Institution
King's College London
Education•London, United Kingdom•
About: King's College London is a education organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Mental health. The organization has 43107 authors who have published 113125 publications receiving 4498103 citations. The organization is also known as: King's & KCL.
Papers published on a yearly basis
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TL;DR: It is shown in mice that the vast majority of adult tissue-resident macrophages originate from a Tie2+ (also known as Tek) cellular pathway generating Csf1r+ erythro-myeloid progenitors (EMPs) distinct from HSCs.
Abstract: Most haematopoietic cells renew from adult haematopoietic stem cells (HSCs), however, macrophages in adult tissues can self-maintain independently of HSCs. Progenitors with macrophage potential in vitro have been described in the yolk sac before emergence of HSCs, and fetal macrophages can develop independently of Myb, a transcription factor required for HSC, and can persist in adult tissues. Nevertheless, the origin of adult macrophages and the qualitative and quantitative contributions of HSC and putative non-HSC-derived progenitors are still unclear. Here we show in mice that the vast majority of adult tissue-resident macrophages in liver (Kupffer cells), brain (microglia), epidermis (Langerhans cells) and lung (alveolar macrophages) originate from a Tie2(+) (also known as Tek) cellular pathway generating Csf1r(+) erythro-myeloid progenitors (EMPs) distinct from HSCs. EMPs develop in the yolk sac at embryonic day (E) 8.5, migrate and colonize the nascent fetal liver before E10.5, and give rise to fetal erythrocytes, macrophages, granulocytes and monocytes until at least E16.5. Subsequently, HSC-derived cells replace erythrocytes, granulocytes and monocytes. Kupffer cells, microglia and Langerhans cells are only marginally replaced in one-year-old mice, whereas alveolar macrophages may be progressively replaced in ageing mice. Our fate-mapping experiments identify, in the fetal liver, a sequence of yolk sac EMP-derived and HSC-derived haematopoiesis, and identify yolk sac EMPs as a common origin for tissue macrophages.
1,626 citations
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German Center for Neurodegenerative Diseases1, University of Bonn2, Harvard University3, Maastricht University4, Aix-Marseille University5, Pierre-and-Marie-Curie University6, French Institute of Health and Medical Research7, University of Melbourne8, VU University Amsterdam9, New York University10, Mayo Clinic11, City University of New York12, University of New South Wales13, Indiana University14, King's College London15, University of Toulouse16
TL;DR: Research criteria for SCD in pre‐mild cognitive impairment (MCI) are presented and a list of core features proposed for reporting in SCD studies is provided, which will enable comparability of research across different settings.
Abstract: There is increasing evidence that subjective cognitive decline (SCD) in individuals with unimpaired performance on cognitive tests may represent the first symptomatic manifestation of Alzheimer's disease (AD). The research on SCD in early AD, however, is limited by the absence of common standards. The working group of the Subjective Cognitive Decline Initiative (SCD-I) addressed this deficiency by reaching consensus on terminology and on a conceptual framework for research on SCD in AD. In this publication, research criteria for SCD in pre-mild cognitive impairment (MCI) are presented. In addition, a list of core features proposed for reporting in SCD studies is provided, which will enable comparability of research across different settings. Finally, a set of features is presented, which in accordance with current knowledge, increases the likelihood of the presence of preclinical AD in individuals with SCD. This list is referred to as SCD plus.
1,626 citations
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Maastricht University Medical Centre1, deCODE genetics2, University of California, Los Angeles3, Utrecht University4, University of Oslo5, University of Bonn6, Ludwig Maximilian University of Munich7, Copenhagen University Hospital8, Wellcome Trust Sanger Institute9, Aarhus University Hospital10, Aarhus University11, University of Iceland12, University of Helsinki13, Bispebjerg Hospital14, Glostrup Hospital15, Heidelberg University16, Semmelweis University17, University of Verona18, Radboud University Nijmegen Medical Centre19, Russian Academy20, University of Valencia21, King's College London22, Royal Cornhill Hospital23, Duke University24, University of Santiago de Compostela25, Hospital General Universitario Gregorio Marañón26, Karolinska Institutet27, Hammersmith Hospital28, GlaxoSmithKline29, Sichuan University30
TL;DR: Findings implicating the MHC region are consistent with an immune component to schizophrenia risk, whereas the association with NRGN and TCF4 points to perturbation of pathways involved in brain development, memory and cognition.
