Mindsets and Failures : Neural Differences in Reactions to Mistakes among 2nd Grade Finnish Girls

Mindsets have been identified as an important factor in explaining learning differences among students. Growth mindset students have been shown to recover from mistakes easier than fixed mindset students, and recent neuroscientific research has shown differences in the brain’s event-related potentials to errors in fixed and growth mindset participants. The purpose of this study was to examine and evaluate these differences in the Finnish elementary school context. To achieve this, event-related potentials of five fixed and five growth mindset 8-9-year-old female students were recorded during a go/no-go task. Differences between the two groups emerged, however, they were different from the results of some previous studies in the field. These findings are discussed in the light of earlier neuroscientific research related to mindsets, including limitations and suggestions for future research in the field.Peer reviewe

Global patterns in endemicity and vulnerability of soil fungi

Fungi are highly diverse organisms, which provide multiple ecosystem services. However, compared with charismatic animals and plants, the distribution patterns and conservation needs of fungi have been little explored. Here, we examined endemicity patterns, global change vulnerability and conservation priority areas for functional groups of soil fungi based on six global surveys using a high-resolution, long-read metabarcoding approach. We found that the endemicity of all fungi and most functional groups peaks in tropical habitats, including Amazonia, Yucatan, West-Central Africa, Sri Lanka, and New Caledonia, with a negligible island effect compared with plants and animals. We also found that fungi are predominantly vulnerable to drought, heat and land-cover change, particularly in dry tropical regions with high human population density. Fungal conservation areas of highest priority include herbaceous wetlands, tropical forests, and woodlands. We stress that more attention should be focused on the conservation of fungi, especially root symbiotic arbuscular mycorrhizal and ectomycorrhizal fungi in tropical regions as well as unicellular early-diverging groups and macrofungi in general. Given the low overlap between the endemicity of fungi and macroorganisms, but high conservation needs in both groups, detailed analyses on distribution and conservation requirements are warranted for other microorganisms and soil organisms

Global patterns in endemicity and vulnerability of soil fungi

Fungi are highly diverse organisms, which provide multiple ecosystem services. However, compared with charismatic animals and plants, the distribution patterns and conservation needs of fungi have been little explored. Here, we examined endemicity patterns, global change vulnerability and conservation priority areas for functional groups of soil fungi based on six global surveys using a high-resolution, long-read metabarcoding approach. We found that the endemicity of all fungi and most functional groups peaks in tropical habitats, including Amazonia, Yucatan, West-Central Africa, Sri Lanka, and New Caledonia, with a negligible island effect compared with plants and animals. We also found that fungi are predominantly vulnerable to drought, heat and land-cover change, particularly in dry tropical regions with high human population density. Fungal conservation areas of highest priority include herbaceous wetlands, tropical forests, and woodlands. We stress that more attention should be focused on the conservation of fungi, especially root symbiotic arbuscular mycorrhizal and ectomycorrhizal fungi in tropical regions as well as unicellular early-diverging groups and macrofungi in general. Given the low overlap between the endemicity of fungi and macroorganisms, but high conservation needs in both groups, detailed analyses on distribution and conservation requirements are warranted for other microorganisms and soil organisms

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 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

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Connecting the multiple dimensions of global soil fungal diversity

