Institution
University of Oxford
Education•Oxford, Oxfordshire, United Kingdom•
About: University of Oxford is a education organization based out in Oxford, Oxfordshire, United Kingdom. It is known for research contribution in the topics: Population & Context (language use). The organization has 99713 authors who have published 258108 publications receiving 12972806 citations. The organization is also known as: Oxford University & Oxon..
Topics: Population, Context (language use), Galaxy, Politics, Medicine
Papers published on a yearly basis
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Max Planck Society1, University of California, Berkeley2, University of California, Los Angeles3, University of California, Santa Barbara4, California Institute of Technology5, Tel Aviv University6, ETH Zurich7, University of Science and Technology of China8, Janssen Pharmaceutica9, University of Paris-Sud10, University of Oxford11, Yonsei University12
TL;DR: The Spectroscopic Imaging Survey in the near-infrared (near-IR) with SINFONI (SINS) of high-redshift galaxies is presented in this article.
Abstract: We present the Spectroscopic Imaging survey in the near-infrared (near-IR) with SINFONI (SINS) of high-redshift galaxies. With 80 objects observed and 63 detected in at least one rest-frame optical nebular emission line, mainly Hα, SINS represents the largest survey of spatially resolved gas kinematics, morphologies, and physical properties of star-forming galaxies at z ~ 1-3. We describe the selection of the targets, the observations, and the data reduction. We then focus on the "SINS Hα sample," consisting of 62 rest-UV/optically selected sources at 1.3 < z < 2.6 for which we targeted primarily the Hα and [N II] emission lines. Only ≈30% of this sample had previous near-IR spectroscopic observations. The galaxies were drawn from various imaging surveys with different photometric criteria; as a whole, the SINS Hα sample covers a reasonable representation of massive M_* ≳ 10^(10) M_☉ star-forming galaxies at z ≈ 1.5-2.5, with some bias toward bluer systems compared to pure K-selected samples due to the requirement of secure optical redshift. The sample spans 2 orders of magnitude in stellar mass and in absolute and specific star formation rates, with median values ≈3 × 10^(10) M_☉, ≈70 M_☉ yr^(–1), and ≈3 Gyr^(–1). The ionized gas distribution and kinematics are spatially resolved on scales ranging from ≈1.5 kpc for adaptive optics assisted observations to typically ≈4-5 kpc for seeing-limited data. The Hα morphologies tend to be irregular and/or clumpy. About one-third of the SINS Hα sample galaxies are rotation-dominated yet turbulent disks, another one-third comprises compact and velocity dispersion-dominated objects, and the remaining galaxies are clear interacting/merging systems; the fraction of rotation-dominated systems increases among the more massive part of the sample. The Hα luminosities and equivalent widths suggest on average roughly twice higher dust attenuation toward the H II regions relative to the bulk of the stars, and comparable current and past-averaged star formation rates.
1,219 citations
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TL;DR: In insights into the role of alcohol consumption in the genetic architecture of hypertension, a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions is conducted.
Abstract: Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in ≈131K individuals across several ancestry groups yielded 3,514 SNVs (245 loci) with suggestive evidence of association (P < 1.0 x 10-5). In Stage 2, these SNVs were tested for independent external replication in ≈440K individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2,159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 x 10-8). For African ancestry samples, we detected 18 potentially novel BP loci (P < 5.0 x 10-8) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2) have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension.
1,218 citations
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TL;DR: An explicit model for the evolution of complex disease loci is proposed, incorporating mutation, random genetic drift, and the possibility of purifying selection against susceptibility mutations, showing that, for the most plausible range of mutation rates, neutral susceptibility alleles are unlikely to be at intermediate frequencies and contribute little to the overall genetic variance for the disease.
Abstract: Little is known about the nature of genetic variation underlying complex diseases in humans. One popular view proposes that mapping efforts should focus on identification of susceptibility mutations that are relatively old and at high frequency. It is generally assumed—at least for modeling purposes—that selection against complex disease mutations is so weak that it can be ignored. In this article, I propose an explicit model for the evolution of complex disease loci, incorporating mutation, random genetic drift, and the possibility of purifying selection against susceptibility mutations. I show that, for the most plausible range of mutation rates, neutral susceptibility alleles are unlikely to be at intermediate frequencies and contribute little to the overall genetic variance for the disease. Instead, it seems likely that the bulk of genetic variance underlying diseases is due to loci where susceptibility mutations are mildly deleterious and where there is a high overall mutation rate to the susceptible class. At such loci, the total frequency of susceptibility mutations may be quite high, but there is likely to be extensive allelic heterogeneity at many of these loci. I discuss some practical implications of these results for gene mapping efforts.
1,218 citations
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TL;DR: The rationale for each of the 30 items on the STARD 2015 checklist is clarified, and what is expected from authors in developing sufficiently informative study reports is described.
Abstract: Diagnostic accuracy studies are, like other clinical studies, at risk of bias due to shortcomings in design and conduct, and the results of a diagnostic accuracy study may not apply to other patient groups and settings. Readers of study reports need to be informed about study design and conduct, in sufficient detail to judge the trustworthiness and applicability of the study findings. The STARD statement (Standards for Reporting of Diagnostic Accuracy Studies) was developed to improve the completeness and transparency of reports of diagnostic accuracy studies. STARD contains a list of essential items that can be used as a checklist, by authors, reviewers and other readers, to ensure that a report of a diagnostic accuracy study contains the necessary information. STARD was recently updated. All updated STARD materials, including the checklist, are available at http://www.equator-network.org/reporting-guidelines/stard. Here, we present the STARD 2015 explanation and elaboration document. Through commented examples of appropriate reporting, we clarify the rationale for each of the 30 items on the STARD 2015 checklist, and describe what is expected from authors in developing sufficiently informative study reports.
1,217 citations
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TL;DR: The third edition of the International Classification of Diseases for Oncology (ICD‐O‐3), which was published in 2000, introduced major changes in coding and classification of neoplasms, notably for leukemias and lymphomas, which are important groups of cancer types that occur in childhood.
Abstract: BACKGROUND
The third edition of the International Classification of Diseases for Oncology (ICD-O-3), which was published in 2000, introduced major changes in coding and classification of neoplasms, notably for leukemias and lymphomas, which are important groups of cancer types that occur in childhood. This necessitated a third revision of the 1996 International Classification of Childhood Cancer (ICCC-3).
METHODS
The tumor categories for the ICCC-3 were designed to respect several principles: agreement with current international standards, integration of the entities defined by newly developed diagnostic techniques, continuity with previous childhood classifications, and exhaustiveness.
RESULTS
The ICCC-3 classifies tumors coded according to the ICD-O-3 into 12 main groups, which are split further into 47 subgroups. These 2 levels of the ICCC-3 allow standardized comparisons of the broad categories of childhood neoplasms in continuity with the previous classifications. The 16 most heterogeneous subgroups are broken down further into 2–11 divisions to allow study of important entities or homogeneous collections of tumors characterized at the cytogenetic or molecular level. Some divisions may be combined across the higher-level categories, such as the B-cell neoplasms within leukemias and lymphomas.
CONCLUSIONS
The ICCC-3 respects currently existing international standards and was designed for use in international, population-based, epidemiological studies and cancer registries. The use of an international classification system is especially important in the field of pediatric oncology, in which the low frequency of cases requires rigorous procedures to ensure data comparability. Cancer 2005. © 2005 American Cancer Society.
1,217 citations
Authors
Showing all 101421 results
Name | H-index | Papers | Citations |
---|---|---|---|
Eric S. Lander | 301 | 826 | 525976 |
Albert Hofman | 267 | 2530 | 321405 |
Douglas G. Altman | 253 | 1001 | 680344 |
Salim Yusuf | 231 | 1439 | 252912 |
George Davey Smith | 224 | 2540 | 248373 |
Yi Chen | 217 | 4342 | 293080 |
David J. Hunter | 213 | 1836 | 207050 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
Christopher J L Murray | 209 | 754 | 310329 |
Cyrus Cooper | 204 | 1869 | 206782 |
Mark J. Daly | 204 | 763 | 304452 |
David Miller | 203 | 2573 | 204840 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Raymond J. Dolan | 196 | 919 | 138540 |
Frank E. Speizer | 193 | 636 | 135891 |