Transparent Helium in Stripped Envelope Supernovae

Using simple arguments based on photometric light curves and velocity evolution, we propose that some stripped envelope supernovae (SNe) show signs that a significant fraction of their helium is effectively transparent. The main pieces of evidence are the relatively low velocities with little velocity evolution, as are expected deep inside an exploding star, along with temperatures that are too low to ionize helium. This means that the helium should not contribute to the shaping of the main SN light curve, and thus the total helium mass may be difficult to measure from simple light curve modeling. Conversely, such modeling may be more useful for constraining the mass of the carbon/oxygen core of the SN progenitor. Other stripped envelope SNe show higher velocities and larger velocity gradients, which require an additional opacity source (perhaps the mixing of heavier elements or radioactive nickel) to prevent the helium from being transparent. We discuss ways in which similar analysis can provide insights into the differences and similarities between SNe Ib and Ic, which will lead to a better understanding of their respective formation mechanisms.Comment: Revised version accepted for publication in The Astrophysical Journal Letters, 4 pages, 4 figure

Exploring the Potential Diversity of Early Type Ia Supernova Light Curves

During the first several days after explosion, Type Ia supernova light curves probe the outer layers of the exploding star and therefore provide important clues for identifying their progenitors. We investigate how both the shallow $^{56}$Ni distribution and the presence of circumstellar material shape these early light curves. This is performed using a series of numerical experiments with parameterized properties for systematic exploration. Although not all of the considered models may be realized in nature (and indeed there are arguments why some of them should not occur), the spirit of this work is to provide a broader exploration of the diversity of possibilities. We find that shallower $^{56}$Ni leads to steeper, bluer light curves. Differences in the shape of the rise can introduce errors in estimating the explosion time and thus impact efforts to infer upper limits on the progenitor or companion radius from a lack of observed shock cooling emission. Circumstellar material can lead to significant luminosity during the first few days, but its presence can be difficult to identify depending on the degree of nickel mixing. In some cases, the hot emission of circumstellar material may even lead to a signature similar to interaction with a companion, and thus in the future additional diagnostics should be gathered for properly assessing early light curves.Comment: Revised version with additional figures and discussions. 8 pages, 15 figures, accepted for publication in The Astrophysical Journa

Explaining the subpulse drift velocity of pulsar magnetosphere within the space-charge limited flow model

We try to explain the subpulse drift phenomena adopting the space-charge limited flow (SCLF) model and comparing the plasma drift velocity in the inner region of pulsar magnetospheres with the observed velocity of drifting subpulses. We apply the approach described in a recent paper of van Leeuwen & Timokhin (2012), where it was shown that the standard estimation of the subpulse drift velocity through the total value of the scalar potential drop in the inner gap gives inaccurate results, while the exact expression relating the drift velocity to the gradient of the scalar potential should be used instead. After considering a selected sample of sources taken from the catalog of Weltevrede, Edwards & Stappers (2006) with coherently drifting subpulses and reasonably known observing geometry, we show that their subpulse drift velocities would correspond to the drift of the plasma located very close or above the pair formation front. Moreover, a detailed analysis of PSR B0826-34 and PSR B0818-41 reveals that the variation of the subpulse separation with the pulse longitude can be successfully explained by the dependence of the plasma drift velocity on the angular coordinates.Comment: 14 pages, 6 figures, 2 table

Nonsingular electrodynamics of a rotating black hole moving in an asymptotically uniform magnetic test field

We extend the Wald solution to a black hole that is also moving at constant velocity. More specifically, we derive analytic solutions for the Maxwell equations for a rotating black hole moving at constant speed in an asymptotically uniform magnetic test field. By adopting Kerr-Schild coordinates we avoid singular behaviors at the horizon and obtain a complete description of the charge and current distributions in terms of the black-hole spin and velocity. Using this solution, we compute the energy losses expected when charged particles are accelerated along the magnetic field lines, improving previous estimates that had to cope with singular electromagnetic fields on the horizon. When used to approximate the emission from binary black holes in a uniform magnetic field, our estimates match reasonably well those from numerical-relativity calculations in the force-free approximation

Hyperphosphorylation of Tau Associates With Changes in Its Function Beyond Microtubule Stability

Tau is a neuronal microtubule associated protein whose main biological functions are to promote microtubule self-assembly by tubulin and to stabilize those already formed. Tau also plays an important role as an axonal microtubule protein. Tau is an amazing protein that plays a key role in cognitive processes, however, deposits of abnormal forms of tau are associated with several neurodegenerative diseases, including Alzheimer disease (AD), the most prevalent, and Chronic Traumatic Encephalopathy (CTE) and Traumatic Brain Injury (TBI), the most recently associated to abnormal tau. Tau post-translational modifications (PTMs) are responsible for its gain of toxic function. Alonso et al. (1996) were the first to show that the pathological tau isolated from AD brains has prion-like properties and can transfer its toxic function to the normal molecule. Furthermore, we reported that the pathological changes are associated with tau phosphorylation at Ser199 and 262 and Thr212 and 231. This pathological version of tau induces subcellular mislocalization in cultured cells and neurons, and translocates into the nucleus or accumulated in the perinuclear region of cells. We have generated a transgenic mouse model that expresses pathological human tau (PH-Tau) in neurons at two different concentrations (4% and 14% of the total endogenous tau). In this model, PH-Tau causes cognitive decline by at least two different mechanisms: one that involves the cytoskeleton with axonal disruption (at high concentration), and another in which the apparent neuronal morphology is not grossly affected, but the synaptic terminals are altered (at lower concentration). We will discuss the putative involvement of tau in proteostasis under these conditions. Understanding tau’s biological activity on and off the microtubules will help shed light to the mechanism of neurodegeneration and of normal neuronal function

Importin-Mediated Pathological Tau Nuclear Translocation Causes Disruption of the Nuclear Lamina, TDP-43 Mislocalization and Cell Death

Tau is a cytosolic protein that has also been observed in the nucleus, where it has multiple proposed functions that are regulated by phosphorylation. However, the mechanism underlying the nuclear import of tau is unclear, as is the contribution of nuclear tau to the pathology of tauopathies. We have previously generated a pathological form of tau, PH-tau (pseudophosphorylation mutants S199E, T212E, T231E, and S262E) that mimics AD pathological behavior in cells, Drosophila, and a mouse model. Here, we demonstrated that PH-tau translocates into the nucleus of transiently transfected HEK-293 cells, but wildtype tau does not. We identified a putative importin binding site in the tau sequence, and showed that disruption of this site prevents tau from entering the nucleus. We further showed that this nuclear translocation is prevented by inhibitors of both importin-α and importin-β. In addition, expression of PH-tau resulted in an enlarged population of dying cells, which is prevented by blocking its entry into the nucleus. PH-tau-expressing cells also exhibited disruption of the nuclear lamina and mislocalization of TDP-43 to the cytoplasm. We found that PH-tau does not bundle microtubules, and this effect is independent of nuclear translocation. These results demonstrate that tau translocates into the nucleus through the importin-α/β pathway, and that PH-tau exhibits toxicity after its nuclear translocation. We propose a model where hyperphosphorylated tau not only disrupts the microtubule network, but also translocates into the nucleus and interferes with cellular functions, such as nucleocytoplasmic transport, inducing mislocalization of proteins like TDP-43 and, ultimately, cell death

Light Curves of Core-Collapse Supernovae with Substantial Mass Loss using the New Open-Source SuperNova Explosion Code (SNEC)

We present the SuperNova Explosion Code (SNEC), an open-source Lagrangian code for the hydrodynamics and equilibrium-diffusion radiation transport in the expanding envelopes of supernovae. Given a model of a progenitor star, an explosion energy, and an amount and distribution of radioactive nickel, SNEC generates the bolometric light curve, as well as the light curves in different wavelength bands assuming black body emission. As a first application of SNEC, we consider the explosions of a grid of 15 M_⊙ (at zero-age main sequence) stars whose hydrogen envelopes are stripped to different extents and at different points in their evolution. The resulting light curves exhibit plateaus with durations of ∼20 − 100 days if & 1.5 − 2 M_⊙ of hydrogen-rich material is left and no plateau if less hydrogen-rich material is left. The shorter plateau lengths are unlike the Type IIP supernova light curves typically observed in nature. This suggests that, at least for zero-age main sequence masses . 20 M_⊙, hydrogen mass loss occurs as an all or nothing process, perhaps pointing to the important role binary interactions play in observed mass-stripped supernovae (i.e., Type Ib/c events). These light curves are also unlike what is typically seen for Type IIL supernovae, arguing that simply varying the amount of mass loss cannot explain these events. The most stripped models begin to show double-peaked light curves similar to what is often seen for Type IIb supernovae, confirming previous work that these supernovae can come from progenitors that have a small amount of hydrogen and a radius of ∼ 500 R_⊙

Hyperphosphorylation of Tau Associates With Changes in Its Function Beyond Microtubule Stability

Tau is a neuronal microtubule associated protein whose main biological functions are to promote microtubule self-assembly by tubulin and to stabilize those already formed. Tau also plays an important role as an axonal microtubule protein. Tau is an amazing protein that plays a key role in cognitive processes, however, deposits of abnormal forms of tau are associated with several neurodegenerative diseases, including Alzheimer disease (AD), the most prevalent, and Chronic Traumatic Encephalopathy (CTE) and Traumatic Brain Injury (TBI), the most recently associated to abnormal tau. Tau post-translational modifications (PTMs) are responsible for its gain of toxic function. Alonso et al. (1996) were the first to show that the pathological tau isolated from AD brains has prion-like properties and can transfer its toxic function to the normal molecule. Furthermore, we reported that the pathological changes are associated with tau phosphorylation at Ser199 and 262 and Thr212 and 231. This pathological version of tau induces subcellular mislocalization in cultured cells and neurons, and translocates into the nucleus or accumulated in the perinuclear region of cells. We have generated a transgenic mouse model that expresses pathological human tau (PH-Tau) in neurons at two different concentrations (4% and 14% of the total endogenous tau). In this model, PH-Tau causes cognitive decline by at least two different mechanisms: one that involves the cytoskeleton with axonal disruption (at high concentration), and another in which the apparent neuronal morphology is not grossly affected, but the synaptic terminals are altered (at lower concentration). We will discuss the putative involvement of tau in proteostasis under these conditions. Understanding tau’s biological activity on and off the microtubules will help shed light to the mechanism of neurodegeneration and of normal neuronal function

Explaining radio emission of magnetars via rotating and oscillating magnetospheres of neutron stars

We investigate the conditions for radio emission in rotating and oscillating magnetars, by focusing on the main physical processes determining the position of their death-lines in the P-\dot{P} diagram, i.e. of those lines that separate the regions where the neutron star may be radio-loud or radio-quiet. After using the general relativistic expression for the electromagnetic scalar potential in the magnetar magnetosphere, we find that larger compactness parameters of the star as well as larger inclination angles between the rotation axis and the magnetic moment produce death-lines well above the majority of known magnetars. This is consistent with the observational evidence of no regular radio emission from the magnetars in the frequency range typical for the ordinary pulsars. On the contrary, when oscillations of the magnetar are taken into account, the death-lines shift downward and the conditions necessary for the generation of radio emission in the magnetosphere are met. Present observations showing a close connection between the burst activity of magnetars and the generation of the radio emission in the magnetar magnetosphere are naturally accounted for within our interpretation.Comment: 9 pages, 4 figures, matches version accepted by MNRA