The Quality-Diversity Transformer: Generating Behavior-Conditioned Trajectories with Decision Transformers

In the context of neuroevolution, Quality-Diversity algorithms have proven effective in generating repertoires of diverse and efficient policies by relying on the definition of a behavior space. A natural goal induced by the creation of such a repertoire is trying to achieve behaviors on demand, which can be done by running the corresponding policy from the repertoire. However, in uncertain environments, two problems arise. First, policies can lack robustness and repeatability, meaning that multiple episodes under slightly different conditions often result in very different behaviors. Second, due to the discrete nature of the repertoire, solutions vary discontinuously. Here we present a new approach to achieve behavior-conditioned trajectory generation based on two mechanisms: First, MAP-Elites Low-Spread (ME-LS), which constrains the selection of solutions to those that are the most consistent in the behavior space. Second, the Quality-Diversity Transformer (QDT), a Transformer-based model conditioned on continuous behavior descriptors, which trains on a dataset generated by policies from a ME-LS repertoire and learns to autoregressively generate sequences of actions that achieve target behaviors. Results show that ME-LS produces consistent and robust policies, and that its combination with the QDT yields a single policy capable of achieving diverse behaviors on demand with high accuracy.Comment: 10+7 page

Phenotypic spectrum of fetal Smith-Lemli-Opitz syndrome.

International audienceThe Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive multiple congenital malformation syndrome caused by dehydrocholesterol reductase deficiency. The diagnosis is confirmed by high 7- and secondarily 8-dehydrocholesterol levels in plasma and tissues and/or by detection of biallelic mutations in the DHCR7 gene. The phenotypic spectrum of SLOS is broad, ranging from a mild phenotype combining subtle physical anomalies with behavioral and learning problems, to a perinatally lethal multiple malformations syndrome. The fetal phenotype of SLOS has been poorly described in the literature. We report a series of 10 fetuses with molecularly proven SLOS. Even in young fetuses, the facial dysmorphism appears characteristic. Genital abnormalities are rare in 46,XX subjects. Gonadal differentiation appears histologically normal and in agreement with the chromosomal sex, contrary to what has been previously stated. We observed some previously unreported anomalies: ulnar hypoplasia, vertebral segmentation anomalies, congenital pulmonary adenomatoid malformation, fused lungs, gastroschisis, holomyelia and hypothalamic hamartoma. This latter malformation proves that SLOS phenotypically overlaps with Pallister-Hall syndrome which remains clinically a major differential diagnosis of SLOS

CNV-association meta-analysis in 191,161 European adults reveals new loci associated with anthropometric traits

Funding Information: This research has been conducted using the UK Biobank Resource. This research has been conducted using the Danish National Biobank resource. The authors are grateful to the Raine Study participants and their families, and to the Raine Study research staff for cohort co-ordination and data collection. QIMR is grateful to the twins and their families for their generous participation in these studies. We would like to thank staff at the Queensland Institute of Medical Research: Anjali Henders, Dixie Statham, Lisa Bowdler, Ann Eldridge, and Marlene Grace for sample collection, processing and genotyping, Scott Gordon, Brian McEvoy, Belinda Cornes and Beben Benyamin for data QC and preparation, and David Smyth and Harry Beeby for IT support. HBCS Acknowledgements: We thank all study participants as well as everybody involved in the Helsinki Birth Cohort Study. Helsinki Birth Cohort Study has been supported by grants from the Academy of Finland, the Finnish Diabetes Research Society, Folkhälsan Research Foundation, Novo Nordisk Foundation, Finska Läkaresällskapet, Juho Vainio Foundation, Signe and Ane Gyllenberg Foundation, University of Helsinki, Ministry of Education, Ahokas Foundation, Emil Aaltonen Foundation. Finrisk study is grateful for the THL DNA laboratory for its skillful work to produce the DNA samples used in this study and thanks the Sanger Institute and FIMM genotyping facilities for genotyping the samples. We thank the MOLGENIS team and Genomics Coordination Center of the University Medical Center Groningen for software development and data management, in particular Marieke Bijlsma and Edith Adriaanse. This work was supported by the Leenards Foundation (to Z.K.), the Swiss National Science Foundation (31003A_169929 to Z.K., Sinergia grant CRSII33-133044 to AR), Simons Foundation (SFARI274424 to AR) and SystemsX.ch (51RTP0_151019 to Z.K.). A.R.W., H.Y. and T.M.F. are supported by the European Research Council grant: 323195:SZ-245. M.A.T., M.N.W. and An.M. are supported by the Wellcome Trust Institutional Strategic Support Award (WT097835MF). For full funding information of all participating cohorts see Supplementary Note 2. Publisher Copyright: © 2017 The Author(s).There are few examples of robust associations between rare copy number variants (CNVs) and complex continuous human traits. Here we present a large-scale CNV association meta-analysis on anthropometric traits in up to 191,161 adult samples from 26 cohorts. The study reveals five CNV associations at 1q21.1, 3q29, 7q11.23, 11p14.2, and 18q21.32 and confirms two known loci at 16p11.2 and 22q11.21, implicating at least one anthropometric trait. The discovered CNVs are recurrent and rare (0.01-0.2%), with large effects on height (> 2.4 cm), weight ( 5 kg), and body mass index (BMI) (> 3.5 kg/m(2)). Burden analysis shows a 0.41 cm decrease in height, a 0.003 increase in waist-to-hip ratio and increase in BMI by 0.14 kg/m2 for each Mb of total deletion burden (P = 2.5 x 10(-10), 6.0 x 10(-5), and 2.9 x 10(-3)). Our study provides evidence that the same genes (e.g., MC4R, FIBIN, and FMO5) harbor both common and rare variants affecting body size and that anthropometric traits share genetic loci with developmental and psychiatric disorders.Peer reviewe

Título: Libri de piscibus marinis

Marca tip. en portColofónSign.: [alfa]8, A-H6, I-K4, L-Z6, 2A-2Z6, 2A-2B6, 2C-2D4, 2E-2F6Las il. son xil., una de ellas, al comienzo del texto, retrato del auto

Limits of event-related potential differences in tracking object processing speed

International audienceWe report results from two experiments in which subjects had to categorize briefly presented upright or inverted natural scenes. In the first experiment, subjects decided whether images contained animals or human faces presented at different scales. Behavioral results showed virtually identical processing speed between the two categories and very limited effects of inversion. One type of event-related potential (ERP) comparison, potentially capturing low-level physical differences, showed large effects with onsets at about 150 msec in the animal task. However, in the human face task, those differences started as early as 100 msec. In the second experiment, subjects responded to close-up views of animal faces or human faces in an attempt to limit physical differences between image sets. This manipulation almost completely eliminated small differences before 100 msec in both tasks. But again, despite very similar behavioral performances and short reaction times in both tasks, human faces were associated with earlier ERP differences compared with animal faces. Finally, in both experiments, as an alternative way to determine processing speed, we compared the ERP with the same images when seen as targets and nontargets in different tasks. Surprisingly, all task-dependent ERP differences had relatively long latencies. We conclude that task-dependent ERP differences fail to capture object processing speed, at least for some categories like faces. We discuss models of object processing that might explain our results, as well as alternative approaches