The VLBA Imaging and Polarimetry Survey at 5 GHz

We present the first results of the VLBA Imaging and Polarimetry Survey (VIPS), a 5 GHz VLBI survey of 1,127 sources with flat radio spectra. Through automated data reduction and imaging routines, we have produced publicly available I, Q, and U images and have detected polarized flux density from 37% of the sources. We have also developed an algorithm to use each source's I image to automatically classify it as a point-like source, a core-jet, a compact symmetric object (CSO) candidate, or a complex source. The mean ratio of the polarized to total 5 GHz flux density for VIPS sources with detected polarized flux density ranges from 1% to 20% with a median value of about 5%. We have also found significant evidence that the directions of the jets in core-jet systems tend to be perpendicular to the electric vector position angles (EVPAs). The data is consistent with a scenario in which ~24% of the polarized core-jets have EVPAs that are anti-aligned with the directions of their jet components and which have a substantial amount of Faraday rotation. In addition to these initial results, plans for future follow-up observations are discussed.Comment: 36 pages, 3 tables, 13 figures; accepted for publication in Ap

Backward-wave medium infra-red down-conversion in proustite

Phase-matched backward-wave down-conversion has been obtained in the medium infrared using proustite (Ag3AsS3) as the mixing crystal. A transmission window between the two-photon lattice band and the high-frequency wing of the reststrahlen permitted 18.6 µm infrared to be generated by mixing the output of a ruby laser with stimulated Raman emission from bromoform (CHBr3)

Parametric generation of infrared radiation between 10 µm and 25 µm in CdSe and proustite

Generation of tunable infrared radiation by difference mixing of signal and idler outputs from a parametric oscillator allows a considerable extension of tuning range into the infrared, The original proposal for this[1] included a demonstration of the principle in a proustite down-converter crystal together with the further suggestion that using a CdSe crystal would allow coverage from 10 μm to 25 μm. This has now been accomplished.The doubly resonant proustite parametric oscillator was pumped by a 1.065 μm Q-switched Nd:YAG laser. 30-kW pump pulses of 20-ns duration produced total signal and idler powers of 3 kW over the signal wavelength range 1.91 μm - 2.04 μm. The corresponding range for the idler was 2.40 μm - 2.23 μm and for the difference wavelength 9.4 μm - 24.3 μm.[1] G.C.Bhar, D.C.Hanna, B.Luther-Davies, and R.C.Smith, Opt. Commun., vol.6, pp.323-326, 1972

Staphylococcus aureus alpha-toxin induces apoptosis in peripheral blood mononuclear cells:role of endogenous tumour necrosis factor-alpha and the mitochondrial death pathway

Staphylococcus aureus infections can result in septic and toxic shock with depletion of immune cells and massive cytokine production. Recently, we showed that, in S. aureus-infected Jurkat T cells, alpha-toxin is the major mediator of caspase activation and apoptosis. Here, we investigated the mechanisms of cell death induced by alpha-toxin in peripheral blood mononuclear cells (MNC). We show that alpha-toxin is required and sufficient for S. aureus-induced cell death not only in transformed Jurkat T cells but also in MNC. Low alpha-toxin doses (3-30 ng ml-1) dose- and time-dependently induced apoptosis in both cell types, which was completely blocked by the caspase inhibitor zVAD-fmk. In Jurkat T cells and MNC, alpha-toxin induced the breakdown of the mitochondrial membrane potential and the intrinsic activation of caspase-3, -8 and -9. Interestingly, unlike in Jurkat T cells, apoptosis in MNC was additionally mediated by a caspase-9-independent component. MNC, but not Jurkat T cells, produced tumour necrosis factor (TNF)-alpha upon alpha-toxin stimulation. Blocking endogenous TNF-alpha with a TNF-alpha receptor antagonist partially decreased apoptosis in MNC. Our data therefore suggest that, whereas in Jurkat T cells apoptosis is solely mediated by the mitochondrial pathway, in MNC endogenous TNF-alpha and a death receptor-dependent pathway are also involved, which may contribute to depletion of immune cells during S. aureus infection

Effects of tezosentan on symptoms and clinical outcomes in patients with acute heart failure: the VERITAS Randomized controlled trials

Context: Plasma concentrations of the vasoconstrictor peptide endothelin-1 are increased in patients with heart failure, and higher concentrations are associated with worse outcomes. Tezosentan is an intravenous short-acting endothelin receptor antagonist that has favorable hemodynamic actions in heart failure. Objective: To determine if tezosentan improves outcomes in patients with acute heart failure. Design, Setting, and Participants: The Value of Endothelin Receptor Inhibition With Tezosentan in Acute Heart Failure Studies, 2 independent, identical, and concurrent randomized, double-blind, placebo-controlled, parallel-group trials conducted from April 2003 through January 2005 at sites in Australia, Europe, Israel, and North America. Patients admitted within the previous 24 hours with persisting dyspnea and a respiratory rate of 24/min or greater were eligible provided they fulfilled 2 of 4 criteria: (1) elevated plasma concentrations of B-type or N-terminal pro–B-type natriuretic peptide, (2) clinical pulmonary edema, (3) radiologic pulmonary congestion or edema, or (4) left ventricular systolic dysfunction. Intervention:Infusion of tezosentan (5 mg/h for 30 minutes, followed by 1 mg/h for 24 to 72 hours [n = 730]) or placebo (n = 718). Main Outcome Measures: The coprimary end points were change in dyspnea (measured at 3, 6, and 24 hours using a visual analog scale from 0-100) over 24 hours (as area under the curve) in the individual trials and incidence of death or worsening heart failure at 7 days in both trials combined. Results: Of the 1435 patients who received treatment as assigned, 855 (60%) were men; mean age was 70 years. Mean left ventricular ejection fraction (measured in 779 patients [54%]) was 29% (SD, 11%). Baseline dyspnea scores were similar in the 2 treatment groups. Tezosentan did not improve dyspnea more than placebo in either trial, with a mean treatment difference of −12 (95% confidence interval [CI], −105 to 81) mm · h (P = .80) in the first trial and −25 (95% CI, −119 to 69) mm · h (P = .60) in the second. The incidence of death or worsening heart failure at 7 days in the combined trials was 26% in each treatment group (odds ratio, 0.99; 95% confidence interval, 0.82-1.21; P = .95). Conclusion: The endothelin receptor antagonist tezosentan did not improve symptoms or clinical outcomes in patients with acute heart failure