Institution
Karolinska Institutet
Education•Stockholm, Sweden•
About: Karolinska Institutet is a education organization based out in Stockholm, Sweden. It is known for research contribution in the topics: Population & Cancer. The organization has 46212 authors who have published 121142 publications receiving 6008130 citations.
Topics: Population, Cancer, Poison control, Cohort study, Health care
Papers published on a yearly basis
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University of California, Irvine1, University of Southern California2, Yale University3, Oslo University Hospital4, Karolinska Institutet5, University of Oslo6, University of California, San Diego7, University of Göttingen8, Trinity College, Dublin9, National University of Ireland, Galway10, University of Amsterdam11, VU University Amsterdam12, University of Pennsylvania13, University of California, San Francisco14, San Francisco VA Medical Center15, University of Minnesota16, Dresden University of Technology17, Harvard University18, University of New Mexico19, University of Iowa20, Utrecht University21, University of California, Los Angeles22, University of Cantabria23, Northwestern University24, University of Edinburgh25, Osaka University26, Georgia State University27
TL;DR: Worldwide cooperative analyses of brain imaging data support a profile of subcortical abnormalities in schizophrenia, which is consistent with that based on traditional meta-analytic approaches, and validates that collaborative data analyses can readily be used across brain phenotypes and disorders.
Abstract: The profile of brain structural abnormalities in schizophrenia is still not fully understood, despite decades of research using brain scans. To validate a prospective meta-analysis approach to analyzing multicenter neuroimaging data, we analyzed brain MRI scans from 2028 schizophrenia patients and 2540 healthy controls, assessed with standardized methods at 15 centers worldwide. We identified subcortical brain volumes that differentiated patients from controls, and ranked them according to their effect sizes. Compared with healthy controls, patients with schizophrenia had smaller hippocampus (Cohen's d=-0.46), amygdala (d=-0.31), thalamus (d=-0.31), accumbens (d=-0.25) and intracranial volumes (d=-0.12), as well as larger pallidum (d=0.21) and lateral ventricle volumes (d=0.37). Putamen and pallidum volume augmentations were positively associated with duration of illness and hippocampal deficits scaled with the proportion of unmedicated patients. Worldwide cooperative analyses of brain imaging data support a profile of subcortical abnormalities in schizophrenia, which is consistent with that based on traditional meta-analytic approaches. This first ENIGMA Schizophrenia Working Group study validates that collaborative data analyses can readily be used across brain phenotypes and disorders and encourages analysis and data sharing efforts to further our understanding of severe mental illness.
919 citations
University of Oxford1, King's College London2, University of Manchester3, Radboud University Nijmegen4, Wellcome Trust Sanger Institute5, University of London6, University of Sheffield7, Trinity College, Dublin8, Wellcome Trust9, Medical University of Graz10, University of Erlangen-Nuremberg11, Queen Mary University of London12, Western Infirmary13, Karolinska Institutet14, St George's, University of London15, University of Dundee16, University of Göttingen17, University of Gothenburg18, Sapienza University of Rome19, University of Cambridge20, University of Münster21, University College London22, Moorfields Eye Hospital23, University of Bristol24
TL;DR: These findings implicate pathways that integrate epidermal barrier dysfunction with innate and adaptive immune dysregulation in psoriasis pathogenesis and report compelling evidence for an interaction between the HLA-C and ERAP1 loci.
Abstract: To identify new susceptibility loci for psoriasis, we undertook a genome-wide association study of 594,224 SNPs in 2,622 individuals with psoriasis and 5,667 controls. We identified associations at eight previously unreported genomic loci. Seven loci harbored genes with recognized immune functions (IL28RA, REL, IFIH1, ERAP1, TRAF3IP2, NFKBIA and TYK2). These associations were replicated in 9,079 European samples (six loci with a combined P < 5 × 10⁻⁸ and two loci with a combined P < 5 × 10⁻⁷). We also report compelling evidence for an interaction between the HLA-C and ERAP1 loci (combined P = 6.95 × 10⁻⁶). ERAP1 plays an important role in MHC class I peptide processing. ERAP1 variants only influenced psoriasis susceptibility in individuals carrying the HLA-C risk allele. Our findings implicate pathways that integrate epidermal barrier dysfunction with innate and adaptive immune dysregulation in psoriasis pathogenesis.
919 citations
TL;DR: Evidence for brain maintenance at different levels is discussed: cellular, neurochemical, gray- and white-matter integrity, and systems-level activation patterns, and it is argued that it constitutes the primary determinant of successful memory aging.
918 citations
TL;DR: The CDP-reductase system was purified from E. coli 13 a low molecular weight, heat-stable protein, hereafter called thioredoxin, and the requirement for reduced lipoate was replaced by either catalytic amounts of thiOREDoxin + TPNH or substrate amounts of chemically reduced dihydrothiored toxin.
916 citations
TL;DR: This work provides the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide.
Abstract: Alternative splicing of pre-messenger RNA is a key feature of transcriptome expansion in eukaryotic cells, yet its regulation is poorly understood. Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing. Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns. Moreover, the rate of transcription elongation has been linked to alternative splicing. Here we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide. We further show that CTCF binding to CD45 exon 5 is inhibited by DNA methylation, leading to reciprocal effects on exon 5 inclusion. These findings provide a mechanistic basis for developmental regulation of splicing outcome through heritable epigenetic marks.
916 citations
Authors
Showing all 46522 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Meir J. Stampfer | 277 | 1414 | 283776 |
| Albert Hofman | 267 | 2530 | 321405 |
| Guido Kroemer | 236 | 1404 | 246571 |
| Eric B. Rimm | 196 | 988 | 147119 |
| Scott M. Grundy | 187 | 841 | 231821 |
| Jing Wang | 184 | 4046 | 202769 |
| Tadamitsu Kishimoto | 181 | 1067 | 130860 |
| John Hardy | 177 | 1178 | 171694 |
| Marc G. Caron | 173 | 674 | 99802 |
| Ramachandran S. Vasan | 172 | 1100 | 138108 |
| Adrian L. Harris | 170 | 1084 | 120365 |
| Douglas F. Easton | 165 | 844 | 113809 |
| Zulfiqar A Bhutta | 165 | 1231 | 169329 |
| Judah Folkman | 165 | 499 | 148611 |
| Ralph A. DeFronzo | 160 | 759 | 132993 |