Institution
Northwestern University
Education•Evanston, Illinois, United States•
About: Northwestern University is a education organization based out in Evanston, Illinois, United States. It is known for research contribution in the topics: Population & Transplantation. The organization has 75430 authors who have published 188857 publications receiving 9463252 citations. The organization is also known as: Northwestern & NU.
Topics: Population, Transplantation, Cancer, Health care, Poison control
Papers published on a yearly basis
Papers
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TL;DR: Data support the hypothesis that high CACS can modify predicted risk obtained from FRS alone, especially among patients in the intermediate-risk category in whom clinical decision making is most uncertain.
Abstract: ContextGuidelines advise that all adults undergo coronary heart disease (CHD)
risk assessment to guide preventive treatment intensity. Although the Framingham
Risk Score (FRS) is often recommended for this, it has been suggested that
risk assessment may be improved by additional tests such as coronary artery
calcium scoring (CACS).ObjectivesTo determine whether CACS assessment combined with FRS in asymptomatic
adults provides prognostic information superior to either method alone and
whether the combined approach can more accurately guide primary preventive
strategies in patients with CHD risk factors.Design, Setting, and ParticipantsProspective observational population-based study, of 1461 asymptomatic
adults with coronary risk factors. Participants with at least 1 coronary risk
factor (>45 years) underwent computed tomography (CT) examination, were screened
between 1990-1992, were contacted yearly for up to 8.5 years after CT scan,
and were assessed for CHD. This analysis included 1312 participants with CACS
results; excluded were 269 participants with diabetes and 14 participants
with either missing data or had a coronary event before CACS was performed.Main Outcome MeasureNonfatal myocardial infarction (MI) or CHD death.ResultsDuring a median of 7.0 years of follow-up, 84 patients experienced MI
or CHD death; 70 patients died of any cause. There were 291 (28%) participants
with an FRS of more than 20% and 221 (21%) with a CACS of more than 300. Compared
with an FRS of less than 10%, an FRS of more than 20% predicted the risk of
MI or CHD death (hazard ratio [HR], 14.3; 95% confidence interval [CI]; 2.0-104; P = .009). Compared with a CACS of zero, a CACS of more
than 300 was predictive (HR, 3.9; 95% CI, 2.1-7.3; P<.001).
Across categories of FRS, CACS was predictive of risk among patients with
an FRS higher than 10% (P<.001) but not with an
FRS less than 10%.ConclusionThese data support the hypothesis that high CACS can modify predicted
risk obtained from FRS alone, especially among patients in the intermediate-risk
category in whom clinical decision making is most uncertain.
1,759 citations
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TL;DR: In this article, the authors present a survey of self-interference mitigation techniques for in-band full-duplex (IBFD) wireless systems and discuss the challenges and opportunities in the design and analysis of IBFD wireless systems.
Abstract: In-band full-duplex (IBFD) operation has emerged as an attractive solution for increasing the throughput of wireless communication systems and networks. With IBFD, a wireless terminal is allowed to transmit and receive simultaneously in the same frequency band. This tutorial paper reviews the main concepts of IBFD wireless. One of the biggest practical impediments to IBFD operation is the presence of self-interference, i.e., the interference that the modem's transmitter causes to its own receiver. This tutorial surveys a wide range of IBFD self-interference mitigation techniques. Also discussed are numerous other research challenges and opportunities in the design and analysis of IBFD wireless systems.
1,752 citations
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Harvard University1, Hospital de Base2, The Heart Research Institute3, University of Groningen4, University of Erlangen-Nuremberg5, University of Wisconsin-Madison6, Northwestern University7, Tufts University8, Washington University in St. Louis9, St. John's University10, University of Copenhagen11, Aarhus University12, University of Texas Southwestern Medical Center13
TL;DR: The use of darbepoetin alfa in patients with diabetes, chronic kidney disease, and moderate anemia who were not undergoing dialysis did not reduce the risk of either of the two primary composite outcomes (either death or a cardiovascular event ordeath or a renal event) and was associated with an increased risk of stroke.
Abstract: Background Anemia is associated with an increased risk of cardiovascular and renal events among patients with type 2 diabetes and chronic kidney disease. Although darbepoetin alfa can effectively increase hemoglobin levels, its effect on clinical outcomes in these patients has not been adequately tested. Methods In this study involving 4038 patients with diabetes, chronic kidney disease, and anemia, we randomly assigned 2012 patients to darbepoetin alfa to achieve a hemoglobin level of approximately 13 g per deciliter and 2026 patients to placebo, with rescue darbepoetin alfa when the hemoglobin level was less than 9.0 g per deciliter. The primary end points were the composite outcomes of death or a cardiovascular event (nonfatal myocardial infarction, congestive heart failure, stroke, or hospitalization for myocardial ischemia) and of death or end-stage renal disease. Results Death or a cardiovascular event occurred in 632 patients assigned to darbepoetin alfa and 602 patients assigned to placebo (hazard...
1,750 citations
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TL;DR: It is shown that renin expression and plasma angiotensin II production were increased severalfold in vitamin D receptor-null (VDR-null) mice, leading to hypertension, cardiac hypertrophy, and increased water intake, and 1,25(OH)(2)D(3) is a novel negative endocrine regulator of the renin-angiotens in system.
Abstract: Inappropriate activation of the renin-angiotensin system, which plays a central role in the regulation of blood pressure, electrolyte, and volume homeostasis, may represent a major risk factor for hypertension, heart attack, and stroke. Mounting evidence from clinical studies has demonstrated an inverse relationship between circulating vitamin D levels and the blood pressure and/or plasma renin activity, but the mechanism is not understood. We show here that renin expression and plasma angiotensin II production were increased severalfold in vitamin D receptor-null (VDR-null) mice, leading to hypertension, cardiac hypertrophy, and increased water intake. However, the salt- and volume-sensing mechanisms that control renin synthesis are still intact in the mutant mice. In wild-type mice, inhibition of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] synthesis also led to an increase in renin expression, whereas 1,25(OH)(2)D(3) injection led to renin suppression. We found that vitamin D regulation of renin expression was independent of calcium metabolism and that 1,25(OH)(2)D(3) markedly suppressed renin transcription by a VDR-mediated mechanism in cell cultures. Hence, 1,25(OH)(2)D(3) is a novel negative endocrine regulator of the renin-angiotensin system. Its apparent critical role in electrolytes, volume, and blood pressure homeostasis suggests that vitamin D analogues could help prevent or ameliorate hypertension.
1,744 citations
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TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
Abstract: The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). Both joint analysis and meta-analysis approaches were used. We obtained genome-wide significant results at MS4A4A (rs4938933; stages 1 and 2, meta-analysis P (P(M)) = 1.7 × 10(-9), joint analysis P (P(J)) = 1.7 × 10(-9); stages 1, 2 and 3, P(M) = 8.2 × 10(-12)), CD2AP (rs9349407; stages 1, 2 and 3, P(M) = 8.6 × 10(-9)), EPHA1 (rs11767557; stages 1, 2 and 3, P(M) = 6.0 × 10(-10)) and CD33 (rs3865444; stages 1, 2 and 3, P(M) = 1.6 × 10(-9)). We also replicated previous associations at CR1 (rs6701713; P(M) = 4.6 × 10(-10), P(J) = 5.2 × 10(-11)), CLU (rs1532278; P(M) = 8.3 × 10(-8), P(J) = 1.9 × 10(-8)), BIN1 (rs7561528; P(M) = 4.0 × 10(-14), P(J) = 5.2 × 10(-14)) and PICALM (rs561655; P(M) = 7.0 × 10(-11), P(J) = 1.0 × 10(-10)), but not at EXOC3L2, to late-onset Alzheimer's disease susceptibility.
1,743 citations
Authors
Showing all 76189 results
Name | H-index | Papers | Citations |
---|---|---|---|
George M. Whitesides | 240 | 1739 | 269833 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
Daniel Levy | 212 | 933 | 194778 |
David Miller | 203 | 2573 | 204840 |
Ronald M. Evans | 199 | 708 | 166722 |
Michael Marmot | 193 | 1147 | 170338 |
Robert C. Nichol | 187 | 851 | 162994 |
Scott M. Grundy | 187 | 841 | 231821 |
Stuart H. Orkin | 186 | 715 | 112182 |
Michael A. Strauss | 185 | 1688 | 208506 |
Ralph Weissleder | 184 | 1160 | 142508 |
Patrick O. Brown | 183 | 755 | 200985 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Valentin Fuster | 179 | 1462 | 185164 |
Ronald C. Petersen | 178 | 1091 | 153067 |