Shepherd My Sheep : Preaching for the Sake of Greater Works Than These

The conversation between Jesus and Peter in John 21:15–19 highlights Peter’s work as an apostle but also reveals our own call to care for the sheep—as Jesus says, to “do the works that I do.” The text offers an opportunity to preach about Christian vocation and daily life

Inferring the Andromeda Galaxy's mass from its giant southern stream with Bayesian simulation sampling

M31 has a giant stream of stars extending far to the south and a great deal of other tidal debris in its halo, much of which is thought to be directly associated with the southern stream. We model this structure by means of Bayesian sampling of parameter space, where each sample uses an N-body simulation of a satellite disrupting in M31's potential. We combine constraints on stellar surface densities from the Isaac Newton Telescope survey of M31 with kinematic data and photometric distances. This combination of data tightly constrains the model, indicating a stellar mass at last pericentric passage of log(M_s / Msun) = 9.5+-0.1, comparable to the LMC. Any existing remnant of the satellite is expected to lie in the NE Shelf region beside M31's disk, at velocities more negative than M31's disk in this region. This rules out the prominent satellites M32 or NGC 205 as the progenitor, but an overdensity recently discovered in M31's NE disk sits at the edge of the progenitor locations found in the model. M31's virial mass is constrained in this model to be log(M200) = 12.3+-0.1, alleviating the previous tension between observational virial mass estimates and expectations from the general galactic population and the timing argument. The techniques used in this paper, which should be more generally applicable, are a powerful method of extracting physical inferences from observational data on tidal debris structures.Comment: 27 pages, 10 figures. Accepted by MNRA

A Global Star Forming Episode in M31 2-4 Gyr Ago

We have identified a major global enhancement of star formation in the inner M31 disk that occurred between 2-4 Gyr ago, producing $\sim$60% of the stellar mass formed in the past 5 Gyr. The presence of this episode in the inner disk was discovered by modeling the optical resolved star color-magnitude diagrams of low extinction regions in the main disk of M31 (3$<$R$<$20 kpc) as part of the Panchromatic Hubble Andromeda Treasury. This measurement confirms and extends recent measurements of a widespread star formation enhancement of similar age in the outer disk, suggesting that this burst was both massive and global. Following the galaxy-wide burst, the star formation rate of M31 has significantly declined. We briefly discuss possible causes for these features of the M31 evolutionary history, including interactions with M32, M33 and/or a merger.Comment: 12 pages, 2 tables, 6 figures, accepted for publication in Ap

The Hubble Space Telescope Survey of M31 Satellite Galaxies. II. The Star Formation Histories of Ultrafaint Dwarf Galaxies

We present the lifetime star formation histories (SFHs) for six ultrafaint dwarf (UFD; M V > − 7.0, 4.9<log10(M*(z=0)/M⊙)<5.5 ) satellite galaxies of M31 based on deep color–magnitude diagrams constructed from Hubble Space Telescope imaging. These are the first SFHs obtained from the oldest main-sequence turnoff of UFDs outside the halo of the Milky Way (MW). We find that five UFDs formed at least 50% of their stellar mass by z = 5 (12.6 Gyr ago), similar to known UFDs around the MW, but that 10%–40% of their stellar mass formed at later times. We uncover one remarkable UFD, And xiii, which formed only 10% of its stellar mass by z = 5, and 75% in a rapid burst at z ∼ 2–3, a result that is robust to choices of underlying stellar model and is consistent with its predominantly red horizontal branch. This “young” UFD is the first of its kind and indicates that not all UFDs are necessarily quenched by reionization, which is consistent with predictions from several cosmological simulations of faint dwarf galaxies. SFHs of the combined MW and M31 samples suggest reionization did not homogeneously quench UFDs. We find that the least-massive MW UFDs (M *(z = 5) ≲ 5 × 104 M ⊙) are likely quenched by reionization, whereas more-massive M31 UFDs (M *(z = 5) ≳ 105 M ⊙) may only have their star formation suppressed by reionization and quench at a later time. We discuss these findings in the context of the evolution and quenching of UFDs

