scholarly journals A NARROW SHORT-DURATION GRB JET FROM A WIDE CENTRAL ENGINE

2015 ◽  
Vol 813 (1) ◽  
pp. 64 ◽  
Author(s):  
Paul C. Duffell ◽  
Eliot Quataert ◽  
Andrew I. MacFadyen
2020 ◽  
Vol 500 (2) ◽  
pp. 1708-1720
Author(s):  
R Ricci ◽  
E Troja ◽  
G Bruni ◽  
T Matsumoto ◽  
L Piro ◽  
...  

ABSTRACT Neutron star mergers produce a substantial amount of fast-moving ejecta, expanding outwardly for years after the merger. The interaction of these ejecta with the surrounding medium may produce a weak isotropic radio remnant, detectable in relatively nearby events. We use late-time radio observations of short duration gamma-ray bursts (sGRBs) to constrain this model. Two samples of events were studied: four sGRBs that are possibly in the local (<200 Mpc) Universe were selected to constrain the remnant non-thermal emission from the sub-relativistic ejecta, whereas 17 sGRBs at cosmological distances were used to constrain the presence of a proto-magnetar central engine, possibly re-energizing the merger ejecta. We consider the case of GRB 170817A/GW170817 and find that in this case the early radio emission may be quenched by the jet blast-wave. In all cases, for ejecta mass range of ${M}_{\rm {ej}}\lesssim 10^{-2}\, (5\times 10^{-2})\, \mathrm{M}_\odot$, we can rule out very energetic merger ejecta ${E}_{\rm {ej}}\gtrsim 5\times 10^{52}\, (10^{53})\, \rm erg$, thus excluding the presence of a powerful magnetar as a merger remnant.


1999 ◽  
Vol 173 ◽  
pp. 249-254
Author(s):  
A.M. Silva ◽  
R.D. Miró

AbstractWe have developed a model for theH2OandOHevolution in a comet outburst, assuming that together with the gas, a distribution of icy grains is ejected. With an initial mass of icy grains of 108kg released, theH2OandOHproductions are increased up to a factor two, and the growth curves change drastically in the first two days. The model is applied to eruptions detected in theOHradio monitorings and fits well with the slow variations in the flux. On the other hand, several events of short duration appear, consisting of a sudden rise ofOHflux, followed by a sudden decay on the second day. These apparent short bursts are frequently found as precursors of a more durable eruption. We suggest that both of them are part of a unique eruption, and that the sudden decay is due to collisions that de-excite theOHmaser, when it reaches the Cometopause region located at 1.35 × 105kmfrom the nucleus.


1990 ◽  
Vol 122 (2) ◽  
pp. 191-200 ◽  
Author(s):  
C. G. J. Sweep ◽  
Margreet D. Boomkamp ◽  
István Barna ◽  
A. Willeke Logtenberg ◽  
Victor M. Wiegant

Abstract The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of β-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4–9) (1.44 fmol), Nα-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of β-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1–9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied β-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel β-endorphin-(1–31), the β-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lifes of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol β-endorphin-(1–31)) significantly enhanced the disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of β-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.


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