Abstract: Schizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative risk of schizophrenia but also of other psychiatric disorders. The structural variations associated with schizophrenia can involve several genes and the phenotypic syndromes, or the 'genomic disorders', have not yet been characterized. Single nucleotide polymorphism (SNP)-based genome-wide association studies with the potential to implicate individual genes in complex diseases may reveal underlying biological pathways. Here we combined SNP data from several large genome-wide scans and followed up the most significant association signals. We found significant association with several markers spanning the major histocompatibility complex (MHC) region on chromosome 6p21.3-22.1, a marker located upstream of the neurogranin gene (NRGN) on 11q24.2 and a marker in intron four of transcription factor 4 (TCF4) on 18q21.2. Our findings implicating the MHC region are consistent with an immune component to schizophrenia risk, whereas the association with NRGN and TCF4 points to perturbation of pathways involved in brain development, memory and cognition.
1,625 citations
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TL;DR: It is shown that hyperactivity of the hypothalamic-pituitary-adrenal axis is one of the most consistent biological findings in major depression psychiatry, but the mechanisms underlying this abnormality are still unclear.
1,621 citations
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Francis Crick Institute1, Fox Chase Cancer Center2, Washington University in St. Louis3, Cold Spring Harbor Laboratory4, Howard Hughes Medical Institute5, Salk Institute for Biological Studies6, Cornell University7, Goethe University Frankfurt8, Fred Hutchinson Cancer Research Center9, Massachusetts Institute of Technology10, Harvard University11, University of Manchester12, New York University13, University of Texas Health Science Center at Houston14, University of Pennsylvania15, Stony Brook University16, Hofstra University17, Weizmann Institute of Science18, Oregon Health & Science University19, University of California, San Francisco20, King's College London21, Johns Hopkins University22
TL;DR: This Consensus Statement issues a call to action for all cancer researchers to standardize assays and report metadata in studies of cancer-associated fibroblasts to advance the understanding of this important cell type in the tumour microenvironment.
Abstract: Cancer-associated fibroblasts (CAFs) are a key component of the tumour microenvironment with diverse functions, including matrix deposition and remodelling, extensive reciprocal signalling interactions with cancer cells and crosstalk with infiltrating leukocytes. As such, they are a potential target for optimizing therapeutic strategies against cancer. However, many challenges are present in ongoing attempts to modulate CAFs for therapeutic benefit. These include limitations in our understanding of the origin of CAFs and heterogeneity in CAF function, with it being desirable to retain some antitumorigenic functions. On the basis of a meeting of experts in the field of CAF biology, we summarize in this Consensus Statement our current knowledge and present a framework for advancing our understanding of this critical cell type within the tumour microenvironment.
1,616 citations
Authors
Showing all 43962 results
Name | H-index | Papers | Citations |
---|---|---|---|
Cyrus Cooper | 204 | 1869 | 206782 |
David Miller | 203 | 2573 | 204840 |
Rob Knight | 201 | 1061 | 253207 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael Rutter | 188 | 676 | 151592 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
John Hardy | 177 | 1178 | 171694 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Barry Halliwell | 173 | 662 | 159518 |
Feng Zhang | 172 | 1278 | 181865 |
Simon Baron-Cohen | 172 | 773 | 118071 |
Phillip A. Sharp | 172 | 614 | 117126 |
Yang Yang | 171 | 2644 | 153049 |