Ivan Robert King (1927–2021)

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Discovery of Extended Blue Horizontal Branches in Two Metal-Rich Globular Clusters

We have used WFPC2 to construct B, V color-magnitude diagrams of four metal-rich globular clusters, NGC 104 (47 Tuc), NGC 5927, NGC 6388, and NGC 6441. All four clusters have well populated red horizontal branches (RHB), as expected for their metallicity. However, NGC 6388 and 6441 also exhibit a prominent blue HB (BHB) extension, including stars reaching as faint in V as the turnoff luminosity. This discovery demonstrates directly for the first time that a major population of hot HB stars can exist in old, metal-rich systems. This may have important implications for the interpretation of the integrated spectra of elliptical galaxies. The cause of the phenomenon remains uncertain. We examine the possibility that NGC 6388 and 6441 are older than the other clusters, but a simple difference in age may not be sufficient to produce the observed distributions along the HB. The high central densities in NGC 6388 and 6441 suggest that the existence of the blue HB (BHB) tails might be caused by stellar interactions in the dense cores of these clusters, which we calculate to have two of the highest collision rates among globular clusters in the Galaxy. Tidal collisions might act in various ways to enhance loss of envelope mass, and therefore populate the blue side of the HB. However, the relative frequency of tidal collisions does not seem large enough (compared to that of the clusters with pure RHBs) to account for such a drastic difference in HB morphology. While a combination of an age difference and dynamical interactions may help, prima facie the lack of a radial gradient in the BHB/RHB star ratio seems to argue against dynamical effects playing a role.Comment: LaTeX, includes one Postscript figure. To appear in ApJ

Further Evidence that Quasar X-Ray Emitting Regions Are Compact: X-Ray and Optical Microlensing in the Lensed Quasar Q J0158-4325

We present four new seasons of optical monitoring data and six epochs of X-ray photometry for the doubly-imaged lensed quasar Q J0158-4325. The high-amplitude, short-period microlensing variability for which this system is known has historically precluded a time delay measurement by conventional methods. We attempt to circumvent this limitation by application of a Monte Carlo microlensing analysis technique, but we are only able to prove that the delay must have the expected sign (image A leads image B). Despite our failure to robustly measure the time delay, we successfully model the microlensing at optical and X-ray wavelengths to find a half light radius for soft X-ray emission log(r_{1/2,X,soft}/cm) = 14.3^{+0.4}_{-0.5}, an upper limit on the half-light radius for hard X-ray emission log(r_{1/2,X,hard}/cm) <= 14.6 and a refined estimate of the inclination-corrected scale radius of the optical R-band (rest frame 3100 Angstrom) continuum emission region of log(r_s/cm) = 15.6+-0.3.Comment: 9 pages, 6 figures, submitted to Ap

Cosmic ray neon, Wolf-Rayet stars, and the superbubble origin of galactic cosmic rays

The abundances of neon isotopes in the galactic cosmic rays (GCRs) are reported using data from the Cosmic Ray Isotope Spectrometer (CRIS) aboard the Advanced Composition Explorer (ACE). We compare our ACE-CRIS data for neon and refractory isotope ratios, and data from other experiments, with recent results from two-component Wolf-Rayet (WR) models. The three largest deviations of GCR isotope ratios from solar-system ratios predicted by these models are indeed present in the GCRs. Since WR stars are evolutionary products of OB stars, and most OB stars exist in OB associations that form superbubbles, the good agreement of these data with WR models suggests that superbubbles are the likely source of at least a substantial fraction of GCRs.Comment: 22 pages, 6 figures Accepted for publication by Ap

Multiple Binding Sites on the Pyrin Domain of ASC Protein Allow Self-association and Interaction with NLRP3 Protein

A key process underlying an innate immune response to pathogens or cellular stress is activation of members of the NOD-like receptor family, such as NLRP3, to assemble caspase- 1-activating inflammasome complexes. Activated caspase-1 processes proinflammatory cytokines into active forms that mediate inflammation. Activation of the NLRP3 inflammasome is also associated with common diseases including cardiovascular disease, diabetes, chronic kidney disease, and Alzheimer disease. However, the molecular details of NLRP3 inflammasome assembly are not established. The adaptor protein ASC plays a key role in inflammasome assembly. It is composed of an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain, which are protein interaction domains of the death fold superfamily. ASC interacts with NLRP3 via a homotypic PYD interaction and recruits procaspase-1 via a homotypic caspase recruitment domain interaction. Here we demonstrate that ASC PYD contains two distinct binding sites important for self-association and interaction with NLRP3 and the modulatory protein POP1. Modeling of the homodimeric ASC PYD complex formed via an asymmetric interaction using both sites resembles a type I interaction found in other death fold domain complexes. This interaction mode also permits assembly of ASC PYDs into filaments. Furthermore, a type I binding mode is likely conserved in interactions with NLRP3 and POP1, because residues critical for interaction of ASC PYD are conserved in these PYDs. We also demonstrate that ASC PYD can simultaneously self-associate and interact with NLRP3, rationalizing the model whereby ASC self-association upon recruitment to NLRP3 promotes clustering and activation of procaspase-1

Estimation and application of the thermodynamic properties of aqueous phenanthrene and isomers of methylphenanthrene at high temperature

Estimates of standard molal Gibbs energy (ΔGf°) and enthalpy (ΔHf°) of formation, entropy (S°), heat capacity (Cp°) and volume (V°) at 25 °C and 1 bar of aqueous phenanthrene (P) and 1-, 2-, 3-, 4- and 9-methylphenanthrene (1-MP, 2-MP, 3-MP, 4-MP, 9-MP) were made by combining reported standard-state properties of the crystalline compounds, solubilities and enthalpies of phenanthrene and 1-MP, and relative Gibbs energies, enthalpies and entropies of aqueous MP isomers from published quantum chemical simulations. The calculated properties are consistent with greater stabilities of the β isomers (2-MP and 3-MP) relative to the α isomers (1-MP and 9-MP) at 25 °C. However, the metastable equilibrium values of the abundance ratios 2-MP/1-MP (MPR) and (2-MP + 3-MP)/(1-MP + 9-MP) (MPI-3) decrease with temperature, becoming <1 at ~375–455 °C. The thermodynamic model is consistent with observations of reversals of these organic maturity parameters at high temperature in hydrothermal and metamorphic settings. Application of the model to data reported for the Paleoproterozoic Here’s Your Chance (HYC) Pb–Zn–Ag ore deposit (McArthur River, Northern Territory, Australia) indicates a likely effect of high-temperature equilibration on reported values of MPR and MPI-3, but this finding is contingent on the location within the deposit. If metastable equilibrium holds, a third aromatic maturity ratio, 1.5 × (2-MP + 3-MP)/(P + 1-MP + 9-MP) (MPI-1), can be used as a proxy for oxidation potential. Values of log aH2(aq) determined from data reported for HYC and for a sequence of deeply buried source rocks are indicative of more reducing conditions at a given temperature than those inferred from data reported for two sets of samples exposed to contact or regional metamorphism. These results are limiting-case scenarios for the modeled systems that do not account for effects of non-ideal mixing or kinetics, or external sources or transport of the organic matter.Nevertheless, quantifying the temperature dependence of equilibrium constants of organic reactions enables the utilization of organic maturity parameters as relative geothermometers at temperatures higher than the nominal limits of the oil window

Pathogen-Mediated Proteolysis of the Cell Death Regulator RIPK1 and the Host Defense Modulator RIPK2 in Human Aortic Endothelial Cells