NK Cells Are Not Required for Spontaneous Autoimmune Diabetes in NOD Mice

NK cells have been shown to either promote or protect from autoimmune diseases. Several studies have examined the role of receptors preferentially expressed by NK cells in the spontaneous disease of NOD mice or the direct role of NK cells in acute induced disease models of diabetes. Yet, the role of NK cells in spontaneous diabetes has not been directly addressed. Here, we used the NOD.NK1.1 congenic mouse model to examine the role of NK cells in spontaneous diabetes. Significant numbers of NK cells were only seen in the pancreas of mice with disease. Pancreatic NK cells displayed an activated surface phenotype and proliferated more than NK cells from other tissues in the diseased mice. Nonetheless, depletion of NK cells had no effect on dendritic cell maturation or T cell proliferation. In spontaneous disease, the deletion of NK cells had no significant impact on disease onset. NK cells were also not required to promote disease induced by adoptively transferred pathogenic CD4+ T cells. Thus, NK cells are not required for spontaneous autoimmune diabetes in NOD mice

Prevalence and correlates of common mental disorders among participants of the Uganda Genome Resource: Opportunities for psychiatric genetics research.

Genetics research has potential to alleviate the burden of mental disorders in low- and middle-income-countries through identification of new mechanistic pathways which can lead to efficacious drugs or new drug targets. However, there is currently limited genetics data from Africa. The Uganda Genome Resource provides opportunity for psychiatric genetics research among underrepresented people from Africa. We aimed at determining the prevalence and correlates of major depressive disorder (MDD), suicidality, post-traumatic stress disorder (PTSD), alcohol abuse, generalised anxiety disorder (GAD) and probable attention-deficit hyperactivity disorder (ADHD) among participants of the Uganda Genome Resource. Standardised tools assessed for each mental disorder. Prevalence of each disorder was calculated with 95% confidence intervals. Multivariate logistic regression models evaluated the association between each mental disorder and associated demographic and clinical factors. Among 985 participants, prevalence of the disorders were: current MDD 19.3%, life-time MDD 23.3%, suicidality 10.6%, PTSD 3.1%, alcohol abuse 5.7%, GAD 12.9% and probable ADHD 9.2%. This is the first study to determine the prevalence of probable ADHD among adult Ugandans from a general population. We found significant association between sex and alcohol abuse (adjusted odds ratio [AOR] = 0.26 [0.14,0.45], p < 0.001) and GAD (AOR = 1.78 [1.09,2.49], p = 0.019) respectively. We also found significant association between body mass index and suicidality (AOR = 0.85 [0.73,0.99], p = 0.041), alcohol abuse (AOR = 0.86 [0.78,0.94], p = 0.003) and GAD (AOR = 0.93 [0.87,0.98], p = 0.008) respectively. We also found a significant association between high blood pressure and life-time MDD (AOR = 2.87 [1.08,7.66], p = 0.035) and probable ADHD (AOR = 1.99 [1.00,3.97], p = 0.050) respectively. We also found a statistically significant association between tobacco smoking and alcohol abuse (AOR = 3.2 [1.56,6.67], p = 0.002). We also found ever been married to be a risk factor for probable ADHD (AOR = 2.12 [0.88,5.14], p = 0.049). The Uganda Genome Resource presents opportunity for psychiatric genetics research among underrepresented people from Africa

Genetic copy number variants, cognition and psychosis: a meta-analysis and a family study

