Forbidden hugs in pandemic times: III. Observations of the luminous red nova AT 2021biy in the nearby galaxy NGC 4631

We present an observational study of the luminous red nova (LRN) AT 2021biy in the nearby galaxy NGC 4631. The field of the object was routinely imaged during the pre-eruptive stage by synoptic surveys, but the transient was detected only at a few epochs from ∼231 days before maximum brightness. The LRN outburst was monitored with unprecedented cadence both photometrically and spectroscopically. AT 2021biy shows a short-duration blue peak, with a bolometric luminosity of ∼1.6×1041 erg s-1, followed by the longest plateau among LRNe to date, with a duration of 210 days. A late-time hump in the light curve was also observed, possibly produced by a shell-shell collision. AT 2021biy exhibits the typical spectral evolution of LRNe. Early-time spectra are characterised by a blue continuum and prominent H emission lines. Then, the continuum becomes redder, resembling that of a K-type star with a forest of metal absorption lines during the plateau phase. Finally, late-time spectra show a very red continuum (TBB ≈ 2050 K) with molecular features (e.g., TiO) resembling those of M-type stars. Spectropolarimetric analysis indicates that AT 2021biy has local dust properties similar to those of V838 Mon in the Milky Way Galaxy. Inspection of archival Hubble Space Telescope data taken on 2003 August 3 reveals a ∼20 M⊙ progenitor candidate with log (L/L⊙) = 5.0 dex and Teff 5900 K at solar metallicity. The above luminosity and colour match those of a luminous yellow supergiant. Most likely, this source is a close binary, with a 17-24 M⊙ primary component

Soliton-induced relativistic-scattering and amplification

Solitons are of fundamental importance in photonics due to applications in optical data transmission and also as a tool for investigating novel phenomena ranging from light generation at new frequencies and wave-trapping to rogue waves. Solitons are also moving scatterers: they generate refractive index perturbations moving at the speed of light. Here we found that such perturbations scatter light in an unusual way: they amplify light by the mixing of positive and negative frequencies, as we describe using a first Born approximation and numerical simulations. The simplest scenario in which these effects may be observed is within the initial stages of optical soliton propagation: a steep shock front develops that may efficiently scatter a second, weaker probe pulse into relatively intense positive and negative frequency modes with amplification at the expense of the soliton. Our results show a novel all-optical amplification scheme that relies on soliton induced scattering.Publisher PDFPeer reviewe

Nucleoside-Diphosphate-Kinase of P. gingivalis is Secreted from Epithelial Cells In the Absence of a Leader Sequence Through a Pannexin-1 Interactome

Nucleoside-diphosphate-kinases (NDKs) are leaderless, multifunctional enzymes. The mode(s) of NDK secretion is currently undefined, while extracellular translocation of bacterial NDKs is critical for avoidance of host pathogen clearance by opportunistic pathogens such as Porphyromonas gingivalis. P. gingivalis-NDK during infection inhibits extracellular-ATP (eATP)/P2X(7)-receptor mediated cell death in gingival epithelial cells (GECs) via eATP hydrolysis. Furthermore, depletion of pannexin-1-hemichannel (PNX1) coupled with P2X(7)-receptor blocks the infection-induced eATP release in GECs, and P. gingivalis-NDK impacts this pathway. Ultrastructural and confocal microscopy of P. gingivalis-co-cultured GECs or green-fluorescent-protein (GFP)-P. gingivalis-NDK transfected GECs revealed a perinuclear/cytoplasmic localization of NDK. eATP stimulation induced NDK recruitment to the cell periphery. Depletion of PNX1 by siRNA or inhibition by probenecid resulted in significant blocking of extracellular NDK activity and secretion using ATPase and ELISA assays. Co-immunoprecipitation-coupled Mass-spectrometry method revealed association of P. gingivalis-NDK to the myosin-9 motor molecule. Interestingly, inhibition of myosin-9, actin, and lipid-rafts, shown to be involved in PNX1-hemichannel function, resulted in marked intracellular accumulation of NDK and decreased NDK secretion from infected GECs. These results elucidate for the first time PNX1-hemichannels as potentially main extracellular translocation pathway for NDKs from an intracellular pathogen, suggesting that PNX1-hemichannels may represent a therapeutic target for chronic opportunistic infections