Porphyromonas gingivalis is the primary etiologic agent of periodontal disease that is associated with other human chronic inflammatory diseases, including atherosclerosis. The ability of P. gingivalis to invade and persist within human aortic endothelial cells (HAEC) has been postulated to contribute to a low to moderate chronic state of inflammation, although how this is specifically achieved has not been well defined. In this study, we demonstrate that P. gingivalis infection of HAEC resulted in the rapid cleavage of receptor interacting protein 1 (RIPK1), a mediator of tumor necrosis factor (TNF) receptor-1 (TNF-R1)-induced cell activation or death, and RIPK2, a key mediator of both innate immune signaling and adaptive immunity. The cleavage of RIPK1 or RIPK2 was not observed in cells treated with apoptotic stimuli, or cells stimulated with agonists to TNF-R1, nucleotide oligomerization domain receptor 1(NOD1), NOD2, Toll-like receptor 2 (TLR2) or TLR4. P. gingivalis-induced cleavage of RIPK1 and RIPK2 was inhibited in the presence of a lysine-specific gingipain (Kgp) inhibitor. RIPK1 and RIPK2 cleavage was not observed in HAEC treated with an isogenic mutant deficient in the lysine-specific gingipain, confirming a role for Kgp in the cleavage of RIPK1 and RIPK2. Similar proteolysis of poly (ADP-ribose) polymerase (PARP) was observed. We also demonstrated direct proteolysis of RIPK2 by P. gingivalis in a cell-free system which was abrogated in the presence of a Kgp-specific protease inhibitor. Our studies thus reveal an important role for pathogen-mediated modification of cellular kinases as a potential strategy for bacterial persistence within target host cells, which is associated with low-grade chronic inflammation, a hallmark of pathogen-mediated chronic inflammatory disorders

Innate Sensing of HIV-Infected Cells

Cell-free HIV-1 virions are poor stimulators of type I interferon (IFN) production. We examined here how HIV-infected cells are recognized by plasmacytoid dendritic cells (pDCs) and by other cells. We show that infected lymphocytes are more potent inducers of IFN than virions. There are target cell-type differences in the recognition of infected lymphocytes. In primary pDCs and pDC-like cells, recognition occurs in large part through TLR7, as demonstrated by the use of inhibitors and by TLR7 silencing. Donor cells expressing replication-defective viruses, carrying mutated reverse transcriptase, integrase or nucleocapsid proteins induced IFN production by target cells as potently as wild-type virus. In contrast, Env-deleted or fusion defective HIV-1 mutants were less efficient, suggesting that in addition to TLR7, cytoplasmic cellular sensors may also mediate sensing of infected cells. Furthermore, in a model of TLR7-negative cells, we demonstrate that the IRF3 pathway, through a process requiring access of incoming viral material to the cytoplasm, allows sensing of HIV-infected lymphocytes. Therefore, detection of HIV-infected lymphocytes occurs through both endosomal and cytoplasmic pathways. Characterization of the mechanisms of innate recognition of HIV-infected cells allows a better understanding of the pathogenic and exacerbated immunologic events associated with HIV infection

Euclid preparation. XXIV. Calibration of the halo mass function in Λ(ν)\Lambda(\nu)CDM cosmologies

Euclid's photometric galaxy cluster survey has the potential to be a very competitive cosmological probe. The main cosmological probe with observations of clusters is their number count, within which the halo mass function (HMF) is a key theoretical quantity. We present a new calibration of the analytic HMF, at the level of accuracy and precision required for the uncertainty in this quantity to be subdominant with respect to other sources of uncertainty in recovering cosmological parameters from Euclid cluster counts. Our model is calibrated against a suite of N-body simulations using a Bayesian approach taking into account systematic errors arising from numerical effects in the simulation. First, we test the convergence of HMF predictions from different N-body codes, by using initial conditions generated with different orders of Lagrangian Perturbation theory, and adopting different simulation box sizes and mass resolution. Then, we quantify the effect of using different halo-finder algorithms, and how the resulting differences propagate to the cosmological constraints. In order to trace the violation of universality in the HMF, we also analyse simulations based on initial conditions characterised by scale-free power spectra with different spectral indexes, assuming both Einstein--de Sitter and standard $\Lambda$CDM expansion histories. Based on these results, we construct a fitting function for the HMF that we demonstrate to be sub-percent accurate in reproducing results from 9 different variants of the $\Lambda$CDM model including massive neutrinos cosmologies. The calibration systematic uncertainty is largely sub-dominant with respect to the expected precision of future mass-observation relations; with the only notable exception of the effect due to the halo finder, that could lead to biased cosmological inference.Comment: 24 pages, 21 figures, 5 tables, 3 appendixes

Euclid preparation. XXI. Intermediate-redshift contaminants in the search for z > 6 galaxies within the Euclid Deep Survey (Corrigendum)

A&amp;A, 666, A200 (2022), https://doi.org/10.1051/0004-6361/20224395