948 research outputs found

    Hyponatraemia and hypokalaemia due to indapamide

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    The document attached has been archived with permission from the editor of the Medical Journal of Australia (10 January 2008). An external link to the publisher’s copy is included.Objectives: To review Australian adverse drug reaction reports describing hyponatraemia and hypokalaemia attributed to indapamide and compare the characteristics of the patients with those in Australian reports implicating two other diuretic products (hydrochlorothiazide and amiloride hydrochloride; chlorothiazide). Design: Descriptive analysis using reports from the database of the Adverse Drug Reactions Advisory Committee (ADRAC). Main outcome measures: Numbers of reports of hyponatraemia and hypokalaemia; proportion of such reports in total reports of adverse reactions to each drug; severity of electrolyte disturbances. Results: Between August 1984 and September 2000, 84 Australian reports of hyponatraemia and 87 reports of hypokalaemia, in which indapamide was the sole suspected drug, were submitted to ADRAC. Most reports involved an indapamide dose of 2.5 mg daily. There was a significantly greater proportion of reports of hyponatraemia with indapamide and with the hydrochlorothiazide and amiloride combination than with chlorothiazide; hypokalaemia was significantly more common for indapamide than for the other two drugs. Of the 87 reports of hypokalaemia with indapamide, 35 patients also had hyponatraemia. For all three drugs, at least 80% of reports of hyponatraemia were in people aged 65 or over, and electrolyte disturbance was most commonly reported in elderly women. Conclusions: Hyponatraemia and hypokalaemia have been described in 20.9% and 21.7%, respectively, of reports to ADRAC in which indapamide was the sole suspected drug. The electrolyte disturbances can be severe.Michael D Chapman, Ross Hanrahan, John McEwen and John E Marle

    Microstructural strain energy of α-uranium determined by calorimetry and neutron diffractometry

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    The microstructural contribution to the heat capacity of α-uranium was determined by measuring the heat-capacity difference between polycrystalline and single-crystal samples from 77 to 320 K. When cooled to 77 K and then heated to about 280 K, the uranium microstructure released (3±1) J/mol of strain energy. On further heating to 300 K, the microstructure absorbed energy as it began to redevelop microstrains. Anisotropic strain-broadening parameters were extracted from neutron-diffraction measurements on polycrystals. Combining the strain-broadening parameters with anisotropic elastic constants from the literature, the microstructural strain energy is predicted in the two limiting cases of statistically isotropic stress and statistically isotropic strain. The result calculated in the limit of statistically isotropic stress was (3.7±0.5) J/mol K at 77 K and (1±0.5) J/mol at room temperature. In the limit of statistically isotropic strain, the values were (7.8±0.5) J/mol K at 77 K and (4.5±0.5) J/mol at room temperature. In both cases the changes in the microstructural strain energy showed good agreement with the calorimetry

    Off-The-Shelf MEMS for Rotary MEMS

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    Angle-resolved photoemission and first-principles electronic structure of single-crystalline α\alpha-uranium (001)

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    Continuing the photoemission study begun with the work of Opeil et al. [Phys. Rev. B \textbf{73}, 165109 (2006)], in this paper we report results of an angle-resolved photoemission spectroscopy (ARPES) study performed on a high-quality single-crystal α\alpha-uranium at 173 K. The absence of surface-reconstruction effects is verified using X-ray Laue and low-energy electron diffraction (LEED) patterns. We compare the ARPES intensity map with first-principles band structure calculations using a generalized gradient approximation (GGA) and we find good correlations with the calculated dispersion of the electronic bands

    Potential sites of CFTR activation by tyrosine kinases

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    The CFTR chloride channel is tightly regulated by phosphorylation at multiple serine residues. Recently it has been proposed that its activity is also regulated by tyrosine kinases, however the tyrosine phosphorylation sites remain to be identified. In this study we examined 2 candidate tyrosine residues near the boundary between the first nucleotide binding domain and the R domain, a region which is important for channel function but devoid of PKA consensus sequences. Mutating tyrosines at positions 625 and 627 dramatically reduced responses to Src or Pyk2 without altering the activation by PKA, suggesting they may contribute to CFTR regulation

    Can Modal Skepticism Defeat Humean Skepticism?

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    My topic is moderate modal skepticism in the spirit of Peter van Inwagen. Here understood, this is a conservative version of modal empiricism that severely limits the extent to which an ordinary agent can reasonably believe “exotic” possibility claims. I offer a novel argument in support of this brand of skepticism: modal skepticism grounds an attractive (and novel) reply to Humean skepticism. Thus, I propose that modal skepticism be accepted on the basis of its theoretical utility as a tool for dissolving philosophical paradox
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