Signatures of Galaxy-Cluster Interactions: Spiral Galaxy Rotation Curve Asymmetry, Shape, and Extent

The environmental dependencies of the characteristics of spiral galaxy rotation curves are studied in this work. We use our large, homogeneously collected sample of 510 cluster spiral galaxy rotation curves to test the claim that the shape of a galaxy's rotation curve strongly depends on its location within the cluster, and thus presumably on the strength of the local intracluster medium and on the frequency and strength of tidal interactions with the cluster and cluster galaxies. Our data do not corroborate such a scenario, consistent with the fact that Tully-Fisher residuals are independent of galaxy location within the cluster; while the average late-type spiral galaxy shows more rise in the outer parts of its rotation curve than does the typical early-type spiral galaxy, there is no apparent trend for either subset with cluster environment. We also investigate as a function of cluster environment rotation curve asymmetry and the radial distribution of H II region tracers within galactic disks. Mild trends with projected cluster-centric distance are observed: (i) the (normalized) radial extent of optical line emission averaged over all spiral galaxy types shows a 4%+/-2% increase per Mpc of galaxy-cluster core separation, and (ii) rotation curve asymmetry falls by a factor of two between the inner and outer cluster for early-type spirals (a negligible decrease is found for late-type spirals). Such trends are consistent with spiral disk perturbations or even the stripping of the diffuse, outermost gaseous regions within the disks as galaxies pass through the dense cluster cores.Comment: 17 pages; to appear in the April 2001 Astronomical Journa

Analysis of Artificial Intelligence Policies for Higher Education in Europe.

This paper analyses 15 AI policies for higher education from eight European countries, drawn from individual universities, from consortia of universities and from government agencies. Based on an overview of current research findings, it focuses the comparison of different aspects among the selected AI policies. The analysis distinguishes between four potential target groups, namely students, teachers, education managers and policy makers. The paper aims at contributing to the further development and improvement of AI policies for higher education through the identification of commonalities and gaps within the existing AI policies. Moreover, it calls for further and in particular evidence-based research to identify the potential and practical impact of AI in higher education and highlights the need to combine AI use in (higher) education with education about AI, often called as AI literacy

A tier-based typed programming language characterizing Feasible Functionals

International audienceThe class of Basic Feasible Functionals BFF 2 is the type-2 counterpart of the class FP of type-1 functions computable in polynomial time. Several characterizations have been suggested in the literature, but none of these present a programming language with a type system guaranteeing this complexity bound. We give a characterization of BFF 2 based on an imperative language with oracle calls using a tier-based type system whose inference is decidable. Such a characterization should make it possible to link higher-order complexity with programming theory. The low complexity (cubic in the size of the program) of the type inference algorithm contrasts with the intractability of the aforementioned methods and does not restrain strongly the expressive power of the language

Variants in CUL4B are Associated with Cerebral Malformations

Variants in cullin 4B (CUL4B) are a known cause of syndromic X-linked intellectual disability. Here, we describe an additional 25 patients from 11 families with variants in CUL4B. We identified nine different novel variants in these families and confirmed the pathogenicity of all nontruncating variants. Neuroimaging data, available for 15 patients, showed the presence of cerebral malformations in ten patients. The cerebral anomalies comprised malformations of cortical development (MCD), ventriculomegaly, and diminished white matter volume. The phenotypic heterogeneity of the cerebral malformations might result from the involvement of CUL-4B in various cellular pathways essential for normal brain development. Accordingly, we show that CUL-4B interacts with WDR62, a protein in which variants were previously identified in patients with microcephaly and a wide range of MCD. This interaction might contribute to the development of cerebral malformations in patients with variants in CUL4B

Autosomal recessive primary microcephaly due to ASPM mutations: An update.

Autosomal recessive microcephaly or microcephaly primary hereditary (MCPH) is a genetically heterogeneous neurodevelopmental disorder characterized by a reduction in brain volume, indirectly measured by an occipitofrontal circumference (OFC) 2 standard deviations or more below the age- and sex-matched mean (-2SD) at birth and -3SD after 6 months, and leading to intellectual disability of variable severity. The abnormal spindle-like microcephaly gene (ASPM), the human ortholog of the Drosophila melanogaster "abnormal spindle" gene (asp), encodes ASPM, a protein localized at the centrosome of apical neuroprogenitor cells and involved in spindle pole positioning during neurogenesis. Loss-of-function mutations in ASPM cause MCPH5, which affects the majority of all MCPH patients worldwide. Here, we report 47 unpublished patients from 39 families carrying 28 new ASPM mutations, and conduct an exhaustive review of the molecular, clinical, neuroradiological, and neuropsychological features of the 282 families previously reported (with 161 distinct ASPM mutations). Furthermore, we show that ASPM-related microcephaly is not systematically associated with intellectual deficiency and discuss the association between the structural brain defects (strong reduction in cortical volume and surface area) that modify the cortical map of these patients and their cognitive abilities

De novo TBR1 variants cause a neurocognitive phenotype with ID and autistic traits:report of 25 new individuals and review of the literature

TBR1, a T-box transcription factor expressed in the cerebral cortex, regulates the expression of several candidate genes for autism spectrum disorders (ASD). Although TBR1 has been reported as a high-confidence risk gene for ASD and intellectual disability (ID) in functional and clinical reports since 2011, TBR1 has only recently been recorded as a human disease gene in the OMIM database. Currently, the neurodevelopmental disorders and structural brain anomalies associated with TBR1 variants are not well characterized. Through international data sharing, we collected data from 25 unreported individuals and compared them with data from the literature. We evaluated structural brain anomalies in seven individuals by analysis of MRI images, and compared these with anomalies observed in TBR1 mutant mice. The phenotype included ID in all individuals, associated to autistic traits in 76% of them. No recognizable facial phenotype could be identified. MRI analysis revealed a reduction of the anterior commissure and suggested new features including dysplastic hippocampus and subtle neocortical dysgenesis. This report supports the role of TBR1 in ID associated with autistic traits and suggests new structural brain malformations in humans. We hope this work will help geneticists to interpret TBR1 variants and diagnose ASD probands

A homozygous ATAD1 mutation impairs postsynaptic AMPA receptor trafficking and causes a lethal encephalopathy

Members of the AAA+ superfamily of ATPases are involved in the unfolding of proteins and disassembly of protein complexes and aggregates. ATAD1 encoding the ATPase family, AAA+ domain containing 1-protein Thorase plays an important role in the function and integrity of mitochondria and peroxisomes. Postsynaptically, Thorase controls the internalization of excitatory, glutamatergic AMPA receptors by disassembling complexes between the AMPA receptor-binding protein, GRIP1, and the AMPA receptor subunit GluA2. Using whole-exome sequencing, we identified a homozygous frameshift mutation in the last exon of ATAD1 [c.1070-1071delAT; p.(His357Argfs 1715)] in three siblings who presented with a severe, lethal encephalopathy associated with stiffness and arthrogryposis. Biochemical and cellular analyses show that the C-terminal end of Thorase mutant gained a novel function that strongly impacts its oligomeric state, reduces stability or expression of a set of Golgi, peroxisomal and mitochondrial proteins and affects disassembly of GluA2 and Thorase oligomer complexes. Atad1 -/- neurons expressing Thorase mutant His357Argfs 1715 display reduced amount of GluA2 at the cell surface suggesting that the Thorase mutant may inhibit the recycling back and/or reinsertion of AMPA receptors to the plasma membrane. Taken together, our molecular and functional analyses identify an activating ATAD1 mutation as a new cause of severe encephalopathy and congenital stiffness