The Role of Environment in the Mass-Metallicity Relation

Using a sample of 57,377 star-forming galaxies drawn from the Sloan Digital Sky Survey, we study the relationship between gas-phase oxygen abundance and environment in the local Universe. We find that there is a strong relationship between metallicity and environment such that more metal-rich galaxies favor regions of higher overdensity. Furthermore, this metallicity-density relation is comparable in strength to the color-density relation along the blue cloud. After removing the mean dependence of environment on color and luminosity, we find a significant residual trend between metallicity and environment that is largely driven by galaxies in high-density regions, such as groups and clusters. We discuss the potential source of this relationship between metallicity and local galaxy density in the context of feedback models, with special attention paid to quantifying the impact of environment on the scatter in the mass-metallicity relation. We find that environment is a non-negligible source of scatter in this fundamental relation, with > 15% of the measured scatter correlated with environment.Comment: Submitted to MNRA

The Chemical Evolution Carousel of Spiral Galaxies : Azimuthal Variations of Oxygen Abundance in NGC1365

19 pages, 13 figures. Accepted to ApJThe spatial distribution of oxygen in the interstellar medium of galaxies is the key to understanding how efficiently metals that are synthesized in massive stars can be redistributed across a galaxy. We present here a case study in the nearby spiral galaxy NGC1365 using 3D optical data obtained in the TYPHOON Program. We find systematic azimuthal variations of the HII region oxygen abundance imprinted on a negative radial gradient. The 0.2 dex azimuthal variations occur over a wide radial range of 0.3 to 0.7 R25 and peak at the two spiral arms in NGC1365. We show that the azimuthal variations can be explained by two physical processes: gas undergoes localized, sub-kpc scale self-enrichment when orbiting in the inter-arm region, and experiences efficient, kpc scale mixing-induced dilution when spiral density waves pass through. We construct a simple chemical evolution model to quantitatively test this picture and find that our toy model can reproduce the observations. This result suggests that the observed abundance variations in NGC1365 are a snapshot of the dynamical local enrichment of oxygen modulated by spiral-driven, periodic mixing and dilution.Peer reviewedFinal Published versio

Characterization of the First SARS-CoV-2 Isolates from Aotearoa New Zealand as Part of a Rapid Response to the COVID-19 Pandemic

SARS-CoV-2, the virus responsible for the COVID-19 pandemic, has wreaked havoc across the globe for the last two years. More than 300 million cases and over 5 million deaths later, we continue battling the first real pandemic of the 21st century. SARS-CoV-2 spread quickly, reaching most countries within the first half of 2020, and New Zealand was not an exception. Here, we describe the first isolation and characterization of SARS-CoV-2 variants during the initial virus outbreak in New Zealand. Patient-derived nasopharyngeal samples were used to inoculate Vero cells and, three to four days later, a cytopathic effect was observed in seven viral cultures. Viral growth kinetics was characterized using Vero and VeroE6/TMPRSS2 cells. The identity of the viruses was verified by RT-qPCR, Western blot, indirect immunofluorescence assays, and electron microscopy. Whole-genome sequences were analyzed using two different yet complementary deep sequencing platforms (MiSeq/Illumina and Ion PGM™/Ion Torrent™), classifying the viruses as SARS-CoV-2 B.55, B.31, B.1, or B.1.369 based on the Pango Lineage nomenclature. All seven SARS-CoV-2 isolates were susceptible to remdesivir (EC50 values from 0.83 to 2.42 µM) and β-D-N4-hydroxycytidine (molnupiravir, EC50 values from 0.96 to 1.15 µM) but not to favipiravir (>10 µM). Interestingly, four SARS-CoV-2 isolates, carrying the D614G substitution originally associated with increased transmissibility, were more susceptible (2.4-fold) to a commercial monoclonal antibody targeting the spike glycoprotein than the wild-type viruses. Altogether, this seminal work allowed for early access to SARS-CoV-2 isolates in New Zealand, paving the way for numerous clinical and scientific research projects in the country, including the development and validation of diagnostic assays, antiviral strategies, and a national COVID-19 vaccine development program

Data supporting the activation of autophagy genes in the diabetic heart

This data article contains full list of autophagy related genes that are altered in diabetic heart. This article also shows data from in vitro cultured cardiomyocytes that are exposed the high glucose treatment to simulate hyperglycemic state in vitro. The interpretation of these data and further extensive insights into the regulation of SG biogenesis by AMPK can be found in “Type-2 diabetes increases autophagy in the human heart through promotion of Beclin-1 mediated pathway” (Munasinghe et al., in press) [1]

Data supporting the activation of autophagy genes in the diabetic heart

This data article contains full list of autophagy related genes that are altered in diabetic heart. This article also shows data from in vitro cultured cardiomyocytes that are exposed the high glucose treatment to simulate hyperglycemic state in vitro. The interpretation of these data and further extensive insights into the regulation of SG biogenesis by AMPK can be found in “Type-2 diabetes increases autophagy in the human heart through promotion of Beclin-1 mediated pathway” (Munasinghe et al., in press) [1]

Type-2 diabetes increases autophagy in the human heart through promotion of Beclin-1 mediated pathway

Background: Diabetes promotes progressive loss of cardiac cells, which are replaced by a fibrotic matrix, resulting in the loss of cardiac function. In the current study we sought to identify if excessive autophagy plays a major role in inducing this progressive loss.Methods and results: Immunofluorescence and western blotting analysis of the right atrial appendages collected from diabetic and non-diabetic patients undergoing coronary artery bypass graft surgery showed a marked increase in the level of autophagy in the diabetic heart, as evidenced by increased expression of autophagy marker LC3B-II and its mediator Beclin-1 and decreased expression of p62, which incorporates into autophagosomes to be efficiently degraded. Moreover, a marked activation of pro-apoptotic caspase-3 was observed. Electron microscopy showed increased autophagosomes in the diabetic heart. In vivo measurement of autophagic flux by choloroquine injection resulted in further enhancement of LC3B-II in the diabetic myocardium, confirming increased autophagic activity in the type-2 diabetic heart. Importantly, in-vitro genetic depletion of beclin-1 in high glucose treated adult rat cardiomyocytes markedly inhibited the level of autophagy and subsequent apoptotic cell death.Conclusions: These findings demonstrate the pathological role of autophagy in the type-2 diabetic heart, opening up a potentially novel therapeutic avenue for the treatment of diabetic heart disease