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Institution

University of Michigan

EducationAnn Arbor, Michigan, United States
About: University of Michigan is a education organization based out in Ann Arbor, Michigan, United States. It is known for research contribution in the topics: Computer science & Chemistry. The organization has 138538 authors who have published 342338 publications receiving 17638979 citations. The organization is also known as: UMich & UM.


Papers
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Book
01 Jan 1998
TL;DR: In Emergence, John Holland dramatically shows that a theory of emergence can predict many complex behaviors, and has much to teach us about life, the mind, and organizations.
Abstract: From the Publisher: From one of today's most innovative thinkers comes the first book to carefully explore emergence - a surprisingly simple notion (the whole is more than the sum of its parts) with enormous implications for science, business, and the arts. In this work, John Holland, a leader in the study of complexity at the Santa Fe Institute, dramatically shows that a theory of emergence can predict many complex behaviors, and has much to teach us about life, the mind, and organizations. In Emergence, Holland demonstrates that a small number of rules of laws can generate systems of surprising complexity. Board games provide an ancient and direct example: Chess is defined by fewer than two dozen rules, but the myriad patterns that result lead to perpetual novelty and emergence. It took centuries of study to recognize certain patterns of play, such as the control of pawn formations. But once recognized, these patterns greatly enhance the possibility of winning the game. The discovery of similar patterns in other facets of our world opens the way to a deeper understanding of the complexity of life, answering such questions as: How does a fertilized egg program the development of a trillion-cell organism? How can we build human organizations that respond rapidly to change through innovation? Throughout the book, Holland compares different systems and models that exhibit emergence in the quest for common rules or laws.

1,881 citations

Journal ArticleDOI
TL;DR: This work derives CRBs and maximum-likelihood estimators (MLEs) under Gaussian and log-normal models for the TOA and RSS measurements, respectively for sensor location estimation when sensors measure received signal strength or time-of-arrival between themselves and neighboring sensors.
Abstract: Self-configuration in wireless sensor networks is a general class of estimation problems that we study via the Cramer-Rao bound (CRB). Specifically, we consider sensor location estimation when sensors measure received signal strength (RSS) or time-of-arrival (TOA) between themselves and neighboring sensors. A small fraction of sensors in the network have a known location, whereas the remaining locations must be estimated. We derive CRBs and maximum-likelihood estimators (MLEs) under Gaussian and log-normal models for the TOA and RSS measurements, respectively. An extensive TOA and RSS measurement campaign in an indoor office area illustrates MLE performance. Finally, relative location estimation algorithms are implemented in a wireless sensor network testbed and deployed in indoor and outdoor environments. The measurements and testbed experiments demonstrate 1-m RMS location errors using TOA, and 1- to 2-m RMS location errors using RSS.

1,881 citations

Journal ArticleDOI
TL;DR: In this paper, the authors provide a theoretical analysis of the process of competition for control of the target and empirical evidence that competition among bidding firms increases the returns to targets and decreases the return to acquirers, and that the supply of target shares is positively sloped.

1,880 citations

Journal ArticleDOI
TL;DR: It is reported that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation and may further explain the epidemiological association of infection with thrombosis.
Abstract: Neutrophil extracellular traps (NETs) are part of the innate immune response to infections. NETs are a meshwork of DNA fibers comprising histones and antimicrobial proteins. Microbes are immobilized in NETs and encounter a locally high and lethal concentration of effector proteins. Recent studies show that NETs are formed inside the vasculature in infections and noninfectious diseases. Here we report that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation. NETs perfused with blood caused platelet adhesion, activation, and aggregation. DNase or the anticoagulant heparin dismantled the NET scaffold and prevented thrombus formation. Stimulation of platelets with purified histones was sufficient for aggregation. NETs recruited red blood cells, promoted fibrin deposition, and induced a red thrombus, such as that found in veins. Markers of extracellular DNA traps were detected in a thrombus and plasma of baboons subjected to deep vein thrombosis, an example of inflammation-enhanced thrombosis. Our observations indicate that NETs are a previously unrecognized link between inflammation and thrombosis and may further explain the epidemiological association of infection with thrombosis.

