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Institution

St George's, University of London

EducationLondon, United Kingdom
About: St George's, University of London is a education organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Health care. The organization has 4953 authors who have published 11675 publications receiving 574153 citations. The organization is also known as: SGUL & St George's Hospital Medical School.


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Journal ArticleDOI
TL;DR: The implementation of an hs-cTnI assay was evaluated in consecutive patients who had been admitted to the hospitals' emergency departments with suspected acute coronary syndrome and its findings question whether the diagnostic threshold for myocardial infarction should be based on the 99th centile derived from a normal reference population.

240 citations

Journal ArticleDOI
TL;DR: These results strengthen the evidence linking long-term ambient air pollution exposure to increased all-cause mortality, however, the stronger associations with respiratory mortality are not consistent with most US studies in which associations with cardiovascular causes of death tend to predominate.
Abstract: Rationale: Cohort evidence linking long-term exposure to outdoor particulate air pollution and mortality has come largely from the United States. There is relatively little evidence from nationally representative cohorts in other countries. Objectives: To investigate the relationship between long-term exposure to a range of pollutants and causes of death in a national English cohort. Methods: A total of 835,607 patients aged 40–89 years registered with 205 general practices were followed from 2003–2007. Annual average concentrations in 2002 for particulate matter with a median aerodynamic diameter less than 10 (PM10) and less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), ozone, and sulfur dioxide (SO2) at 1 km2 resolution, estimated from emission-based models, were linked to residential postcode. Deaths (n = 83,103) were ascertained from linkage to death certificates, and hazard ratios (HRs) for all- and cause-specific mortality for pollutants were estimated for interquartile pollutant changes from Cox models adjusting for age, sex, smoking, body mass index, and area-level socioeconomic status markers. Measurements and Main Results: Residential concentrations of all pollutants except ozone were positively associated with all-cause mortality (HR, 1.02, 1.03, and 1.04 for PM2.5, NO2, and SO2, respectively). Associations for PM2.5, NO2, and SO2 were larger for respiratory deaths (HR, 1.09 each) and lung cancer (HR, 1.02, 1.06, and 1.05) but nearer unity for cardiovascular deaths (1.00, 1.00, and 1.04). Conclusions: These results strengthen the evidence linking long-term ambient air pollution exposure to increased all-cause mortality. However, the stronger associations with respiratory mortality are not consistent with most US studies in which associations with cardiovascular causes of death tend to predominate.

240 citations

Journal ArticleDOI
Louise V. Wain1, Louise V. Wain2, Nick Shrine1, María Soler Artigas1, A. Mesut Erzurumluoglu1, Boris Noyvert1, Lara Bossini-Castillo3, Ma'en Obeidat4, Amanda P. Henry5, Michael A. Portelli5, Robert J. Hall5, Charlotte K. Billington5, Tracy L. Rimington5, Anthony G. Fenech6, Catherine John1, Tineka Blake1, Victoria E. Jackson1, Richard J. Allen1, Bram P. Prins3, Archie Campbell7, David J. Porteous7, Marjo-Riitta Järvelin8, Marjo-Riitta Järvelin9, Matthias Wielscher8, Alan James10, Alan James11, Jennie Hui11, Jennie Hui10, Nicholas J. Wareham12, Jing Hua Zhao12, James F. Wilson7, Peter K. Joshi7, Beate Stubbe13, Rajesh Rawal14, Holger Schulz, Medea Imboden15, Nicole Probst-Hensch15, Stefan Karrasch16, Christian Gieger14, Ian J. Deary7, Sarah E. Harris7, Jonathan Marten7, Igor Rudan7, Stefan Enroth17, Ulf Gyllensten17, Shona M. Kerr7, Ozren Polasek18, Ozren Polasek7, Mika Kähönen19, Ida Surakka20, Veronique Vitart7, Caroline Hayward7, Terho Lehtimäki19, Olli T. Raitakari21, David M. Evans22, David M. Evans23, A. John Henderson23, Craig E. Pennell10, Carol A. Wang10, Peter D. Sly22, Emily S. Wan24, Robert Busch24, Brian D. Hobbs24, Augusto A. Litonjua24, David Sparrow25, Amund Gulsvik26, Per Bakke26, James D. Crapo27, Terri H. Beaty28, Nadia N. Hansel28, Rasika A. Mathias28, Ingo Ruczinski28, Kathleen C. Barnes29, Yohan Bossé30, Philippe Joubert31, Maarten van den Berge32, Corry-Anke Brandsma32, Peter D. Paré4, Don D. Sin4, David C. Nickle33, Ke Hao34, Omri Gottesman35, Frederick E. Dewey35, Shannon Bruse35, David J. Carey36, H. Lester Kirchner36, Stefan Jonsson37, Gudmar Thorleifsson37, Ingileif Jonsdottir37, Ingileif Jonsdottir38, Thorarinn Gislason38, Kari Stefansson38, Kari Stefansson37, Claudia Schurmann34, Girish N. Nadkarni34, Erwin P. Bottinger34, Ruth J. F. Loos34, Robin G. Walters39, Zhengming Chen39, Iona Y Millwood39, Julien Vaucher39, Om P Kurmi39, Liming Li40, Liming Li41, Anna Hansell8, Christopher E. Brightling1, Christopher E. Brightling2, Eleftheria Zeggini3, Michael H. Cho24, Edwin K. Silverman24, Ian Sayers5, Gosia Trynka3, Andrew P. Morris42, David P. Strachan43, Ian P. Hall5, Martin D. Tobin1, Martin D. Tobin2 
TL;DR: In this article, a genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (∼6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 × 10(-49)), and they observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest GA risk score deciles in UK Biobank.
Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is the third leading cause of death globally. Through genome-wide association discovery in 48,943 individuals, selected from extremes of the lung function distribution in UK Biobank, and follow-up in 95,375 individuals, we increased the yield of independent signals for lung function from 54 to 97. A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (∼6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 × 10(-49)), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest genetic risk score deciles in UK Biobank. The 97 signals show enrichment in genes for development, elastic fibers and epigenetic regulation pathways. We highlight targets for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and describe targets for potential drug repositioning from other clinical indications.

240 citations

Journal ArticleDOI
TL;DR: TB meningitis is probably underdiagnosed by laboratory investigation, as evidence by the large numbers presenting with sterile lymphocytic markedly abnormal CSFs.
Abstract: The presentation and causes of adult meningitis in South Africa have changed substantially as a result of HIV. Knowledge of aetiology and laboratory findings in patients presenting with meningitis are important in guiding management. We performed a retrospective study to determine these findings in a setting of high HIV and TB prevalence in Cape Town. Patients undergoing lumbar punctures between 1st January 2006 and 31st December 2008 at a public sector referral hospital were studied. Cases were classified by microbiological diagnosis, or in the absence of definitive microbiology as 1) normal CSF (neutrophils ≤ 1 × 106/L, lymphocytes ≤ 5 × 106/L, protein ≤ 0.5 g/dL, glucose ≥1.5 mmol/L), 2) minor abnormalities (neutrophils 2-5, lymphocytes 6-20, protein 0.51-1.0, glucose 1.0-1.49) or 3) markedly abnormal (neutrophils>5, lymphocytes>20, protein>1.0, glucose<1.0). 5578 LPs were performed on 4549 patients, representing 4961 clinical episodes. Of these, 2293 had normal CSF and 931 had minor abnormalities and no aetiology identified. Of the remaining 1737, microbiological diagnoses were obtained in 820 (47%). Cryptococcus accounted for 63% (514) of microbiological diagnoses, TB for 28% (227), bacterial meningitis for 8% (68). Of the remaining 917 who had marked abnormalities, the majority (59%) had a sterile lymphocytic CSF. Of note 16% (81) patients with confirmed Cryptococcus, 5% (12) with TB and 4% (3) with bacterial meningitis had normal CSF cell-counts and biochemistry. Cryptococcal and tuberculous meningitis are now the commonest causes of adult meningitis in this setting. TB meningitis is probably underdiagnosed by laboratory investigation, as evidence by the large numbers presenting with sterile lymphocytic markedly abnormal CSFs.

239 citations

Journal ArticleDOI
TL;DR: Evidence is found linking long-term exposure to particulate matter and NO2 with the development of heart failure in an English national cohort, which did not replicate associations for other cardiovascular outcomes that have been reported elsewhere.
Abstract: Background:Evidence based largely on US cohorts suggests that long-term exposure to fine particulate matter is associated with cardiovascular mortality. There is less evidence for other pollutants and for cardiovascular morbidity. By using a cohort of 836,557 patients age 40 to 89 years registered w

238 citations


Authors

Showing all 5006 results

NameH-indexPapersCitations
JoAnn E. Manson2701819258509
Paul M. Ridker2331242245097
George Davey Smith2242540248373
Peer Bork206697245427
Grant W. Montgomery157926108118
Naveed Sattar1551326116368
Alan S. Verkman14677170434
David P. Strachan143472105256
Sekar Kathiresan14147998784
Nick C. Fox13974893036
Andrew Steptoe137100373431
Daniel I. Chasman13448472180
Joel N. Hirschhorn133431101061
Dan M. Roden13285967578
Hugh Watkins12852491317
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202313
202293
20211,153
2020999
2019873
2018789