This study characterises the radio luminosity functions (RLFs) for star forming galaxies (SFGs) and active galactic nuclei (AGN) using statistical redshift estimation in the absence of comprehensive spectroscopic data. Sensitive radio surveys over large areas detect many sources with faint optical and infrared counterparts, for which redshifts and spectra are unavailable. This challenges our attempt to understand the population of radio sources. Statistical tools are often used to model parameters (such as redshift) as an alternative to observational data. Using the data from GAMA G23 and EMU early science observations, we explore simple statistical techniques to estimate the redshifts in order to measure the RLFs of the G23 radio sources as a whole and for SFGs and AGN separately. Redshifts and AGN/SFG classifications are assigned statistically for those radio sources without spectroscopic data. The calculated RLFs are compared with existing studies, and the results suggest that the RLFs match remarkably well for low redshift galaxies with an optical counterpart. We use a more realistic high redshift distribution to model the redshifts of (most likely) high redshift radio sources and find that the LFs from our approach match well with measured LFs. We also look at strategies to compare the RLFs of radio sources without an optical counterpart to existing studies.

With wide-field phased array feed technology, the Australian Square Kilometre Array Pathfinder (ASKAP) is ideally suited to search for seemingly rare radio transient sources that are difficult to discover previous-generation narrow-field telescopes. The Commensal Real-time ASKAP Fast Transient (CRAFT) Survey Science Project has developed instrumentation to continuously search for fast radio transients (duration $\lesssim$ 1 s) with ASKAP, with a particular focus on finding and localising fast radio bursts (FRBs). Since 2018, the CRAFT survey has been searching for FRBs and other fast transients by incoherently adding the intensities received by individual ASKAP antennas, and then correcting for the impact of frequency dispersion on these short-duration signals in the resultant incoherent sum (ICS) in real time. This low-latency detection enables the triggering of voltage buffers, which facilitates the localisation of the transient source and the study of spectro-polarimetric properties at high time resolution. Here we report the sample of 43 FRBs discovered in this CRAFT/ICS survey to date. This includes 22 FRBs that had not previously been reported: 16 FRBs localised by ASKAP to $\lesssim 1$ arcsec and 6 FRBs localised to $\sim 10$ arcmin. Of the new arcsecond-localised FRBs, we have identified and characterised host galaxies (and measured redshifts) for 11. The median of all 30 measured host redshifts from the survey to date is $z=0.23$. We summarise results from the searches, in particular those contributing to our understanding of the burst progenitors and emission mechanisms, and on the use of bursts as probes of intervening media. We conclude by foreshadowing future FRB surveys with ASKAP using a coherent detection system that is currently being commissioned. This will increase the burst detection rate by a factor of approximately ten and also the distance to which ASKAP can localise FRBs.

Female fertility is a complex trait with age-specific changes in spontaneous dizygotic (DZ) twinning and fertility. To elucidate factors regulating female fertility and infertility, we conducted a genome-wide association study (GWAS) on mothers of spontaneous DZ twins (MoDZT) versus controls (3273 cases, 24,009 controls). This is a follow-up study to the Australia/New Zealand (ANZ) component of that previously reported (Mbarek et al., 2016), with a sample size almost twice that of the entire discovery sample meta-analysed in the previous article (and five times the ANZ contribution to that), resulting from newly available additional genotyping and representing a significant increase in power. We compare analyses with and without male controls and show unequivocally that it is better to include male controls who have been screened for recent family history, than to use only female controls. Results from the SNP based GWAS identified four genomewide significant signals, including one novel region, ZFPM1 (Zinc Finger Protein, FOG Family Member 1), on chromosome 16. Previous signals near FSHB (Follicle Stimulating Hormone beta subunit) and SMAD3 (SMAD Family Member 3) were also replicated (Mbarek et al., 2016). We also ran the GWAS with a dominance model that identified a further locus ADRB2 on chr 5. These results have been contributed to the International Twinning Genetics Consortium for inclusion in the next GWAS meta-analysis (Mbarek et al., in press).