1,880 citations

Journal ArticleDOI
Benjamin F. Voight1, Benjamin F. Voight2, Benjamin F. Voight3, Gina M. Peloso4, Gina M. Peloso5, Marju Orho-Melander6, Ruth Frikke-Schmidt7, Maja Barbalić8, Majken K. Jensen2, George Hindy6, Hilma Holm9, Eric L. Ding2, Toby Johnson10, Heribert Schunkert11, Nilesh J. Samani12, Nilesh J. Samani13, Robert Clarke14, Jemma C. Hopewell14, John F. Thompson13, Mingyao Li3, Gudmar Thorleifsson9, Christopher Newton-Cheh, Kiran Musunuru2, Kiran Musunuru1, James P. Pirruccello1, James P. Pirruccello2, Danish Saleheen15, Li Chen16, Alexandre F.R. Stewart16, Arne Schillert11, Unnur Thorsteinsdottir17, Unnur Thorsteinsdottir9, Gudmundur Thorgeirsson17, Sonia S. Anand18, James C. Engert19, Thomas M. Morgan20, John A. Spertus21, Monika Stoll22, Klaus Berger22, Nicola Martinelli23, Domenico Girelli23, Pascal P. McKeown24, Christopher Patterson24, Stephen E. Epstein25, Joseph M. Devaney25, Mary Susan Burnett25, Vincent Mooser26, Samuli Ripatti27, Ida Surakka27, Markku S. Nieminen27, Juha Sinisalo27, Marja-Liisa Lokki27, Markus Perola5, Aki S. Havulinna5, Ulf de Faire28, Bruna Gigante28, Erik Ingelsson28, Tanja Zeller29, Philipp S. Wild29, Paul I.W. de Bakker, Olaf H. Klungel30, Anke-Hilse Maitland-van der Zee30, Bas J M Peters30, Anthonius de Boer30, Diederick E. Grobbee30, Pieter Willem Kamphuisen31, Vera H.M. Deneer, Clara C. Elbers30, N. Charlotte Onland-Moret30, Marten H. Hofker31, Cisca Wijmenga31, W. M. Monique Verschuren, Jolanda M. A. Boer, Yvonne T. van der Schouw30, Asif Rasheed, Philippe M. Frossard, Serkalem Demissie4, Serkalem Demissie5, Cristen J. Willer32, Ron Do2, Jose M. Ordovas33, Jose M. Ordovas34, Gonçalo R. Abecasis32, Michael Boehnke32, Karen L. Mohlke35, Mark J. Daly1, Mark J. Daly2, Candace Guiducci1, Noël P. Burtt1, Aarti Surti1, Elena Gonzalez1, Shaun Purcell1, Shaun Purcell2, Stacey Gabriel1, Jaume Marrugat, John F. Peden14, Jeanette Erdmann11, Patrick Diemert11, Christina Willenborg11, Inke R. König11, Marcus Fischer36, Christian Hengstenberg36, Andreas Ziegler11, Ian Buysschaert37, Diether Lambrechts37, Frans Van de Werf37, Keith A.A. Fox38, Nour Eddine El Mokhtari39, Diana Rubin, Jürgen Schrezenmeir, Stefan Schreiber39, Arne Schäfer39, John Danesh15, Stefan Blankenberg29, Robert Roberts16, Ruth McPherson16, Hugh Watkins14, Alistair S. Hall40, Kim Overvad41, Eric B. Rimm2, Eric Boerwinkle8, Anne Tybjærg-Hansen7, L. Adrienne Cupples5, L. Adrienne Cupples4, Muredach P. Reilly3, Olle Melander6, Pier Mannuccio Mannucci42, Diego Ardissino, David S. Siscovick43, Roberto Elosua, Kari Stefansson17, Kari Stefansson9, Christopher J. O'Donnell2, Christopher J. O'Donnell5, Veikko Salomaa5, Daniel J. Rader3, Leena Peltonen44, Leena Peltonen27, Stephen M. Schwartz43, David Altshuler, Sekar Kathiresan 
11 Aug 2012
TL;DR: In this paper, a Mendelian randomisation analysis was performed to compare the effect of HDL cholesterol, LDL cholesterol, and genetic score on risk of myocardial infarction.
Abstract: Methods We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20 913 myocardial infarction cases, 95 407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12 482 cases of myocardial infarction and 41 331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol. – ¹³) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with noncarriers. This diff erence in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84–0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88–1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58–0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93, 95% CI 0·68–1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45–1·63) was concordant with that from genetic score (OR 2·13, 95% CI 1·69–2·69, p=2×10

1,878 citations


Authors

Showing all 142736 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Robert Langer2812324326306
Ronald C. Kessler2741332328983
Graham A. Colditz2611542256034
George M. Whitesides2401739269833
Salim Yusuf2311439252912
Richard A. Flavell2311328205119
John Q. Trojanowski2261467213948
Irving L. Weissman2011141172504
Francis S. Collins196743250787
Eric B. Rimm196988147119
Robert M. Califf1961561167961
Martin White1962038232387
Craig B. Thompson195557173172
Eric J. Topol1931373151025
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
2023508
2022375,426
202117,451
202017,549
201916,234