Detector Description and Performance for the First Coincidence Observations between LIGO and GEO

For 17 days in August and September 2002, the LIGO and GEO interferometer gravitational wave detectors were operated in coincidence to produce their first data for scientific analysis. Although the detectors were still far from their design sensitivity levels, the data can be used to place better upper limits on the flux of gravitational waves incident on the earth than previous direct measurements. This paper describes the instruments and the data in some detail, as a companion to analysis papers based on the first data.Comment: 41 pages, 9 figures 17 Sept 03: author list amended, minor editorial change

The Earth: Plasma Sources, Losses, and Transport Processes

This paper reviews the state of knowledge concerning the source of magnetospheric plasma at Earth. Source of plasma, its acceleration and transport throughout the system, its consequences on system dynamics, and its loss are all discussed. Both observational and modeling advances since the last time this subject was covered in detail (Hultqvist et al., Magnetospheric Plasma Sources and Losses, 1999) are addressed

Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron.

The epithelial Na <sup>+</sup> channel (ENaC) constitutes the rate-limiting step for Na <sup>+</sup> absorption in the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), connecting tubule (CNT), and collecting duct (CD). Previously, we demonstrated that ENaC activity in the DCT2/CNT transition zone is constitutively high and independent of aldosterone, in contrast to its aldosterone dependence in the late CNT/initial cortical CD (CCD). The mineralocorticoid receptor (MR) is expressed in the entire ASDN. Its activation by glucocorticoids is prevented through 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) abundantly expressed in the late but probably not early part of the ASDN. We hypothesized that ENaC function in the early part of the ASDN is aldosterone independent but may depend on MR activated by glucocorticoids due to low 11β-HSD2 abundance. To test this hypothesis, we used doxycycline-inducible nephron-specific MR-deficient [MR knockout (KO)] mice. Whole cell ENaC currents were investigated in isolated nephron fragments from the DCT2/CNT or CNT/CCD transition zones using the patch-clamp technique. ENaC activity was detectable in the CNT/CCD of control mice but absent or barely detectable in the majority of CNT/CCD preparations from MR KO mice. Importantly, ENaC currents in the DCT2/CNT were greatly reduced in MR KO mice compared with ENaC currents in the DCT2/CNT of control mice. Immunofluorescence for 11β-HSD2 was abundant in the CCD, less prominent in the CNT, and very low in the DCT2. We conclude that MR is critically important for maintaining aldosterone-independent ENaC activity in the DCT2/CNT. Aldosterone-independent MR activation is probably mediated by glucocorticoids due to low expression of 11β-HSD2.NEW & NOTEWORTHY Using a mouse model with inducible nephron-specific mineralocorticoid receptor (MR) deficiency, we demonstrated that MR is not only critical for maintaining aldosterone-dependent ENaC activity in CNT/CCD but also for aldosterone-independent ENaC activity in DCT2/CNT. Furthermore, we demonstrated that cells of this latter nephron segment express little 11β-HSD2, which probably allows glucocorticoids to stimulate MR, resulting in aldosterone-independent ENaC activity in DCT2/CNT. This site-specific ENaC regulation has physiologically relevant implications for renal sodium and potassium homeostasis

Inhibition of electrical activity in mouse pancreatic beta- cells by the Atp/Adp translocase inhibitor, Bongkrekic Acid

Bongkrekic acid causes fatal food poisoning which is associated with hyperglycaemia. Here we demonstrate that bongkrekic acid, a potent inhibitor of the mitochondrial ATP/ADP translocase, inhibits glucose-induced electrical activity in the pancreatic β-cell through the simulation of ATP-sensitive potassium channel (K-ATP-channel) activity. By comparison of its effects with those of oligomycin, we suggest that bongkrekic acid acts by the inhibition of glucose metabolism and may induce hyperglycaemia by impairing β-cel function

Pendrin-null mice develop severe hypokalemia following dietary Na⁺ and K⁺ restriction: role of ENaC.

Pendrin is an intercalated cell Cl <sup>-</sup> /[Formula: see text] exchanger thought to participate in K <sup>+</sup> -sparing NaCl absorption. However, its role in K <sup>+</sup> homeostasis has not been clearly defined. We hypothesized that pendrin-null mice will develop hypokalemia with dietary K <sup>+</sup> restriction. We further hypothesized that pendrin knockout (KO) mice mitigate urinary K <sup>+</sup> loss by downregulating the epithelial Na <sup>+</sup> channel (ENaC). Thus, we examined the role of ENaC in Na <sup>+</sup> and K <sup>+</sup> balance in pendrin KO and wild-type mice following dietary K <sup>+</sup> restriction. To do so, we examined the relationship between Na <sup>+</sup> and K <sup>+</sup> balance and ENaC subunit abundance in K <sup>+</sup> -restricted pendrin-null and wild-type mice that were NaCl restricted or replete. Following a NaCl-replete, K <sup>+</sup> -restricted diet, K <sup>+</sup> balance and serum K <sup>+</sup> were similar in both groups. However, following a Na <sup>+</sup> , K <sup>+</sup> , and Cl <sup>-</sup> -deficient diet, pendrin KO mice developed hypokalemia from increased K <sup>+</sup> excretion. The fall in serum K <sup>+</sup> observed in K <sup>+</sup> -restricted pendrin KO mice was enhanced with ENaC stimulation but eliminated with ENaC inhibition. The fall in serum K <sup>+</sup> observed in K <sup>+</sup> -restricted pendrin KO mice was enhanced with ENaC stimulation but eliminated with ENaC inhibition. However, reducing ENaC activity also reduced blood pressure and increased apparent intravascular volume contraction, since KO mice had lower serum Na <sup>+</sup> , higher blood urea nitrogen and hemoglobin, greater weight loss, greater metabolic alkalosis, and greater NaCl excretion. We conclude that dietary Na <sup>+</sup> and K <sup>+</sup> restriction induces hypokalemia in pendrin KO mice. Pendrin-null mice limit renal K <sup>+</sup> loss by downregulating ENaC. However, this ENaC downregulation occurs at the expense of intravascular volume.NEW & NOTEWORTHY Pendrin is an apical Cl <sup>-</sup> /[Formula: see text] exchanger that provides renal K <sup>+</sup> -sparing NaCl absorption. The pendrin-null kidney has an inability to fully conserve K <sup>+</sup> and limits renal K <sup>+</sup> loss by downregulating the epithelial Na <sup>+</sup> channel (ENaC). However, with Na <sup>+</sup> restriction, the need to reduce ENaC for K <sup>+</sup> balance conflicts with the need to stimulate ENaC for intravascular volume. Therefore, NaCl restriction stimulates ENaC less in pendrin-null mice than in wild-type mice, which mitigates their kaliuresis and hypokalemia but exacerbates volume contraction