Strong associations between neural tube defects (NTDs) and monozygotic (MZ) twinning have long been noted, and it has been suggested that NTD cases who do not present as MZ twins may be the survivors of MZ twinning events. We have recently shown that MZ twins carry a strong, distinctive DNA methylation signature and have developed an algorithm based on genomewide DNA methylation array data that distinguishes MZ twins from dizygotic twins and other relatives at well above chance level. We have applied this algorithm to published methylation data from five fetal tissues (placental chorionic villi, kidney, spinal cord, brain and muscle) collected from spina bifida cases (n = 22), anencephalic cases (n = 15) and controls (n = 19). We see no difference in signature between cases and controls, providing no support for a common etiological role of MZ twinning in NTDs. The strong associations therefore continue to await elucidation.

Previous genetic association studies have failed to identify loci robustly associated with sepsis, and there have been no published genetic association studies or polygenic risk score analyses of patients with septic shock, despite evidence suggesting genetic factors may be involved. We systematically collected genotype and clinical outcome data in the context of a randomized controlled trial from patients with septic shock to enrich the presence of disease-associated genetic variants. We performed genomewide association studies of susceptibility and mortality in septic shock using 493 patients with septic shock and 2442 population controls, and polygenic risk score analysis to assess genetic overlap between septic shock risk/mortality with clinically relevant traits. One variant, rs9489328, located in AL589740.1 noncoding RNA, was significantly associated with septic shock (p = 1.05 × 10–10); however, it is likely a false-positive. We were unable to replicate variants previously reported to be associated (p < 1.00 × 10–6 in previous scans) with susceptibility to and mortality from sepsis. Polygenic risk scores for hematocrit and granulocyte count were negatively associated with 28-day mortality (p = 3.04 × 10–3; p = 2.29 × 10–3), and scores for C-reactive protein levels were positively associated with susceptibility to septic shock (p = 1.44 × 10–3). Results suggest that common variants of large effect do not influence septic shock susceptibility, mortality and resolution; however, genetic predispositions to clinically relevant traits are significantly associated with increased susceptibility and mortality in septic individuals.

OBJECTIVES/GOALS: Human placentation requires complex coordination between maternal and fetal cell types but remains incompletely understood. We hypothesize that uterine natural killer (uNK) cells, an immune cell type that increases in abundance during the implantation window, is essential for appropriate implantation and placentation. METHODS/STUDY POPULATION: We plan to examine stromal cell (SC) decidualization, spiral artery remodeling, and EVT invasion, processes vital for early pregnancy establishment, in the presence or absence of secretory phase uNK cells. Fetal extravillous trophoblasts (EVTs) will be isolated from first trimester pregnancy tissue; maternal SCs, endothelial cells (ECs) and uNK cells will be obtained from secretory phase uterine tissue. SCs will be placed in monoculture and coculture with uNK cells and prolactin will be measured to evaluate decidualization. To study EVT invasion, we will utilize our novel “implantation-on-a-chip” device to determine how addition of uNK cells affects EVT migration through a collagen-matrigel matrix. In this system, we will also examine spiral artery remodeling with or without uNK cells via TUNEL staining. RESULTS/ANTICIPATED RESULTS: We anticipate that uNK cell addition to SCs will lead to a significant increase in SC prolactin levels, suggesting a role of uNK cells in endometrial decidualization. In vitro, we expect the addition of uNK cells will increase EC apoptosis and promote EVT invasion. DISCUSSION/SIGNIFICANCE OF IMPACT: Although decidual NK cells are known to participate in placentation, the role of pre-pregnancy uNK cells is unknown. uNK cell involvement in processes important for the earliest stages of pregnancy would provide a potential marker for abnormal placentation and offer avenues for intervention to decrease placentation associated perinatal morbidity.