Discovery of a rapid, luminous nova in NGC 300 by the KMTNet Supernova Program

We present the discovery of a rapidly evolving transient by the Korean Microlensing Telescope Network Supernova Program (KSP). KSP is a novel high-cadence supernova survey that offers deep ($\sim21.5$ mag in $BVI$ bands) nearly continuous wide-field monitoring for the discovery of early and/or fast optical transients. KSP-OT-201509a, reported here, was discovered on 2015 September 27 during the KSP commissioning run in the direction of the nearby galaxy NGC~300, and stayed above detection limit for $\sim$ 22 days. We use our $BVI$ light-curves to constrain the ascent rate, $-3.7(7)$ mag day$^{-1}$ in $V$, decay time scale, $t^{V}_{2}=1.7(6)$ days, and peak absolute magnitude, $-9.65\leq M_{V}\leq -9.25$ mag. We also find evidence for a short-lived pre-maximum halt in all bands. The peak luminosity and lightcurve evolution make KSP-OT-201509a consistent with a bright, rapidly decaying nova outburst. We discuss constraints on the nature of the progenitor and its environment using archival HST/ACS images and conclude with a broad discussion on the nature of the system.Comment: 7 pages in aastex6 two-column format, 4 figures; accepted in Ap

Ice-Water-Gas Interaction during Icebreaking by an Airgun Bubble

When an airgun releases high-pressure gas underwater below an ice plate, it is observed that a bubble is formed rapidly while the ice plate is broken fiercely. In order to study the ice-water-gas interaction during this transient and violent phenomenon, a set of laboratory-scale devices was designed and a series of icebreaking experiments were carried out. High-speed photography was used to capture the evolution of the bubble and the ice plate. It was found that the airgun bubble had a unique ‘pear’ shape compared with the spherical bubble generated by electric sparking. The pressure induced by the pulsation of the airgun bubble near a rigid wall was measured by the pressure sensor. The initial shockwave, oscillatory pressure peaks caused by the directional fast air injection, secondary shockwave, and pressure peak caused by the bubble jet impact were clearly recorded. Three damage patterns of ice plates were observed and corresponding reasons were analyzed. The influence of dimensionless parameters, such as airgun-ice distance (Formula presented.) and ice thickness (Formula presented.), was also investigated. The physical mechanism of ice-water-gas interaction was summarized

Up-Regulation Thioredoxin Inhibits Advanced Glycation End Products-Induced Neurodegeneration

Background/Aims: Diabetic retinopathy (DR) is one of the most serious complications of diabetes and is the leading cause of adult blindness in developed countries. Advanced glycation end products (AGEs) accumulation in diabetes is associated with its complications. Thioredoxin (Trx) is a small molecule (12kDa) antioxidant protein widely distributed in mammalian tissues, which has important biological functions including anti-apoptosis and transcriptional regulation. In a previous study, we found that Trx plays a key role in retinal neurodegeneration prior to the occurrence of endothelial damage in diabetic mice. In this study, our aim is to determine the effect of Trx on neurodegeneration induced by AGEs in order to identify new therapeutic targets for the clinical treatment and prevention of DR. Methods: In vivo, a high-fat diet and Streptozotocin (STZ) injection were used to generate a mouse model of diabetes. Histology was utilized to examine tissue morphology and measure the outer nuclear layer (ONL) thickness. Electroretinography (ERG) was used to assess retinal function and Western blot was used to examine protein expression. In vitro, three methods of Trx up-regulation were used, including a stable cell line that overexpresses Trx, treatment with Sulforaphane, and shRNA down-regulation Txnip. Cells were treated with AGEs, and level of apoptosis was performed to quantify this by flow cytometry and TUNEL. Quantitative Reverse Transcription PCR (qRT-PCR), Western blotting and immunofluorescence were used to measure gene and protein expression. Transmission electron microscopy (TEM) was used to observe autophagosomes. Results: We found that diabetic mice display decreased retinal function and reduced ONL thickness with AGEs accumulation and a reduction of Trx expression. Up-regulation Trx can prevent the ONL thickness decrease in diabetic mice, as observed by H&E staining. In vitro, up-regulation Trx resulted in decreased intracellular ROS generation, reduced apoptosis by inhibited autophagy. Conclusion: Up-regulating Trx inhibited neurodegeneration induced by AGEs. The underlying mechanism may be related to inhibit Txnip/mTOR pathway-mediated autophagy

A New Cationic Fluorescent Probe for HSO3− Based on Bisulfite Induced Aggregation Self-Assembly

In comparison with the numerous studies that have centered on developing molecular frameworks for the functionalization of fluorescent materials, less research has addressed the influence of the side chains, despite such appendages contributing significantly to the properties and applications of fluorescent materials. In this work, a new series of cationic fluorescent probes with AIE characteristics have been developed, which exhibit unique sensitivity for charge-diffusion anions, namely HSO3−, via the interactions of ions and the cooperation of the controllable hydrophobicity. The impact of the alkyl chain length attached at the cationic probes suggested that the fluorescent intensity and sensitivity of the probes could be partially enhanced by adjusting their aggregation tendency through the action of the hydrophobic effect under aqueous conditions. DLS and SEM images indicated that different particle sizes and new morphologies of the probes were formed in the anion-recognition-triggered self-assembly process, which could be attributed to the composite effect of electrostatic actions, Van der Waals forces and π-π stacking

Origin of high-velocity ejecta and early red excess emission in the infant Type Ia supernova 2021aefx

\object{SN 2021aefx} is a normal Type Ia Supernova (SN) with red excess emission over the first $\sim$ 2 days. We present detailed analysis of this SN using our high-cadence KMTNet multi-band photometry, spectroscopy, and publicly available data. We provide the first measurements of its epochs of explosion (MJD 59529.32 $\pm$ 0.16) as well as ``first light'' (MJD 59529.85 $\pm$ 0.55) associated with the main ejecta ${\rm{^{56}Ni}}$ distribution. This places our first detection of SN 2021aefx at $\sim -$0.5 hours since ``first light'', indicating the presence of additional power sources. Our peak-spectrum confirms its Type Ia sub-classification as intermediate between Core-Normal and Broad-Line, and we estimate the ejecta mass to be $\sim$ 1.34 $M_{\odot}$. The pre-peak spectral evolution identifies fast-expanding material reaching $>$ 40,000 km s$^{-1}$ (the fastest ever observed in Type Ia SNe) and at least two distinct homologously-expanding ejecta components: (1) a normal-velocity (12,400 km s$^{-1}$) component consistent with the typical photospheric evolution of Chandrasekhar-mass ejecta; and (2) a high-velocity (23,500 km s$^{-1}$) component visible during the first $\sim$ 3.6 days post-explosion, which locates the component within the outer $<$ 16\% of the ejecta mass. Asymmetric, subsonic explosion processes producing a non-spherical photosphere provide an explanation for the simultaneous presence of the two components, as well as the red excess emission via a slight ${\rm{^{56}Ni}}$ enrichment in the outer $\sim$ 0.5\% of the ejecta mass. Our spectrum from 300 days post-peak advances the constraint against non-degenerate companions and further supports a near-Chandrasekhar-mass explosion origin. Off-center ignited delayed-detonations of Chandrasekhar-mass white dwarfs may be responsible for the observed features of SN 2021aefx in some normal Type Ia SNe.Comment: Submitted for publication in ApJ. 29 pages, 14 figures, 4 table

The genetic correlation and causal association between key factors that influence vascular calcification and cardiovascular disease incidence

Background: Serum calcium (Ca), vitamin D (VD), and vitamin K (VK) levels are key determinants of vascular calcification, which itself impacts cardiovascular disease (CVD) risk. The specific relationships between the levels of these different compounds and particular forms of CVD, however, remain to be fully defined. Objective: This study was designed to explore the associations between these serum levels and CVDs with the goal of identifying natural interventions capable of controlling vascular calcification and thereby protecting against CVD pathogenesis, extending the healthy lifespan of at-risk individuals.Methods: Linkage disequilibrium score (LDSC) regression and a two-sample Mendelian randomization (MR) framework were leveraged to systematically examine the causal interplay between these serum levels and nine forms of CVD, as well as longevity through the use of large publically accessible Genome-Wide Association Studies (GWAS) datasets. The optimal concentrations of serum Ca and VD to lower CVD risk were examined through a restrictive cubic spline (RCS) approach.Results: After Bonferroni correction, the positive genetic correlations were observed between serum Ca levels and myocardial infarction (MI) (p = 1.356E–04), as well as coronary artery disease (CAD) (p = 3.601E–04). Negative genetic correlations were detected between levels of VD and CAD (p = 0.035), while elevated VK1 concentrations were causally associated with heart failure (HF) [odds ratios (OR) per 1-standard deviation (SD) increase: 1.044], large artery stroke (LAS) (OR per 1-SD increase: 1.172), and all stroke (AS) (OR per 1-SD increase: 1.041). Higher serum Ca concentrations (OR per 1-SD increase: 0.865) and VD levels (OR per 1-SD increase: 0.777) were causally associated with reduced odds of longevity. These findings remained consistent in sensitivity analyses, and serum Ca and VD concentrations of 2.376 mmol/L and 46.8 nmol/L, respectively, were associated with a lower CVD risk (p &lt; 0.001). Conclusion: Our findings support a genetic correlation between serum Ca and VD and CVD risk, and a causal relationship between VK1 levels and CVD risk. The optimal serum Ca (2.376 mmol/L) and VD levels (46.8 nmol/L) can reduce cardiovascular risk.</p

The genetic correlation and causal association between key factors that influence vascular calcification and cardiovascular disease incidence

Background: Serum calcium (Ca), vitamin D (VD), and vitamin K (VK) levels are key determinants of vascular calcification, which itself impacts cardiovascular disease (CVD) risk. The specific relationships between the levels of these different compounds and particular forms of CVD, however, remain to be fully defined. Objective: This study was designed to explore the associations between these serum levels and CVDs with the goal of identifying natural interventions capable of controlling vascular calcification and thereby protecting against CVD pathogenesis, extending the healthy lifespan of at-risk individuals.Methods: Linkage disequilibrium score (LDSC) regression and a two-sample Mendelian randomization (MR) framework were leveraged to systematically examine the causal interplay between these serum levels and nine forms of CVD, as well as longevity through the use of large publically accessible Genome-Wide Association Studies (GWAS) datasets. The optimal concentrations of serum Ca and VD to lower CVD risk were examined through a restrictive cubic spline (RCS) approach.Results: After Bonferroni correction, the positive genetic correlations were observed between serum Ca levels and myocardial infarction (MI) (p = 1.356E–04), as well as coronary artery disease (CAD) (p = 3.601E–04). Negative genetic correlations were detected between levels of VD and CAD (p = 0.035), while elevated VK1 concentrations were causally associated with heart failure (HF) [odds ratios (OR) per 1-standard deviation (SD) increase: 1.044], large artery stroke (LAS) (OR per 1-SD increase: 1.172), and all stroke (AS) (OR per 1-SD increase: 1.041). Higher serum Ca concentrations (OR per 1-SD increase: 0.865) and VD levels (OR per 1-SD increase: 0.777) were causally associated with reduced odds of longevity. These findings remained consistent in sensitivity analyses, and serum Ca and VD concentrations of 2.376 mmol/L and 46.8 nmol/L, respectively, were associated with a lower CVD risk (p &lt; 0.001). Conclusion: Our findings support a genetic correlation between serum Ca and VD and CVD risk, and a causal relationship between VK1 levels and CVD risk. The optimal serum Ca (2.376 mmol/L) and VD levels (46.8 nmol/L) can reduce cardiovascular risk.</p

GABA, progesterone and zona pellucida activation of PLA2 and regulation by MEK-ERK1/2 during acrosomal exocytosis in guinea pig spermatozoa

AbstractWe investigated whether GABA activates phospholipase A2 (PLA2) during acrosomal exocytosis, and if the MEK-ERK1/2 pathway modulates PLA2 activation initiated by GABA, progesterone or zona pellucida (ZP). In guinea pig spermatozoa prelabelled with [14C]arachidonic acid or [14C]choline chloride, GABA stimulated a decrease in phosphatidylcholine (PC), and release of arachidonic acid and lysoPC, during exocytosis. These lipid changes are indicative of PLA2 activation and appear essential for exocytosis since inclusion of aristolochic acid (a PLA2 inhibitor) abrogated them, along with exocytosis. GABA activation of PLA2 seems to be mediated, at least in part, by diacylglycerol (DAG) and protein kinase C since inclusion of the DAG kinase inhibitor R59022 enhanced PLA2 activity and exocytosis stimulated by GABA, whereas exposure to staurosporine decreased both. GABA-, progesterone- and ZP-induced release of arachidonic acid and exocytosis were prevented by U0126 and PD98059 (MEK inhibitors). Taken together, our results suggest that PLA2 plays a fundamental role in agonist-stimulated exocytosis and that MEK-ERK1/2 are involved in PLA2 regulation during this process