Summary of demographic and clinical data at baseline and retest (mean ± SD).

<p>DOI, duration of illness; PANSS, Positive and Negative Syndrome Scale;</p><p>CPZ, chlorpromazine.</p><p>^aχ² test;</p>b<p><i>t</i>-test for independent samples,</p>c<p><i>t</i>-test for paired samples.</p

Test-retest correlations of CPT-IP performance measures (mean ± SD).

*<p><i>p</i><.05;</p>**<p><i>p</i><.01,</p>***<p><i>p</i><.001.</p

Overview of meditation types in detail.

N = 739. b Participants could choose multiple options; the total percentage may exceed 100%. (DOCX)</p

Correlations between predictors.

Correlations between predictors.</p

Descriptive statistics of questionnaire scores.

Descriptive statistics of questionnaire scores.</p

Model 4 Mediation model of mindfulness, cognitive fusion and negative affect.

Model 4 mediation model of mindfulness, cognitive fusion and negative affect. SMQ: Southampton Mindfulness Questionnaire; CFQ: Cognitive fusion questionnaire; BSCL: Brief Symptom Checklist. Model controlled for age.</p

Sociodemographic and meditation-related characteristics.

Sociodemographic and meditation-related characteristics.</p

S1 Dataset -

(SAV)</p

Model 7 moderated mediation model of mindfulness, cognitive fusion and negative affect with moderators extraversion, conscientiousness, and neuroticism.

Model 7 moderated mediation model of mindfulness, cognitive fusion and negative affect with moderators extraversion, conscientiousness, and neuroticism. SMQ: Southampton Mindfulness Questionnaire, CFQ: Cognitive fusion questionnaire, BSCL: Brief Symptom Checklist, BFI: Big Five Inventory. Model controlled for age. Indexes of mediation refer to path-a.</p

Mapping genomic loci implicates genes and synaptic biology in schizophrenia

Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies