SKA studies of nearby galaxies : star-formation, accretion processes and molecular gas across all environments

Copyright owned by the author(s) under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike LicenceThe SKA will be a transformational instrument in the study of our local Universe. In particular, by virtue of its high sensitivity (both to point sources and diffuse low surface brightness emission), angular resolution and the frequency ranges covered, the SKA will undertake a very wide range of astrophysical research in the field of nearby galaxies. By surveying vast numbers of nearby galaxies of all types with $\mu$Jy sensitivity and sub-arcsecond angular resolutions at radio wavelengths, the SKA will provide the cornerstone of our understanding of star-formation and accretion activity in the local Universe. In this chapter we outline the key continuum and molecular line science areas where the SKA, both during phase-1 and when it becomes the full SKA, will have a significant scientific impact.Peer reviewedFinal Published versio

MALS SALT-NOT survey of MIR-selected powerful radio-bright AGN at 0<z<3.5

We present results of an optical spectroscopic survey using SALT and NOT to build a WISE mid-infrared color-based, dust-unbiased sample of powerful radio-bright ($>$200 mJy at 1.4 GHz) AGN for the MeerKAT Absorption Line Survey (MALS). Our sample has 250 AGN (median $z=1.8$) showing emission lines, 26 with no emission lines, and 27 without optical counterparts. Overall, our sample is fainter ($\Delta i$=0.6 mag) and redder ($\Delta(g-i)$=0.2 mag) than radio-selected quasars, and representative of fainter quasar population detected in optical surveys. About 20% of the sources are narrow line AGN (NLAGN) $-$ 65% of these, at $z < 0.5$ are galaxies without strong nuclear emission, and 10% at $z>1.9$, have emission line ratios similar to radio galaxies. The farthest NLAGN in our sample is M1513$-$2524 ($z_{em}=3.132$), and the largest (size$\sim$330 kpc) is M0909$-$3133 ($z_{em}=0.884$). We discuss in detail 110 AGN at $1.9 < z < 3.5$. Despite representing the radio loudest quasars (median $R$=3685), their Eddington ratios are similar to the SDSS quasars having lower $R$. We detect 4 CIV BALQSOs, all among AGN with least $R$, and highest black hole masses and Eddington ratios. The BAL detection rate ($4^{+3}_{-2}$%) is consistent with that seen in extremely powerful ($L_{1.4GHz}>10^{25}$ WHz$^{-1}$) quasars. Using optical light-curves, radio polarization and $\gamma$-ray detections, we identify 7 high-probability BL Lacs. We also summarize the full MALS footprint to search for HI 21-cm and OH 18-cm lines at $z<2$.Comment: 62 pages, 15 figures and 3 tables; accepted in ApJ (updated the redshift of M1312-2026 to z=0.977

Discovery of Hydrogen Radio Recombination Lines at z = 0.89 toward PKS 1830-211

We report the detection of stimulated hydrogen radio recombination line (RRL) emission from ionized gas in a z = 0.89 galaxy using 580-1670 MHz observations from the MeerKAT Absorption Line Survey. The RRL emission originates in a galaxy that intercepts and strongly lenses the radio blazar PKS 1830−211 (z = 2.5). This is the second detection of RRLs outside of the local Universe and the first clearly associated with hydrogen. We detect effective H144α (and H163α) transitions at observed frequencies of 1156 (798) MHz by stacking 17 (27) RRLs with 21σ (14σ) significance. The RRL emission contains two main velocity components and is coincident in velocity with H i 21 cm and OH 18 cm absorption. We use the RRL spectral line energy distribution and a Bayesian analysis to constrain the density (n e ) and the volume-averaged path length (ℓ) of the ionized gas. We determine log ( n e ) = 2.0 − 0.7 + 1.0 cm−3 and log ( ℓ ) = − 0.7 − 1.1 + 1.1 pc toward the northeast (NE) lensed image, likely tracing the diffuse thermal phase of the ionized ISM in a thin disk. Toward the southwest (SW) lensed image, we determine log ( n e ) = 3.2 − 1.0 + 0.4 cm−3 and log ( ℓ ) = − 2.7 − 0.2 + 1.8 pc, tracing gas that is more reminiscent of H scii regions. We estimate a star formation (surface density) rate of ΣSFR ∼ 0.6 M ⊙ yr−1 kpc−2 or SFR ∼ 50 M ⊙ yr−1, consistent with a star-forming main-sequence galaxy of M ⋆ ∼ 1011 M ⊙. The discovery presented here opens up the possibility of studying ionized gas at high redshifts using RRL observations from current and future (e.g., SKA and ngVLA) radio facilities

RyRCa2+ Leak Limits Cardiac Ca2+ Window Current Overcoming the Tonic Effect of Calmodulin in Mice

