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We present the first relativistic magnetohydrodynamics numerical simulation of a magnetic jet that propagates through and emerges from the dynamical ejecta of a binary neutron star merger. Generated by the magnetized rotation of the merger remnant, the jet propagates through the ejecta and produces an energetic cocoon that expands at mildly relativistic velocities and breaks out of the ejecta.We show that if the ejecta has a low-mass (∼10-7M☉) high-velocity (v ∼ 0.85c) tail, the cocoon shock breakout will generate γ -ray emission that is comparable to the observed short GRB170817A that accompanied the recent gravitational wave event GW170817. Thus, we propose that this gamma-ray burst (GRB), which is quite different from all other short GRBs observed before, was produced by a different mechanism. We expect, however, that such events are numerous and many will be detected in coming LIGO-Virgo runs. [ABSTRACT FROM AUTHOR]

Every supernova so far observed has been considered to be the terminal explosion of a star. Moreover, all supernovae with absorption lines in their spectra show those lines decreasing in velocity over time, as the ejecta expand and thin, revealing slower-moving material that was previously hidden. In addition, every supernova that exhibits the absorption lines of hydrogen has one main light-curve peak, or a plateau in luminosity, lasting approximately 100 days before declining. Here we report observations of iPTF14hls, an event that has spectra identical to a hydrogen-rich core-collapse supernova, but characteristics that differ extensively from those of known supernovae. The light curve has at least five peaks and remains bright for more than 600 days; the absorption lines show little to no decrease in velocity; and the radius of the line-forming region is more than an order of magnitude bigger than the radius of the photosphere derived from the continuum emission. These characteristics are consistent with a shell of several tens of solar masses ejected by the progenitor star at supernova-level energies a few hundred days before a terminal explosion. Another possible eruption was recorded at the same position in 1954. Multiple energetic pre-supernova eruptions are expected to occur in stars of 95 to 130 solar masses, which experience the pulsational pair instability. That model, however, does not account for the continued presence of hydrogen, or the energetics observed here. Another mechanism for the violent ejection of mass in massive stars may be required.

The origin of gamma-ray bursts (GRBs) is one of the most interesting puzzles in recent astronomy. During the last decade a consensus has formed that long GRBs (LGRBs) arise from the collapse of massive stars, and that short GRBs (SGRBs) have a different origin, most likely neutron star mergers. A key ingredient of the collapsar model that explains how the collapse of massive stars produces a GRB is the emergence of a relativistic jet that penetrates the stellar envelope. The condition that the emerging jet penetrates the envelope imposes strong constraints on the system. Using these constraints we show the following. (i) Low-luminosity GRBs (llGRBs), a subpopulation of GRBs with very low luminosities (and other peculiar properties: single-peaked, smooth and soft), cannot be formed by collapsars. llGRBs must have a different origin (most likely a shock breakout). (ii) On the other hand, regular LGRBs must be formed by collapsars. (iii) While for BATSE the dividing line between collapsars and non-collapsars is indeed at approximately 2 s, the dividing line is different for other GRB detectors. In particular, most Swift bursts longer than 0.8 s are of a collapsar origin. This last result requires a revision of many conclusions concerning the origin of Swift SGRBs, which were based on the commonly used 2 s limit.

Hematopoietic stem and progenitor cells (HSPCs), which continuously maintain all mature blood cells, are regulated within the marrow microenvironment. We previously reported that pharmacologic treatment of naïve mice with prostaglandin E2 (PGE2) expands HSPCs. However, the cellular mechanisms mediating this expansion remain unknown. Here, we demonstrate that PGE2 treatment in naïve mice inhibits apoptosis of HSPCs without changing their proliferation rate. In a murine model of sublethal total body irradiation (TBI), in which HSPCs are rapidly lost, treatment with a long-acting PGE2 analog (dmPGE2) reversed the apoptotic program initiated by TBI. dmPGE2 treatment in vivo decreased the loss of functional HSPCs following radiation injury, as demonstrated both phenotypically and by their increased reconstitution capacity. The antiapoptotic effect of dmPGE2 on HSPCs did not impair their ability to differentiate in vivo, resulting instead in improved hematopoietic recovery after TBI. dmPGE2 also increased microenvironmental cyclooxygenase-2 expression and expanded the α-smooth muscle actin-expressing subset of marrow macrophages, thus enhancing the bone marrow microenvironmental response to TBI. Therefore, in vivo treatment with PGE2 analogs may be particularly beneficial to HSPCs in the setting of injury by targeting them both directly and also through their niche. The current data provide rationale for in vivo manipulation of the HSPC pool as a strategy to improve recovery after myelosuppression., (Copyright © 2012 AlphaMed Press.)

Hematopoietic stem cell (HSC) regulation is highly dependent on interactions with the marrow microenvironment. Controversy exists on N-cadherin's role in support of HSCs. Specifically, it is unknown whether microenvironmental N-cadherin is required for normal marrow microarchitecture and for hematopoiesis. To determine whether osteoblastic N-cadherin is required for HSC regulation, we used a genetic murine model in which deletion of Cdh2, the gene encoding N-cadherin, has been targeted to cells of the osteoblastic lineage. Targeted deletion of N-cadherin resulted in an age-dependent bone phenotype, ultimately characterized by decreased mineralized bone, but no difference in steady-state HSC numbers or function at any time tested, and normal recovery from myeloablative injury. Intermittent parathyroid hormone (PTH) treatment is well established as anabolic to bone and to increase marrow HSCs through microenvironmental interactions. Lack of osteoblastic N-cadherin did not block the bone anabolic or the HSC effects of PTH treatment. This report demonstrates that osteoblastic N-cadherin is not required for regulation of steady-state hematopoiesis, HSC response to myeloablation, or for rapid expansion of HSCs through intermittent treatment with PTH.

Microenvironmental expansion of hematopoietic stem cells (HSCs) is induced by treatment with parathyroid hormone (PTH) or activation of the PTH receptor (PTH1R) in osteoblastic cells; however, the osteoblastic subset mediating this action of PTH is unknown. Osteocytes are terminally differentiated osteoblasts embedded in mineralized bone matrix but are connected with the BM. Activation of PTH1R in osteocytes increases osteoblastic number and bone mass. To establish whether osteocyte-mediated PTH1R signaling expands HSCs, we studied mice expressing a constitutively active PTH1R in osteocytes (TG mice). Osteoblasts, osteoclasts, and trabecular bone were increased in TG mice without changes in BM phenotypic HSCs or HSC function. TG mice had progressively increased trabecular bone but decreased HSC function. In severely affected TG mice, phenotypic HSCs were decreased in the BM but increased in the spleen. TG osteocytes had no increase in signals associated with microenvironmental HSC support, and the spindle-shaped osteoblastic cells that increased with PTH treatment were not present in TG bones. These findings demonstrate that activation of PTH1R signaling in osteocytes does not expand BM HSCs, which are instead decreased in TG mice. Therefore, osteocytes do not mediate the HSC expansion induced by PTH1R signaling. Further, osteoblastic expansion is not sufficient to increase HSCs.

A system of equations governing the structure of a steady, relativistic radiation-dominated shock is derived, starting from the general form of the transfer equation obeyed by the photon distribution function. Closure is obtained by truncating the system of moment equations at some order. The anisotropy of the photon distribution function inside the shock is shown to increase with increasing shock velocity, approaching nearly perfect beaming at upstream Lorentz factors Gamma(-) >>1. Solutions of the shock equations are presented for some range of upstream conditions. These solutions are shown to converge as the truncation order is increased.