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We report the results of an experiment conducted near the High Flux Isotope Reactor of Oak Ridge National Laboratory, designed to address the question of whether a flux of reactor-generated electron antineutrinos (ν¯ e ) can alter the rates of weak nuclear interaction induced decays of 54 Mn, 22 Na, and 60 Co. This experiment has small statistical errors but, when systematic uncertainties are included, has null results. Perturbations greater than one part in 10 4 are excluded at 95% confidence level in β ± decay and electron capture processes, in the presence of an antineutrino flux of 3 × 10 12  cm -2 s -1 . The present experimental methods are applicable to a wide range of radionuclides. Improved sensitivity in future experiments can be anticipated as we continue to better understand and reduce the dominant systematic uncertainties., (Copyright © 2019. Published by Elsevier Ltd.)

We have directly compared the effects of the nitrates isosorbide-5-mononitrate, nitroglycerin and isosorbide dinitrate and of the nitric oxide-containing sodium nitroprusside and 3-morpholino-sydnonimine (SIN 1) as well as of the bioinactive precursor of SIN 1, molsidomine, on platelet activating factor-induced platelet aggregation and activation of soluble guanylate cyclase. The effects of these agents on the aggregation and on soluble guanylate cyclase activity of human platelets were closely correlated. Whereas nitroprusside and SIN 1 were very potent inhibitors of aggregation and activators of soluble guanylate cyclase in micromolar concentrations, the other drugs were effective only at millimolar concentrations. Preincubation of platelets with cysteine did not or only slightly increase the ability of isosorbide-5'-mononitrate and isosorbide dinitrate to inhibit aggregation, but a clear increase was observed after preincubation with nitroglycerin. These data support the concept that cyclic GMP is the mediator of nitric oxide-induced inhibition of platelet aggregation and indicate that nitrates cannot directly inhibit aggregation or be converted to nitric oxide-containing agents by a specific mechanism in platelets. The data also suggest that SIN 1 and nitroprusside, but not or only to a certain degree the nitrates, can be considered as exogenous endothelium-derived relaxing factors.