Ca2+ mediates the functional coupling between L-type Ca2+ channel (LTCC) and sarcoplasmic reticulum (SR) Ca2+ release channel (ryanodine receptor, RyR), participating in key pathophysiological processes. This crosstalk manifests as the orthograde Ca2+-induced Ca2+-release (CICR) mechanism triggered by Ca2+ influx, but also as the retrograde Ca2+-dependent inactivation (CDI) of LTCC, which depends on both Ca2+ permeating through the LTCC itself and on SR Ca2+ release through the RyR. This latter effect has been suggested to rely on local rather than global Ca2+ signaling, which might parallel the nanodomain control of CDI carried out through calmodulin (CaM). Analyzing the CICR in catecholaminergic polymorphic ventricular tachycardia (CPVT) mice as a model of RyR-generated Ca2+ leak, we evidence here that increased occurrence of the discrete local SR Ca2+ releases through the RyRs (Ca2+ sparks) causea depolarizing shift in activation and a hyperpolarizing shift inisochronic inactivation of cardiac LTCC current resulting in the reduction of window current. Both increasing fast [Ca2+]i buffer capacity or depleting SR Ca2+ store blunted these changes, which could be reproduced in WT cells by RyRCa2+ leak induced with Ryanodol and CaM inhibition.Our results unveiled a new paradigm for CaM-dependent effect on LTCC gating and further the nanodomain Ca2+ control of LTCC, emphasizing the importance of spatio-temporal relationships between Ca2+ signals and CaM function

Signal transduction underlying the control of urinary bladder smooth muscle tone by muscarinic receptors and β-adrenoceptors

The normal physiological contraction of the urinary bladder, which is required for voiding, is predominantly mediated by muscarinic receptors, primarily the M3 subtype, with the M2 subtype providing a secondary backup role. Bladder relaxation, which is required for urine storage, is mediated by β-adrenoceptors, in most species involving a strong β3-component. An excessive stimulation of contraction or a reduced relaxation of the detrusor smooth muscle during the storage phase of the micturition cycle may contribute to bladder dysfunction known as the overactive bladder. Therefore, interference with the signal transduction of these receptors may be a viable approach to develop drugs for the treatment of overactive bladder. The prototypical signaling pathway of M3 receptors is activation of phospholipase C (PLC), and this pathway is also activated in the bladder. Nevertheless, PLC apparently contributes only in a very minor way to bladder contraction. Rather, muscarinic-receptor-mediated bladder contraction involves voltage-operated Ca2+ channels and Rho kinase. The prototypical signaling pathway of β-adrenoceptors is an activation of adenylyl cyclase with the subsequent formation of cAMP. Nevertheless, cAMP apparently contributes in a minor way only to β-adrenoceptor-mediated bladder relaxation. BKCa channels may play a greater role in β-adrenoceptor-mediated bladder relaxation. We conclude that apart from muscarinic receptor antagonists and β-adrenoceptor agonists, inhibitors of Rho kinase and activators of BKCa channels may have potential to treat an overactive bladder

VizieR Online Data Catalog: LOFAR Bootes and 3C295 field sources (van Weeren+, 2014)

The Bootes and 3C 295 fields were simultaneously observed on 2012 April 12 as part of a multi-beam observation with the LOFAR LBA stations. The idea behind the multi-beam setup is that we use the 3C 295 observations as a calibrator field to transfer the gain amplitudes to the (target) Bootes field. The total integration time on both fields was 10.25 hr. Complete frequency coverage was obtained between 54 and 70 MHz for both fields, while non-contiguous frequency coverage was obtained between 30 and 54 MHz for the 3C 295 only. All four correlation products were recorded. By default, the frequency band was divided into sub-bands, each 195.3125 kHz wide. Each sub-band was further divided in 64 channels and the integration time was 1 s. (1 data file)

Heterozygous ANKRD17 loss-of-function variants cause a syndrome with intellectual disability, speech delay, and dysmorphism

ANKRD17 is an ankyrin repeat-containing protein thought to play a role in cell cycle progression, whose ortholog in Drosophila functions in the Hippo pathway as a co-factor of Yorkie. Here, we delineate a neurodevelopmental disorder caused by de novo heterozygous ANKRD17 variants. The mutational spectrum of this cohort of 34 individuals from 32 families is highly suggestive of haploinsufficiency as the underlying mechanism of disease, with 21 truncating or essential splice site variants, 9 missense variants, 1 in-frame insertion-deletion, and 1 microdeletion (1.16 Mb). Consequently, our data indicate that loss of ANKRD17 is likely the main cause of phenotypes previously associated with large multi-gene chromosomal aberrations of the 4q13.3 region. Protein modeling suggests that most of the missense variants disrupt the stability of the ankyrin repeats through alteration of core structural residues. The major phenotypic characteristic of our cohort is a variable degree of developmental delay/intellectual disability, particularly affecting speech, while additional features include growth failure, feeding difficulties, non-specific MRI abnormalities, epilepsy and/or abnormal EEG, predisposition to recurrent infections (mostly bacterial), ophthalmological abnormalities, gait/balance disturbance, and joint hypermobility. Moreover, many individuals shared similar dysmorphic facial features. Analysis of single-cell RNA-seq data from the developing human telencephalon indicated ANKRD17 expression at multiple stages of neurogenesis, adding further evidence to the assertion that damaging ANKRD17 variants cause a neurodevelopmental disorder.Neurolog