Multi-messenger observations of a binary neutron star merger

On 2017 August 17 a binary neutron star coalescence candidate (later designated GW170817) with merger time 12:41:04 UTC was observed through gravitational waves by the Advanced LIGO and Advanced Virgo detectors. The Fermi Gamma-ray Burst Monitor independently detected a gamma-ray burst (GRB 170817A) with a time delay of ~1.7 s with respect to the merger time. From the gravitational-wave signal, the source was initially localized to a sky region of 31 deg2 at a luminosity distance of 40+8-8 Mpc and with component masses consistent with neutron stars. The component masses were later measured to be in the range 0.86 to 2.26 Mo. An extensive observing campaign was launched across the electromagnetic spectrum leading to the discovery of a bright optical transient (SSS17a, now with the IAU identification of AT 2017gfo) in NGC 4993 (at ~40 Mpc) less than 11 hours after the merger by the One- Meter, Two Hemisphere (1M2H) team using the 1 m Swope Telescope. The optical transient was independently detected by multiple teams within an hour. Subsequent observations targeted the object and its environment. Early ultraviolet observations revealed a blue transient that faded within 48 hours. Optical and infrared observations showed a redward evolution over ~10 days. Following early non-detections, X-ray and radio emission were discovered at the transient’s position ~9 and ~16 days, respectively, after the merger. Both the X-ray and radio emission likely arise from a physical process that is distinct from the one that generates the UV/optical/near-infrared emission. No ultra-high-energy gamma-rays and no neutrino candidates consistent with the source were found in follow-up searches. These observations support the hypothesis that GW170817 was produced by the merger of two neutron stars in NGC4993 followed by a short gamma-ray burst (GRB 170817A) and a kilonova/macronova powered by the radioactive decay of r-process nuclei synthesized in the ejecta

Public Data Archiving in Ecology and Evolution:How Well Are We Doing?

Policies that mandate public data archiving (PDA) successfully increase accessibility to data underlying scientific publications. However, is the data quality sufficient to allow reuse and reanalysis? We surveyed 100 datasets associated with nonmolecular studies in journals that commonly publish ecological and evolutionary research and have a strong PDA policy. Out of these datasets, 56% were incomplete, and 64% were archived in a way that partially or entirely prevented reuse. We suggest that cultural shifts facilitating clearer benefits to authors are necessary to achieve high-quality PDA and highlight key guidelines to help authors increase their data’s reuse potential and compliance with journal data policies.12 page(s

Studies of the cardiovascular effects of nociceptin and related peptides

Nociceptin, a novel opioid peptide, and its ORL1 receptor share structural similarities with other opioid ligands and receptors. Although NC exerts evident cardiovascular effects at a central and peripheral level, its role in homeostatic mechanisms and disease states are just beginning to be understood, as only recently selective receptor antagonists became available. In this review, some of the new observations regarding the cardiovascular actions of NC, related peptides and newly synthesized receptor antagonists are discussed

Cardiovascular effects of nociceptin in unanesthetized mice

We evaluated the systemic hemodynamic effects induced by nociceptin (NC) and NC-related peptides, including the NC receptor antagonist [Phe1c(CH2-NH)Gly2]NC(1–13)NH2 ([F/G]NC(1–13)NH2) in unanesthetized normotensive Swiss Morini mice. Bolus intravenous injection of NC decreased mean blood pressure and heart rate. The hypotensive response to 10 nmol/kg NC lasted ,10 minutes, whereas a more prolonged hypotension was evoked by 100 nmol/kg (from 11463 to 9762 mm Hg at 10 minutes, P,0.01). The latter dose reduced heart rate from 542643 to 479631 beats/min (P,0.05) and increased aortic blood flow by 4165% (P,0.05). Hypotension and bradycardia were also evoked by NC(1–17)NH2 and NC(1–13)NH2 fragments, whereas NC(1–13)OH and NC(1–9)NH2 were ineffective. Thiorphan, an inhibitor of neutral endopeptidase 24.11, enhanced the hypotension induced by NC(1–13)NH2 and revealed the ability of NC(1–13)OH to decrease mean blood pressure. [F/G]NC(1–13)NH2, a recently synthesized antagonist of the NC receptor, did not alter basal mean blood pressure or heart rate, but it prevented the hypotension, bradycardia, and increase in aortic blood flow evoked by NC. In contrast, [F/G]NC(1–13)NH2 did not alter the hypotension induced by bradykinin or endomorphin-1 (a m-receptor agonist), and the bradycardia induced by leu-enkephalin (a d-receptor agonist) or U504885 (a synthetic k-receptor agonist). In conclusion, NC and some of its fragments cause hypotension and bradycardia and increase aortic blood flow in mice, with the NC(1–13) sequence being critical for these biological effects. Our results also demonstrate that the compound [F/G]NC(1–13)NH2 is a potent and selective antagonist of the NC receptor in vivo

Cardiovascular effects of nociceptin in unanesthetized mice

We evaluated the systemic hemodynamic effects induced by nociceptin (NC) and NC-related peptides, including the NC receptor antagonist [Phe1c(CH2-NH)Gly2]NC(1\u201313)NH2 ([F/G]NC(1\u201313)NH2) in unanesthetized normotensive Swiss Morini mice. Bolus intravenous injection of NC decreased mean blood pressure and heart rate. The hypotensive response to 10 nmol/kg NC lasted ,10 minutes, whereas a more prolonged hypotension was evoked by 100 nmol/kg (from 11463 to 9762 mm Hg at 10 minutes, P,0.01). The latter dose reduced heart rate from 542643 to 479631 beats/min (P,0.05) and increased aortic blood flow by 4165% (P,0.05). Hypotension and bradycardia were also evoked by NC(1\u201317)NH2 and NC(1\u201313)NH2 fragments, whereas NC(1\u201313)OH and NC(1\u20139)NH2 were ineffective. Thiorphan, an inhibitor of neutral endopeptidase 24.11, enhanced the hypotension induced by NC(1\u201313)NH2 and revealed the ability of NC(1\u201313)OH to decrease mean blood pressure. [F/G]NC(1\u201313)NH2, a recently synthesized antagonist of the NC receptor, did not alter basal mean blood pressure or heart rate, but it prevented the hypotension, bradycardia, and increase in aortic blood flow evoked by NC. In contrast, [F/G]NC(1\u201313)NH2 did not alter the hypotension induced by bradykinin or endomorphin-1 (a m-receptor agonist), and the bradycardia induced by leu-enkephalin (a d-receptor agonist) or U504885 (a synthetic k-receptor agonist). In conclusion, NC and some of its fragments cause hypotension and bradycardia and increase aortic blood flow in mice, with the NC(1\u201313) sequence being critical for these biological effects. Our results also demonstrate that the compound [F/G]NC(1\u201313)NH2 is a potent and selective antagonist of the NC receptor in vivo