Photometry of the Stingray Nebula (V839 Ara) from 1889-2015 Across the Ionization of Its Planetary Nebula

Up until around 1980, the Stingray was an ordinary B1 post-AGB star, but then it suddenly sprouted bright emission lines like in a planetary nebula (PN), and soon after this the Hubble Space Telescope (HST) discovered a small PN around the star, so apparently we have caught a star in the act of ionizing a PN. We report here on a well-sampled light curve from 1889 to 2015, with unique coverage of the prior century plus the entire duration of the PN formation plus three decades of its aftermath. Surprisingly, the star anticipated the 1980's ionization event by declining from B=10.30 in 1889 to B=10.76 in 1980. Starting in 1980, the central star faded fast, at a rate of 0.20 mag/year, reaching B=14.64 in 1996. This fast fading is apparently caused by the central star shrinking in size. From 1994-2015, the V-band light curve is almost entirely from the flux of two bright [OIII] emission lines from the unresolved nebula, and it shows a consistent decline at a rate of 0.090 mag/year. This steady fading (also seen in the radio and infrared) has a time scale equal to that expected for ordinary recombination within the nebula, immediately after a short-duration ionizing event in the 1980s. We are providing the first direct measure of the rapidly changing luminosity of the central star on both sides of a presumed thermal pulse in 1980, with this providing a strong and critical set of constraints, and these are found to sharply disagree with theoretical models of PN evolution.Comment: ApJ accepted, 54 pages, 4 figures, one long data tabl

A Gettysburg Streetscape, North Washington Street in 1925

This paper explores life in Gettysburg on North Washington Street in 1925. It was the final project for Dr. Michael Birkner\u27s Spring 2017 Historical Methods class

Neuropilins: Role in Signalling, Angiogenesis and Disease

Neuropilins (NRPs) are co-receptors for class 3 semaphorins and for members of the vascular endothelial growth factor (VEGF) family of angiogenic cytokines. Genetic analysis of the role of NRPs in mice shows that NRP1 is essential for embryonic neuronal pathfinding and cardiovascular development, mediated via semaphorins and VEGF, respectively, while NRP2 has a more restricted role in neuronal patterning and lymphangiogenesis. NRPs are thought to mediate functional responses, most importantly cell migration, as a result of complex formation with other receptors, such as plexins in the case of semaphorins and the VEGF receptor, VEGFR2, resulting in enhanced signalling via some intracellular pathways. Recent findings indicate that NRPs may have important biological roles in other physiological and disease-related processes. In particular, NRPs are highly expressed in diverse tumour cell lines and human neoplasms and have been implicated in several biological processes regulating tumour growth in vivo, suggesting that NRP1 may be a future therapeutic target in cancer

Position and Momentum Uncertainties of the Normal and Inverted Harmonic Oscillators under the Minimal Length Uncertainty Relation

We analyze the position and momentum uncertainties of the energy eigenstates of the harmonic oscillator in the context of a deformed quantum mechanics, namely, that in which the commutator between the position and momentum operators is given by [x,p]=i\hbar(1+\beta p^2). This deformed commutation relation leads to the minimal length uncertainty relation \Delta x > (\hbar/2)(1/\Delta p +\beta\Delta p), which implies that \Delta x ~ 1/\Delta p at small \Delta p while \Delta x ~ \Delta p at large \Delta p. We find that the uncertainties of the energy eigenstates of the normal harmonic oscillator (m>0), derived in Ref. [1], only populate the \Delta x ~ 1/\Delta p branch. The other branch, \Delta x ~ \Delta p, is found to be populated by the energy eigenstates of the `inverted' harmonic oscillator (m<0). The Hilbert space in the 'inverted' case admits an infinite ladder of positive energy eigenstates provided that \Delta x_{min} = \hbar\sqrt{\beta} > \sqrt{2} [\hbar^2/k|m|]^{1/4}. Correspondence with the classical limit is also discussed.Comment: 16 pages, 31 eps figure

XMM-Newton Survey of the Brightest Supernova Remnants in the Large Magellanic Cloud

Therefore, a realistic understanding of SN contribution from SNRs populations is needed to model the evolution of a galaxy

Magnetic measurements at pressures above 10 GPa in a miniature ceramic anvil cell for a superconducting quantum interference device magnetometer

A miniature ceramic anvil high pressure cell (mCAC) was earlier designed by us for magnetic measurements at pressures up to 7.6 GPa in a commercial superconducting quantum interference (SQUID) magnetometer [N. Tateiwa et al., Rev. Sci. Instrum. 82, 053906 (2011)]. Here, we describe methods to generate pressures above 10 GPa in the mCAC. The efficiency of the pressure generation is sharply improved when the Cu-Be gasket is sufficiently preindented. The maximum pressure for the 0.6 mm culet anvils is 12.6 GPa when the Cu-Be gasket is preindented from the initial thickness of 0.30 to 0.06 mm. The 0.5 mm culet anvils were also tested with a rhenium gasket. The maximum pressure attainable in the mCAC is about 13 GPa. The present cell was used to study YbCu2Si2 which shows a pressure induced transition from the non-magnetic to magnetic phases at 8 GPa. We confirm a ferromagnetic transition from the dc magnetization measurement at high pressure. The mCAC can detect the ferromagnetic ordered state whose spontaneous magnetic moment is smaller than 1 mB per unit cell. The high sensitivity for magnetic measurements in the mCAC may result from the the simplicity of cell structure. The present study shows the availability of the mCAC for precise magnetic measurements at pressures above 10 GPa

Neuropilins 1 and 2 mediate neointimal hyperplasia and re-endothelialization following arterial injury

AIMS: Neuropilins 1 and 2 (NRP1 and NRP2) play crucial roles in endothelial cell migration contributing to angiogenesis and vascular development. Both NRPs are also expressed by cultured vascular smooth muscle cells (VSMCs) and are implicated in VSMC migration stimulated by PDGF-BB, but it is unknown whether NRPs are relevant for VSMC function in vivo. We investigated the role of NRPs in the rat carotid balloon injury model, in which endothelial denudation and arterial stretch induce neointimal hyperplasia involving VSMC migration and proliferation. METHODS AND RESULTS: NRP1 and NRP2 mRNAs and proteins increased significantly following arterial injury, and immunofluorescent staining revealed neointimal NRP expression. Down-regulation of NRP1 and NRP2 using shRNA significantly reduced neointimal hyperplasia following injury. Furthermore, inhibition of NRP1 by adenovirally overexpressing a loss-of-function NRP1 mutant lacking the cytoplasmic domain (ΔC) reduced neointimal hyperplasia, whereas wild-type (WT) NRP1 had no effect. NRP-targeted shRNAs impaired, while overexpression of NRP1 WT and NRP1 ΔC enhanced, arterial re-endothelialization 14 days after injury. Knockdown of either NRP1 or NRP2 inhibited PDGF-BB-induced rat VSMC migration, whereas knockdown of NRP2, but not NRP1, reduced proliferation of cultured rat VSMC and neointimal VSMC in vivo. NRP knockdown also reduced the phosphorylation of PDGFα and PDGFβ receptors in rat VSMC, which mediate VSMC migration and proliferation. CONCLUSION: NRP1 and NRP2 play important roles in the regulation of neointimal hyperplasia in vivo by modulating VSMC migration (via NRP1 and NRP2) and proliferation (via NRP2), independently of the role of NRPs in re-endothelialization