15 páginas.- 5 figuras.- 99 referenciasHow the multiple facets of soil fungal diversity vary worldwide remains virtually unknown, hindering the management of this essential species-rich group. By sequencing high-resolution DNA markers in over 4000 topsoil samples from natural and human-altered ecosystems across all continents, we illustrate the distributions and drivers of different levels of taxonomic and phylogenetic diversity of fungi and their ecological groups. We show the impact of precipitation and temperature interactions on local fungal species richness (alpha diversity) across different climates. Our findings reveal how temperature drives fungal compositional turnover (beta diversity) and phylogenetic diversity, linking them with regional species richness (gamma diversity). We integrate fungi into the principles of global biodiversity distribution and present detailed maps for biodiversity conservation and modeling of global ecological processes.This work was supported by the Estonian Science Foundation: PRG632 (to L.T.), Estonian Research Council: PRG1615 (to R.D.), Estonian Research Council: PRG1170 (to U.K. and Ka.Po.), Estonian Science Foundation: MOBTP198 (to St.An.), Novo Nordisk Fonden: NNF20OC0059948 (to L.T.), Norway-Baltic financial mechanism: EMP442 (to L.T., K.-A.B., and M.T.), King Saud University: DFSP-2020-2 (to L.T.), King Saud University: Highly Cited Program (to L.T.), European Regional Development Fund: Centre of Excellence EcolChange TK131 (to M.O., M.Z., Ü.M., U.K., and M.E.), Estonian Research Council: PRG1789 (to M.O. and I.H.), British Ecological Society: LRB17\1019 (MUSGONET) (to M.D.-B.), Spanish Ministry of Science and Innovation: PID2020-115813RA-I00 (to M.D.-B.), Spanish Ministry of Science and Innovation: SOIL4GROWTH (to M.D.-B.), Marie Sklodowska-Curie: 702057 (CLIMIFUN) (to M.D.- B.), European Research Council (ERC): grant 647038 [BIODESERT] (to F.T.M.), Generalitat Valenciana: CIDEGENT/2018/041 (to F.T.M.), Spanish Ministry of Science and Innovation: EUR2022-134048 (to F.T.M.), Estonian Research Council: PRG1065 (to M.M. and M.Z.), Swedish Research Council Formas: 2020-00807 (to Mo.Ba.), Swedish Research Council: 2019-05191 (to Al. An.), Swedish Foundation for Strategic Environmental Research MISTRA: Project BioPath (to Al. An.), Kew Foundation (to Al.An.), EEA Financial Mechanism Baltic Research Programme in Estonia: EMP442 (to Ke.Ar. and Je.An.), Ghent University Special Research Fund (BOF): Metusalem (to N.S.), Estonian Research Council: PSG825 (to K.R.), European Research Council (ERC): 101096403 (MLTOM23415R) (to Ü.M.), European Regional Development Fund (ERDF): 1.1.1.2/VIAA/2/18/298 (to D.K.), Estonian Research Council: PUT1170 (to I.H.), German Federal Ministry of Education and Research (BMBF): 01DG20015FunTrAf (to K.T.I., M.P., and N.Y.), Proyecto SIA: SA77210019 (ANID—Chile) (to C.M.), Fondecyt: 1190642 (ANID—Chile) (to R.G.), European Research Council (ERC): Synergy Grant 856506—LIFEPLAN (to T.R.), Academy of Finland: grant 322266 (to T.R.), U.S. National Science Foundation: DEB-0918591 (to T.H.), U.S. National Science Foundation: DEB-1556338 (to T.H.), U.S. National Science Foundation: DEB 1737898 (to G.B.), UNAM-PAPIIT: IV200223 (to R.G.-O.), Czech Science Foundation: 21-26883S (to J.D.), Estonian Research Council: PRG352 (to M.E.), NERC core funding: the BAS Biodiversity, Evolution and Adaptation Team (to K.K.N.), NERC-CONICYT: NE/P003079/1 (to E.M.B.), Carlsberg Foundation: CF18-0267 (to E.M.B.), Qatar Petroleum: QUEX-CAS-QP-RD-18/19 (to Ju.Al.), Russian Ministry of Science and Higher Education: 075-15-2021-1396 (to V.F. and V.O.), Secretaria de Ciencia y Técnica (SECYT) of Universidad Nacional de Córdoba and CONICET (to E.N.), HighLevel Talent Recruitment Plan of Yunnan Province 2021:“High-End Foreign Experts” (to Pe.Mo.), AUA grant from research council of UAE University: G00003654 (to S.M.), Ghent University: Bijzonder Onderzoeksfonds (to A.V.), Ghent University: Bijzonder Onderzoeksfonds (BOF-PDO2017-001201) (to E.D.C.), Ghent University: The Faculty Committee Scientific Research, FCWO (to E.D.C. and A.V.), The King Leopold III Fund for Nature Exploration and Conservation (to A.V. and E.D.C.), The Research Foundation—Flanders (FWO) (to E.D.C. and A.V.), The High-Level Talent Recruitment Plan of Yunnan Provinces: “Young Talents” Program (to D.-Q.D.), The HighLevel Talent Recruitment Plan of Yunnan Provinces: “High-End Foreign Experts" Program (to N. N.W.), IRIS scholarship for progressive and ambitious women (to L.H.), Estonian University of Life Sciences: P190250PKKH (to Kr.Pa.), Hungarian Academy of Sciences: Lendület Programme (96049) (to J.G.), Eötvös Loránd Research Network (to J.G.), Botswana International University of Science and Technology (to C.N.), and Higher Education Commision (HEC, Islamabad, Pakistan): Indigenous and International research support initiative program (IRSIP) scholarship (to M.S.)Peer reviewe

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

A first update on mapping the human genetic architecture of COVID-19

peer reviewe