Institution
Boston University
Education•Boston, Massachusetts, United States•
About: Boston University is a education organization based out in Boston, Massachusetts, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 48688 authors who have published 119622 publications receiving 6276020 citations. The organization is also known as: BU & Boston U.
Papers published on a yearly basis
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TL;DR: The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21 and provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome.
Abstract: Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. Several families have been described in which Alzheimer's disease is caused by an autosomal dominant gene defect. The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21. The localization on chromosome 21 provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome. Isolation and characterization of the gene at this locus may yield new insights into the nature of the defect causing familial Alzheimer's disease and possibly, into the etiology of all forms of Alzheimer's disease.
1,158 citations
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30 Aug 2004TL;DR: A general method based on a separation of the high-dimensional space occupied by a set of network traffic measurements into disjoint subspaces corresponding to normal and anomalous network conditions to diagnose anomalies is proposed.
Abstract: Anomalies are unusual and significant changes in a network's traffic levels, which can often span multiple links. Diagnosing anomalies is critical for both network operators and end users. It is a difficult problem because one must extract and interpret anomalous patterns from large amounts of high-dimensional, noisy data.In this paper we propose a general method to diagnose anomalies. This method is based on a separation of the high-dimensional space occupied by a set of network traffic measurements into disjoint subspaces corresponding to normal and anomalous network conditions. We show that this separation can be performed effectively by Principal Component Analysis.Using only simple traffic measurements from links, we study volume anomalies and show that the method can: (1) accurately detect when a volume anomaly is occurring; (2) correctly identify the underlying origin-destination (OD) flow which is the source of the anomaly; and (3) accurately estimate the amount of traffic involved in the anomalous OD flow.We evaluate the method's ability to diagnose (i.e., detect, identify, and quantify) both existing and synthetically injected volume anomalies in real traffic from two backbone networks. Our method consistently diagnoses the largest volume anomalies, and does so with a very low false alarm rate.
1,157 citations
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TL;DR: The reduction of atherosclerotic arterial disease (REACH) registry as discussed by the authors is an international, prospective cohort of 68,236 patients with either established coronary artery disease (CAD, PAD, CVD), or at least three risk factors for atherothrombosis (n = 12,422).
Abstract: ContextFew data document current cardiovascular (CV) event rates in stable patients with atherothrombosis in a community setting. Differential event rates for patients with documented coronary artery disease (CAD), cerebrovascular disease (CVD), or peripheral arterial disease (PAD) or those at risk of these diseases have not been previously evaluated in a single international cohort.ObjectiveTo establish contemporary, international, 1-year CV event rates in outpatients with established arterial disease or with multiple risk factors for atherothrombosis.Design, Setting, and ParticipantsThe Reduction of Atherothrombosis for Continued Health (REACH) Registry is an international, prospective cohort of 68 236 patients with either established atherosclerotic arterial disease (CAD, PAD, CVD; n = 55 814) or at least 3 risk factors for atherothrombosis (n = 12 422), who were enrolled from 5587 physician practices in 44 countries in 2003-2004.Main Outcome MeasuresRates of CV death, myocardial infarction (MI), and stroke.ResultsAs of July 2006, 1-year outcomes were available for 95.22% (n = 64 977) of participants. Cardiovascular death, MI, or stroke rates were 4.24% overall: 4.69% for those with established atherosclerotic arterial disease vs 2.15% for patients with multiple risk factors only. Among patients with established disease, CV death, MI, or stroke rates were 4.52% for patients with CAD, 6.47% for patients with CVD, and 5.35% for patients with PAD. The incidences of the end point of CV death, MI, or stroke or of hospitalization for atherothrombotic event(s) were 15.20% for CAD, 14.53% for CVD, and 21.14% for PAD patients with established disease. These event rates increased with the number of symptomatic arterial disease locations, ranging from 5.31% for patients with risk factors only to 12.58% for patients with 1, 21.14% for patients with 2, and 26.27% for patients with 3 symptomatic arterial disease locations (P<.001 for trend).ConclusionsIn this large, contemporary, international study, outpatients with established atherosclerotic arterial disease, or at risk of atherothrombosis, experienced relatively high annual CV event rates. Multiple disease locations increased the 1-year risk of CV events.
1,156 citations
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TL;DR: In this paper, the structural relationships of dimensions of key features of selected emotional disorders and dimensions of the tripartite model of anxiety and depression were tested using outpatients with mood disorders (N = 350).
Abstract: Using outpatients with anxiety and mood disorders (N = 350), Ihe authors tested several models of the structural relationships of dimensions of key features of selected emotional disorders and dimensions of the tripartite model of anxiety and depression. Results supported the discriminant validity of the 5 symptom domains examined (mood disorders; generalized anxiety disorder, GAD; panic disorder; obsessive-compulsive disorder; social phobia). Of various structural models evaluated, the best fitting involved a structure consistent with the tripartite model (e.g., the higher order factors, negative affect and positive affect, influenced emotional disorder factors in the expected manner). The latent factor, GAD, influenced the latent factor, autonomic arousal, in a direction consistent with recent laboratory findings (autonomic suppression). Findings are discussed in the context of the growing literature on higher order trait dimensions (e.g., negative affect) that may be of considerable importance to the understanding of the pathogenesis, course, and co-occurrence of emotional disorders.
1,150 citations
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TL;DR: The possibility that interventions to promote normal weight may reduce the population burden of AF is raised, as the excess risk of AF associated with obesity appears to be mediated by left atrial dilatation.
Abstract: ContextObesity is associated with atrial enlargement and ventricular diastolic
dysfunction, both known predictors of atrial fibrillation (AF). However, it
is unclear whether obesity is a risk factor for AF.ObjectiveTo examine the association between body mass index (BMI) and the risk
of developing AF.Design, Setting, and ParticipantsProspective, community-based observational cohort in Framingham, Mass.
We studied 5282 participants (mean age, 57 [SD, 13] years; 2898 women [55%])
without baseline AF (electrocardiographic AF or arterial flutter). Body mass
index (calculated as weight in kilograms divided by square of height in meters)
was evaluated as both a continuous and a categorical variable (normal defined
as <25.0; overweight, 25.0 to <30.0; and obese, ≥30.0). In addition
to adjusting for clinical confounders by multivariable techniques, we also
examined models including echocardiographic left atrial diameter to examine
whether the influence of obesity was mediated by changes in left atrial dimensions.Main Outcome MeasureAssociation between BMI or BMI category and risk of developing new-onset
AF.ResultsDuring a mean follow-up of 13.7 years, 526 participants (234 women)
developed AF. Age-adjusted incidence rates for AF increased across the 3 BMI
categories in men (9.7, 10.7, and 14.3 per 1000 person-years) and women (5.1,
8.6, and 9.9 per 1000 person-years). In multivariable models adjusted for
cardiovascular risk factors and interim myocardial infarction or heart failure,
a 4% increase in AF risk per 1-unit increase in BMI was observed in men (95%
confidence interval [CI], 1%-7%; P = .02)
and in women (95% CI, 1%-7%; P = .009).
Adjusted hazard ratios for AF associated with obesity were 1.52 (95% CI, 1.09-2.13; P = .02) and 1.46 (95% CI, 1.03-2.07; P = .03) for men and women, respectively, compared with individuals
with normal BMI. After adjustment for echocardiographic left atrial diameter
in addition to clinical risk factors, BMI was no longer associated with AF
risk (adjusted hazard ratios per 1-unit increase in BMI, 1.00 [95% CI, 0.97-1.04], P = .84 in men; 0.99 [95% CI, 0.96-1.02], P = .56 in women).ConclusionsObesity is an important, potentially modifiable risk factor for AF.
The excess risk of AF associated with obesity appears to be mediated by left
atrial dilatation. These prospective data raise the possibility that interventions
to promote normal weight may reduce the population burden of AF.
1,148 citations
Authors
Showing all 49233 results
Name | H-index | Papers | Citations |
---|---|---|---|
Walter C. Willett | 334 | 2399 | 413322 |
Robert Langer | 281 | 2324 | 326306 |
Meir J. Stampfer | 277 | 1414 | 283776 |
Ronald C. Kessler | 274 | 1332 | 328983 |
JoAnn E. Manson | 270 | 1819 | 258509 |
Albert Hofman | 267 | 2530 | 321405 |
George M. Whitesides | 240 | 1739 | 269833 |
Paul M. Ridker | 233 | 1242 | 245097 |
Eugene Braunwald | 230 | 1711 | 264576 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
David J. Hunter | 213 | 1836 | 207050 |
Daniel Levy | 212 | 933 | 194778 |
Christopher J L Murray | 209 | 754 | 310329 |
Tamara B. Harris | 201 | 1143 | 163979 |
André G. Uitterlinden | 199 | 1229 | 156747 |