Non-Relativistic QCD for Heavy Quark Systems

We employ a nonrelativistic version of QCD (NRQCD) to study heavy quark-antiquark bound states in the lowest approximation without fine structure. We use gluon configurations on a 16^3 by 48 lattice at beta=6.2 from the UKQCD collaboration. For quark masses in the vicinity of the b we obtain bound state masses for S, P and both types of D wave. We also detect signals for two types of hybrids (quark,antiquark,gluon states). The results are sufficiently accurate to confirm that the values of the D wave mass from both lattice D waves coincide indicating that the cubical invariance of the lattice is restored to full rotational invariance at large distance. Our results also show that the S-P splitting is indeed insensitive to variations in the bare quark mass from Ma=1.0 to Ma=1.9.Comment: 13 pages, DAMTP-92-7

Radial Excited States for Heavy Quark Systems in NRQCD

Following the Non-Relativistic QCD approach we use a gauge invariant smearing method with factorization to measure the excitation energies for a heavy $Q\bar{Q}$ system on a $24^3\times 48$ lattice at $\beta=6.2$. The results come from averaging over an ensemble of 60 QCD configurations. In order to enhance the signal from each configuration we use wall sources for quark propagators. The quark Hamiltonian contains only the simplest non-relativistic kinetic energy term. The results are listed for a range of bare quark masses. The mass splittings are insensitive to this variable though there are a slight trends with increasing quark mass. For an appropriate choice of UV cut-off ($a^{-1}=3.2$Gev) the mass spectrum compares reasonably well with the experimental values for the spin-averaged energy gaps of the $\Upsilon$ system. We also present results for the $DE$ and $DT$ waves for the lowest bare quark mass. The results are consistent with degeneracy between the two types of $D$ wave. This encourages the idea that even with our simple quark Hamiltonian the departure from rotational invariance is not great.Comment: 12 page

The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism

Although multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions

The Atacama Cosmology Telescope: A Catalog of >4000 Sunyaev–Zel’dovich Galaxy Clusters

We present a catalog of 4195 optically confirmed Sunyaev–Zel'dovich (SZ) selected galaxy clusters detected with signal-to-noise ratio >4 in 13,211 deg2 of sky surveyed by the Atacama Cosmology Telescope (ACT). Cluster candidates were selected by applying a multifrequency matched filter to 98 and 150 GHz maps constructed from ACT observations obtained from 2008 to 2018 and confirmed using deep, wide-area optical surveys. The clusters span the redshift range 0.04 1 clusters, and a total of 868 systems are new discoveries. Assuming an SZ signal versus mass-scaling relation calibrated from X-ray observations, the sample has a 90% completeness mass limit of M500c > 3.8 × 1014 M⊙, evaluated at z = 0.5, for clusters detected at signal-to-noise ratio >5 in maps filtered at an angular scale of 2farcm4. The survey has a large overlap with deep optical weak-lensing surveys that are being used to calibrate the SZ signal mass-scaling relation, such as the Dark Energy Survey (4566 deg2), the Hyper Suprime-Cam Subaru Strategic Program (469 deg2), and the Kilo Degree Survey (825 deg2). We highlight some noteworthy objects in the sample, including potentially projected systems, clusters with strong lensing features, clusters with active central galaxies or star formation, and systems of multiple clusters that may be physically associated. The cluster catalog will be a useful resource for future cosmological analyses and studying the evolution of the intracluster medium and galaxies in massive clusters over the past 10 Gyr

'Duck to water' or 'fish out of water'? Diversity in the experience of negotiating the transition to university

Winstone and Hulme present a critical discussion of the notion of transition to university. They argue that the common emphasis on the challenging nature of the transition fails to acknowledge the diversity in students’ experiences; for some students, the liminality and discomfort experienced during this critical period in their educational journey can be a transformational and empowering rite of passage. Rather than homogenising students’ experiences, Winstone and Hulme argue that it is beneficial to explore the transition experience through the lens of students’ expectations and subsequent experiences and to view the transition to university as part of a trajectory of transition experience within a student’s educational journey. The chapter also presents practical suggestions for engaging multiple student voices in understanding and facilitating positive transition experiences

Identification of common genetic risk variants for autism spectrum disorder

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD.Peer reviewe

Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci

Analysis of de novo CNVs (dnCNVs) from the full Simons Simplex Collection (SSC) (N = 2,591 families) replicates prior findings of strong association with autism spectrum disorders (ASDs) and confirms six risk loci (1q21.1, 3q29, 7q11.23, 16p11.2, 15q11.2-13, and 22q11.2). The addition of published CNV data from the Autism Genome Project (AGP) and exome sequencing data from the SSC and the Autism Sequencing Consortium (ASC) shows that genes within small de novo deletions, but not within large dnCNVs, significantly overlap the high-effect risk genes identified by sequencing. Alternatively, large dnCNVs are found likely to contain multiple modest-effect risk genes. Overall, we find strong evidence that de novo mutations are associated with ASD apart from the risk for intellectual disability. Extending the transmission and de novo association test (TADA) to include small de novo deletions reveals 71 ASD risk loci, including 6 CNV regions (noted above) and 65 risk genes (FDR ≤ 0.1). Through analysis of de novo mutations in autism spectrum disorder (ASD), Sanders et al. find that small deletions, but not large deletions/duplications, contain one critical gene. Combining CNV and sequencing data, they identify 6 loci and 65 genes associated with ASD. © 2015 Elsevier Inc

Vascular Remodeling in Health and Disease

The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall