Simultaneous VLBI Astrometry of H2O and SiO Masers toward the Semiregular Variable R Crateris

We obtained, for the first time, astrometrically registered maps of the 22.2 GHz H2O and 42.8, 43.1, and 86.2 GHz SiO maser emission toward the semiregular b-type variable (SRb) R Crateris, at three epochs (2015 May 21, and 2016 January 7 and 26) using the Korean Very-long-baseline Interferometry Network. The SiO masers show a ring-like spatial structure, while the H2O maser shows a very asymmetric one-side outflow structure, which is located at the southern part of the ring-like SiO maser feature. We also found that the 86.2 GHz SiO maser spots are distributed in an inner region, compared to those of the 43.1 GHz SiO maser, which is different from all previously known distributions of the 86.2 GHz SiO masers in variable stars. The different distribution of the 86.2 GHz SiO maser seems to be related to the complex dynamics caused by the overtone pulsation mode of the SRb R Crateris. Furthermore, we estimated the position of the central star based on the ring fitting of the SiO masers, which is essential for interpreting the morphology and kinematics of a circumstellar envelope. The estimated stellar coordinate corresponds well to the position measured by Gaia

Chromatin and transcriptional signatures for Nodal signaling during endoderm formation in hESCs

AbstractThe first stages of embryonic differentiation are driven by signaling pathways hardwired to induce particular fates. Endoderm commitment is controlled by the TGF-β superfamily member, Nodal, which utilizes the transcription factors, SMAD2/3, SMAD4 and FOXH1, to drive target gene expression. While the role of Nodal is well defined within the context of endoderm commitment, mechanistically it is unknown how this signal interacts with chromatin on a genome wide scale to trigger downstream responses. To elucidate the Nodal transcriptional network that governs endoderm formation, we used ChIP-seq to identify genomic targets for SMAD2/3, SMAD3, SMAD4, FOXH1 and the active and repressive chromatin marks, H3K4me3 and H3K27me3, in human embryonic stem cells (hESCs) and derived endoderm. We demonstrate that while SMAD2/3, SMAD4 and FOXH1 associate with DNA in a highly dynamic fashion, there is an optimal bivalent signature at 32 gene loci for driving endoderm commitment. Initially, this signature is marked by both H3K4me3 and H3K27me3 as a very broad bivalent domain in hESCs. Within the first 24h, SMAD2/3 accumulation coincides with H3K27me3 reduction so that these loci become monovalent marked by H3K4me3. JMJD3, a histone demethylase, is simultaneously recruited to these promoters, suggesting a conservation of mechanism at multiple promoters genome-wide. The correlation between SMAD2/3 binding, monovalent formation and transcriptional activation suggests a mechanism by which SMAD proteins coordinate with chromatin at critical promoters to drive endoderm specification

Electrochemical detection of mismatched DNA using a MutS probe

A direct and label-free electrochemical biosensor for the detection of the protein–mismatched DNA interaction was designed using immobilized N-terminal histidine tagged Escherichia coli. MutS on a Ni-NTA coated Au electrode. General electrochemical methods, cyclic voltammetry (CV), electrochemical quartz crystal microbalance (EQCM) and impedance spectroscopy, were used to ascertain the binding affinity of mismatched DNAs to the MutS probe. The direct results of CV and impedance clearly reveal that the interaction of MutS with the CC heteroduplex was much stronger than that with AT homoduplex, which was not differentiated in previous results (GT > CT > CC ≈ AT) of a gel mobility shift assay. The EQCM technique was also able to quantitatively analyze MutS affinity to heteroduplexes

Asymmetric distributions of H2O and SiO masers towards V627 Cas

We performed simultaneous observations of the H2O 6(1,6) - 5(2,3) (22.235080 GHz) and SiO v= 1, 2, J = 1 - 0, SiO v = 1, J = 2 - 1, 3 - 2 (43.122080, 42.820587, 86.243442, and 129.363359 GHz) masers towards the suspected D-type symbiotic star, V627 Cas, using the Korean VLBI Network. Here, we present astrometrically registered maps of the H2O and SiO v = 1, 2, J = 1 - 0, SiO v = 1, J = 2 - 1 masers for five epochs from January 2016 to June 2018. Distributions of the SiO maser spots do not show clear ring-like structures, and those of the H2O maser are biased towards the north-north-west to west with respect to the SiO maser features according to observational epochs. These asymmetric distributions of H2O and SiO masers are discussed based on two scenarios of a bipolar outflow and the presence of the hot companion, a white dwarf, in V627 Cas. We carried out ring fitting of SiO v = 1, and v = 2 masers and estimated the expected position of the cool red giant. The ring radii of the SiO v = 1 maser are slightly larger than those of the SiO v = 2 maser, as previously known. Our assumption for the physical size of the SiO maser ring of V627 Cas to be the typical size of a SiO maser ring radius (\sim4 au) of red giants yields the distance of V627 Cas to be \sim1 kpc.Comment: 7 pages, 4 figures, 1 table, Published in MNRA

Umbilical Arterial Blood Gas and Perinatal Outcome in the Second Twin according to the Planned Mode of Delivery

Purpose: To compare umbilical arterial gas parameters in the second twin of twin pregnancies according to the mode of deliver

Cell type–dependent variation in paracrine potency determines therapeutic efficacy against neonatal hyperoxic lung injury

AbstractBackground aimsThe aim of this study was to determine the optimal cell type for transplantation to protect against neonatal hyperoxic lung injury. To this end, the in vitro and in vivo therapeutic efficacies and paracrine potencies of human umbilical cord blood–derived mesenchymal stromal cells (HUMs), human adipose tissue–derived mesenchymal stromal cells (HAMs) and human umbilical cord blood mononuclear cells (HMNs) were compared.MethodsHyperoxic injury was induced in vitro in A549 cells by challenge with H2O2. Alternatively, hyperoxic injury was induced in newborn Sprague-Dawley rats in vivo by exposure to hyperoxia (90% oxygen) for 14 days. HUMs, HAMs or HMNs (5 × 105 cells) were given intratracheally at postnatal day 5.ResultsHyperoxia-induced increases in in vitro cell death and in vivo impaired alveolarization were significantly attenuated in both the HUM and HAM groups but not in the HMN group. Hyperoxia impaired angiogenesis, increased the cell death and pulmonary macrophages and elevated inflammatory cytokine levels. These effects were significantly decreased in the HUM group but not in the HAM or HMN groups. The levels of human vascular endothelial growth factor and hepatocyte growth factor produced by donor cells were highest in HUM group, followed by HAM group and then HMN group.ConclusionsHUMs exhibited the best therapeutic efficacy and paracrine potency than HAMs or HMNs in protecting against neonatal hyperoxic lung injury. These cell type-dependent variations in therapeutic efficacy might be associated or mediated with the paracrine potency of the transplanted donor cells

Function of COP9 Signalosome in Regulation of Mouse Oocytes Meiosis by Regulating MPF Activity and Securing Degradation

The COP9 (constitutive photomorphogenic) signalosome (CSN), composed of eight subunits, is a highly conserved protein complex that regulates processes such as cell cycle progression and kinase signalling. Previously, we found the expression of the COP9 constitutive photomorphogenic homolog subunit 3 (CSN3) and subunit 5 (CSN5) changes as oocytes mature for the first time, and there is no report regarding roles of COP9 in the mammalian oocytes. Therefore, in the present study, we examined the effects of RNA interference (RNAi)-mediated transient knockdown of each subunit on the meiotic cell cycle in mice oocytes. Following knockdown of either CSN3 or CSN5, oocytes failed to complete meiosis I. These arrested oocytes exhibited a disrupted meiotic spindle and misarranged chromosomes. Moreover, down-regulation of each subunit disrupted the activity of maturation-promoting factor (MPF) and concurrently reduced degradation of the anaphase-promoting complex/cyclosome (APC/C) substrates Cyclin B1 and Securin. Our data suggest that the CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C