Joint analysis of BICEP2/keck array and Planck Data.

We report the results of a joint analysis of data from BICEP2/Keck Array and Planck. BICEP2 and Keck Array have observed the same approximately 400 deg^{2} patch of sky centered on RA 0 h, Dec. -57.5°. The combined maps reach a depth of 57 nK deg in Stokes Q and U in a band centered at 150 GHz. Planck has observed the full sky in polarization at seven frequencies from 30 to 353 GHz, but much less deeply in any given region (1.2 µK deg in Q and U at 143 GHz). We detect 150×353 cross-correlation in B modes at high significance. We fit the single- and cross-frequency power spectra at frequencies ≥150 GHz to a lensed-ΛCDM model that includes dust and a possible contribution from inflationary gravitational waves (as parametrized by the tensor-to-scalar ratio r), using a prior on the frequency spectral behavior of polarized dust emission from previous Planck analysis of other regions of the sky. We find strong evidence for dust and no statistically significant evidence for tensor modes. We probe various model variations and extensions, including adding a synchrotron component in combination with lower frequency data, and find that these make little difference to the r constraint. Finally, we present an alternative analysis which is similar to a map-based cleaning of the dust contribution, and show that this gives similar constraints. The final result is expressed as a likelihood curve for r, and yields an upper limit r_{0.05}<0.12 at 95% confidence. Marginalizing over dust and r, lensing B modes are detected at 7.0σ significance.

Biocompatibility of haemodialysis membranes: haemodialysis-related leukotriene B4 and C4 generation. France.

UNLABELLED: The aim of our study was (1) to verify whether haemodialysis (HD) with cuprophane (CUP) and polyacrylonitrile (PAN) membranes is associated with the release of vasoactive leukotriene (LT) C4 and chemotactic LTB4 and (2) to analyse the respective roles of lipoxygenase and cyclo-oxygenase metabolites of arachidonic acid in membrane bio-incompatibility. The investigation was performed in 10 uremic patients using hollow-fibre dialysers and dialysed successively, in random order, with CUP and PAN membranes. The arterial and venous (from dialyser) blood was sampled for the measurement of biochemical parameters, plasma LTC4, LTB4 and prostaglandins (PG) 6-keto-F1 alpha, E2, F2 alpha and thromboxane B2 before and after 15, 30 and 240 min of HD. Eicosanoids were measured by RIA after prior extraction and HPLC separation. RESULTS: CUP HD was associated with a marked early leukopenia and a delayed decrease in blood pO2. Simultaneously, plasma LTB4 and LTC4 increased significantly in arterial blood after 30 min of HD and in venous blood at the end of session of 240 min. Cyclo-oxygenase metabolites increased as well, but nonsignificantly, with a maximum at the end of HD. PAN HD did not significantly change white blood cell count, pO2, or plasma eicosanoid levels. CONCLUSION: CUP membranes stimulate the release of proinflammatory and vasoactive LTB4 and LTC4. PAN membrane haemodialysis is without such side effects. The release of LTs may be an additional valuable marker of membrane bioincompatibility.

Plasma prostaglandins, leukotrienes and thromboxane in acute high altitude hypoxia.

To explore the hypothesis that acute exposure to altitude hypoxia and acute mountain sickness (AMS) are associated with the release of vasoactive eicosanoids, 10 adult subjects were studied at sea-level and after 1-8 days (H1-H8) of exposure to an altitude of 4350 m (Observatoire Vallot). Plasma concentrations of 6 eicosanoids were determined in peripheral venous blood samples by radioimmunoassay after extraction with cooled ethanol and chromatographic separation by HPLC. All subjects experienced symptoms of AMS. Maximal clinical scores were observed at H1 or H2. Symptoms were no longer noted at H8. Hypoxia induced a very large increase in plasma concentration of most eicosanoids; thromboxane B2 (TxB2) and leukotriene B4 (LTB4) were maximum at H1 and H2 (about 5 times the normoxic value); prostaglandins PGE2, 6-keto-PGF1 alpha and PGF2 alpha were maximum at H3 or H4 (about 2.5-5 times of normoxic value). All eicosanoids returned almost to normoxic values by H8. Vasoconstricting mediators were released mostly at the initial phase (H1, H2), vasodilating mediators becoming predominant thereafter (H3, H4). The time pattern of appearance in blood of mediators acting on vascular permeability was strikingly parallel to the clinical score of AMS. In conclusion, exposure to acute hypoxia induced a large increase in plasma concentration of eicosanoids, the variation with time of which is compatible with a hydrostatic-permeability hypothesis of AMS pathophysiology.

The influence of age on renal prostaglandin synthesis in man.

The purpose of our study was to determine influence of age on renal prostaglandin (PG) synthesis in man. Urinary prostaglandins 6-Keto-PGF1 alpha, TxB2, PGE2 and PGF2 alpha were measured in 45 normotensive subjects aged from 20-95 years. Urinary 6-Keto-PGF1 alpha excretion, reflecting mainly renal cortical prostacyclin synthesis, decreased significantly with age, while urinary TxB2 showed the opposite development. The ratio of urinary 6-Keto-PGF1 alpha/TxB2 decreased with age. PGE2 excretion was preserved in old subjects probably because the age-dependent decrease in renal function concerns mainly the cortex and spares the medulla. PGF2 alpha synthesis was least influenced by age. This age-dependent decrease in renal prostacyclin synthesis may play a role in the renal alterations of the elderly.

Urinary prostaglandins in Bartter's and pseudo-Bartter's syndrome.

Renal secretion of prostaglandins (PG) in Bartter's syndrome and in different forms of hypokalemic normotensive syndromes (pseudo-Bartter's syndrome) was measured to determine if it is possible to use the measurement of urinary prostaglandins for the discrimination of different etiologies. Prostaglandins E2, F2 alpha, 6-keto-PGF1 alpha and thromboxane B2 (TxB2) were measured after extraction and chromatography by radioimmunoassay in 19 patients and in 26 control healthy subjects. Bartter's syndrome may be characterized as primary renal hyperprostaglandinism with high urinary PGE2 excretion. It can be dissociated from pseudo-Bartter's syndrome because the urinary PGE2 excretion is always in the normal range in the pseudosyndrome. Abuse of loop diuretics may have effects that mimic Bartter's syndrome since these diuretics stimulate urinary prostaglandin excretion. Therefore, loop diuretics should always be excluded prior to the diagnosis of Bartter's syndrome.