufficient Na+ to ENaC for K+ secretion. K+ may inhibit NCC through WNK4 and help activate ENaC through Nedd4-2.

The Analysis of the Built-in Electric Field and the Migration of Carries in Thermal/Electric-Field Poled Fused Silica

The thermal/electric poling process of fused silica glass is analyzed based on the multi-carriers’ model. The carrier continuity equation is applied to calculate the variation of the carrier concentration with time. The border of positive charge and negative charge is analogous to a p-n junction. Calculation of the built-in electric field is based on the Poisson equation. The result shows that the second-order nonlinearity effect is mainly formed by the Na+ depletion in the poled fused silica glass. The non-linear coefficient is calculated, it is agree well with the literature values, which verifies the reliability of the theory. The study provided theoretical foundation for manufacture optical communication components.

Conservation of Na+ vs. K+ by the rat cortical collecting duct

Regulation of transport by principal cells of the distal nephron contributes to maintenance of Na+ and K+ homeostasis. To assess which of these ions is given a higher priority by these cells, we investigated the upregulation of epithelial Na+ channels (ENaC) in the rat cortical collecting duct (CCD) during Na depletion with and without simultaneous K depletion. ENaC activity, assessed as whole cell amiloride-sensitive current in split-open tubules, was 260 ± 40 pA/cell in K-repleted but virtually undetectable (3 ± 1 pA/cell) in K-depleted animals. This difference was confirmed biochemically by the reduced amounts of the cleaved forms of both the α-ENaC and γ-ENaC subunits measured in immunoblots. In contrast, in K-depleted rats, simultaneously reducing Na intake did not affect the activity of ROMK channels, assessed as tertiapin-Q-sensitive whole cell currents, in the CCDs. The lack of Na current in K-depleted animals was the result of reduced levels of aldosterone in plasma, rather than a reduced sensitivity to the hormone. However, rats on a low-Na, low-K diet for 1 wk did not excrete more Na than those on a low-Na, control-K diet for the same period of time. Immunoblot analysis indicated increased levels of the thiazide-sensitive NaCl cotransporter and the apical Na-H exchanger NHE3. This suggests that with reduced K intake, Na balance is maintained despite reduced aldosterone and Na+ channel activity by upregulation of Na+ transport in upstream segments. Under these conditions, Na+ transport by the aldosterone-sensitive distal nephron is reduced, despite the low-Na intake to minimize K+ secretion and urinary K losses.