The burden of large and rare copy number genetic variants (CNVs) as well as certain specific CNVs increase the risk of developing schizophrenia. Several cognitive measures are purported schizophrenia endophenotypes and may represent an intermediate point between genetics and the illness. This paper investigates the influence of CNVs on cognition. We conducted a systematic review and meta-analysis of the literature exploring the effect of CNV burden on general intelligence. We included ten primary studies with a total of 18,847 participants and found no evidence of association. In a new psychosis family study, we investigated the effects of CNVs on specific cognitive abilities. We examined the burden of large and rare CNVs (>200 kb, <1% MAF) as well as known schizophrenia-associated CNVs in patients with psychotic disorders, their unaffected relatives and controls (N = 3428) from the Psychosis Endophenotypes International Consortium (PEIC). The carriers of specific schizophrenia-associated CNVs showed poorer performance than non-carriers in immediate (P = 0.0036) and delayed (P = 0.0115) verbal recall. We found suggestive evidence that carriers of schizophrenia-associated CNVs had poorer block design performance (P = 0.0307). We do not find any association between CNV burden and cognition. Our findings show that the known high-risk CNVs are not only associated with schizophrenia and other neurodevelopmental disorders, but are also a contributing factor to impairment in cognitive domains such as memory and perceptual reasoning, and act as intermediate biomarkers of disease risk.This work was supported by the Medical Research Council (G0901310) and the Wellcome Trust (grants 085475/B/08/Z, 085475/Z/08/Z). This study was supported by the NIHR Biomedical Research Centre at University College London Hospitals NHS Foundation Trust and University College London and by the NIHR Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust at King’s College London. Further support to EB: Mental Health Research UK’s John Grace QC award, BMA Margaret Temple grants 2016 and 2006, MRC—Korean Health Industry Development Institute Partnering Award (MC_PC_16014), MRC New Investigator Award and a MRC Centenary Award (G0901310), National Institute of Health Research UK post-doctoral fellowship, the Psychiatry Research Trust, the Schizophrenia Research Fund, the Brain and Behaviour Research foundation’s NARSAD Young Investigator Awards 2005, 2008, Wellcome Trust Research Training Fellowship, the NIHR Biomedical Research Centre at UCLH, and the NIHR Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust and Institute of Psychiatry King’s College London. Further support to co-authors: The Brain and Behaviour Research foundation’s (NARSAD’s) Young Investigator Award (Grant 22604, awarded to CI). The BMA Margaret Temple grant 2016 to JT. A 2014 European Research Council Marie Curie award to A Díez-Revuelta. HI has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 747429. A Medical Research Council doctoral studentship to JH-S, IA-Z and AB. A Mental Health Research UK studentship to RM. VB is supported by a Wellcome Trust Seed Award in Science (200589/Z/16/Z). FWO Senior Clinical Fellowship to RvW. The infrastructure for the GROUP consortium is funded through the Geestkracht programme of the Dutch Health Research Council (ZON-MW, grant number 10-000-1001), and matching funds from participating pharmaceutical companies (Lundbeck, AstraZeneca, Eli Lilly, Janssen Cilag) and universities and mental health care organisations (Amsterdam: Academic Psychiatric Centre of the Academic Medical Centre and the mental health institutions: GGZ Ingeest, Arkin, Dijk en Duin, GGZ Rivierduinen, Erasmus Medical Centre, GGZ Noord Holland Noord. Groningen: University Medical Centre Groningen and the mental health institutions: Lentis, GGZ Friesland, GGZ Drenthe, Dimence, Mediant, GGNet Warnsveld, Yulius Dordrecht and Parnassia psycho-medical centre The Hague. Maastricht: Maastricht University Medical Centre and the mental health institutions: GGZ Eindhoven en De Kempen, GGZ Breburg, GGZ Oost-Brabant, Vincent van Gogh voor Geestelijke Gezondheid, Mondriaan, Virenze riagg, Zuyderland GGZ, MET ggz, Universitair Centrum Sint-Jozef Kortenberg, CAPRI University of Antwerp, PC Ziekeren Sint-Truiden, PZ Sancta Maria Sint-Truiden, GGZ Overpelt, OPZ Rekem. Utrecht: University Medical Centre Utrecht and the mental health institutions Altrecht, GGZ Centraal and Delta). The Santander cohort was supported by Instituto de Salud Carlos III (PI020499, PI050427, PI060507), SENY Fundació (CI 2005-0308007), Fundacion Ramón Areces and Fundacion Marqués de Valdecilla (API07/011, API10/13). We thank Valdecilla Biobank for providing the biological PAFIP samples and associated data included in this study and for its help in the technical execution of this work; we also thank IDIVAL Neuroimaging Unit for its help in the acquisition and processing of imaging PAFIP data