Mutualistic Coupling Between Vocabulary and Reasoning Supports Cognitive Development During Late Adolescence and Early Adulthood.

One of the most replicable findings in psychology is the positive manifold: the observation that individual differences in cognitive abilities are universally positively correlated. Investigating the developmental origin of the positive manifold is crucial to understanding it. In a large longitudinal cohort of adolescents and young adults ( N = 785; n = 566 across two waves, mean interval between waves = 1.48 years; age range = 14-25 years), we examined developmental changes in two core cognitive domains, fluid reasoning and vocabulary. We used bivariate latent change score models to compare three leading accounts of cognitive development: g-factor theory, investment theory, and mutualism. We showed that a mutualism model, which proposes that basic cognitive abilities directly and positively interact during development, provides the best account of developmental changes. We found that individuals with higher scores in vocabulary showed greater gains in matrix reasoning and vice versa. These dynamic coupling pathways are not predicted by other accounts and provide a novel mechanistic window into cognitive development.The Neuroscience in Psychiatry Network is supported by a strategic award from the Wellcome Trust to the University of Cambridge and University College London (095844/Z/11/Z). R. A. Kievit is supported by the Wellcome Trust (Grant No. 107392/Z/15/Z) and the UK Medical Research Council (MC-A060-5PR61). P. Fonagy is funded by a National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0514-10157). P. Fonagy was in part supported by the NIHR Collaboration for Leadership in Applied Health Research and Care (CLAHRC) North Thames at Barts Health National Health Service (NHS) Trust. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the UK Department of Health

Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Abstract Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

The Role of Insulin and Glucagon in Mammalian Ammonia Homeostasis. Studies With Ammonia-Induced Orotic Aciduria in Rats

237 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1980.Ammonia is a neural toxin, and this thesis proposes that the prevention of ammonia intoxication is a primary metabolic "concern" of mammals. The infrequency of ammonia intoxication indicates that an effective mechanism for controlling ammonia homeostasis exists. Extensive review of the literature on ammonia metabolism, glucose metabolism, urea synthesis and insulin and glucagon function has provided a basis for proposing a simple model accounting for ammonia homeostasis.Only three enzymes initiate the removal of ammonia. These are: carbamyl phosphate synthetase I (CPS I), glutamate dehydrogenase (GDH), and glutamine synthetase (GS). Their tissue distribution underlies a basic pattern of ammonia metabolism. CPS I is the first enzyme in the synthesis of urea, which accounts for most of the nitrogen loss by mammals. However, urea synthesis is limited primarily to the liver. Therefore, transport of ammonia from extrahepatic tissues, especially the brain, to the liver must occur to prevent ammonia intoxication. This removal and transport of ammonia depends on GDH, GS and related transaminase activity. These reactions require a supply of (alpha)-ketoacids, which depends principally upon the availability of glucose. Therefore, the prevention of ammonia intoxication depends on the controlled presentation of glucose to extrahepatic tissues, its metabolism to (alpha)-ketoacids, their use with ammonia in the synthesis of amino acids and the return of these amino acids to the liver. Hepatic ureagenesis and gluconeogenesis then allow for the final removal of ammonia and the return of glucose for further peripheral ammonia removal. This thesis hypothesizes that ammonia homeostasis depends on the control of glucose metabolism and urea synthesis and that insulin and glucagon initiate control of these to provide for appropriate removal of ammonia.This proposal was tested in studies with fed and fasted mature male rats, using ammonia-induced orotic aciduria (AIOA) as an index. Extensive evidence reviewed in this thesis show that AIOA results because mitochondrially generated carbamyl phosphate is shunted into hepatic pyrimidine synthesis following ammonia intoxication or loss of ureagenic capacity. Data presented show that AIOA is an inverse function of the in vivo ureagenic capacity and is directly related to the degree of ammonia intoxication. Thus the evidence suggests that AIOA may be useful in assessing ureagenic capacity and ammonia status in vivo. These characteristics of AIOA were exploited in studies designed to test the role of glucose metabolism and insulin and glucagon in maintaining ammonia homeostasis.In general the evidence is consistent with the interpretation that glucose, insulin and glucagon play a central role in ammonia homeostasis. That is, glucagon, by increasing peripheral glucose availability and hepatic ureagenesis, and insulin, by causing the reverse, have the capacity to control ammonia homeostasis. Also, the literature reviewed and data presented support the conclusion that changes in ammonia supply are associated with changes in glucose, insulin and glucagon which are appropriate for control of ammonia removal. That is, increased ammonia leads to increased glucagon and/or decreased insulin.In short, this thesis proposes that the control of glucose metabolism is related to its role in ammonia removal and that insulin and glucagon, by appropriately controlling the availability of glucose and the capacity for ureagenesis, lead to the maintenance of ammonia homeostasis. This proposal demands significant reevaluation of the role of glucose, insulin and glucagon in mammals, giving emphasis to their relation to ammonia homeostasis. If valid, this proposed reinterpretation has broad implications of ammonia in mammalian health and disease.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD