Anticipatory Smiling: Linking Early Affective Communication and Social Outcome

In anticipatory smiles, infants appear to communicate pre-existing positive affect by smiling at an object and then turning the smile toward an adult. We report two studies in which the precursors, development, and consequences of anticipatory smiling were investigated. Study 1 revealed a positive correlation between infant smiling at 6 months and the level of anticipatory smiling at 8 and 10 months during joint attention episodes, as well as a positive correlation between anticipatory smiling and parent-rated social expressivity scores at 30 months. Study 2 confirmed a developmental increase in the number of infants using anticipatory smiles between 9 and 12 months that had been initially documented in the Study 1 sample [Venezia, M., Messinger, D. S., Thorp, D., & Mundy, P. (2004). The development of anticipatory smiling. Infancy, 6(3), 397–406]. Additionally, anticipatory smiling at 9 months positively predicted parent-rated social competence scores at 30 months. Findings are discussed with regard to the importance of anticipatory smiling in early socioemotional development

Infant Responding to Joint Attention, Executive Processes, and Self-Regulation in Preschool Children

Infant joint attention is related to behavioral and social outcomes, as well as language in childhood. Recent research and theory suggests that the relations between joint attention and social–behavioral outcomes may reflect the role of executive self-regulatory processes in the development of joint attention. To test this hypothesis two studies were conducted. The first, cross-sectional study examined the development of responding to joint attention (RJA) skill in terms of increasing executive efficiency of responding between 9 and 18 months of age. The results indicated that development of RJA was characterized by a decreased latency to shift attention in following another person\u27s gaze and head turn, as well as an increase in the proportion of correct RJA responses exhibited by older infants. The second study examined the longitudinal relations between 12-month measures of responding to joint attention and 36-month attention regulation in a delay of gratification task. The results indicated that responding to joint attention at 12-months was significantly related to children\u27s use of three types of self-regulation behaviors while waiting for a snack reward at 36 months of age. These observations are discussed in light of a developmental theory of attention regulation and joint attention in infancy

Gaze following, temperament, and language development in 6-month-olds: A replication and extension

This study examined the age of onset of the capacity to align with direction of gaze, and the relations between individual differences in this capacity, temperament and language acquisition. Infants demonstrated the capacity to match mother’s direction of gaze, and individual differences in this capacity were related to temperament and vocabulary development

Responding to Joint Attention Across the 6- Through 24-Month Age Period and Early Language Acquisition

This study examined individual differences in the development of the capacity of infants to respond to the joint attention bids of others (e.g., gaze shift, pointing, and vocalizing) across the first and second year. The primary aim of the study was to determine if responding to joint attention (RJA) in the first and second year was related to subsequent vocabulary acquisition and whether a specific period of development during the first 2 years was optimal for the assessment of individual differences in this skill. The study was also designed to determine if RJA provided unique predictive information about language development over and above that provided by parent reports of early vocabulary acquisition. Findings indicated that RJA at 6, 8, 10, 12, and 18 months was positively related to individual differences in vocabulary development. Furthermore, both a 6- to 18-month aggregate measure of RJA and a parent report measure of language development made unique contributions to the predictions of vocabulary acquisition. Finally, individual differences in RJA measured at 21 and 24 months were not related to language development

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease