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Institution

Boston University

EducationBoston, 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.


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Journal ArticleDOI
22 Oct 1997-JAMA
TL;DR: The APOE∈4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women.
Abstract: Objective. —To examine more closely the association between apolipoprotein E (APOE) genotype and Alzheimer disease (AD) by age and sex in populations of various ethnic and racial denominations. Data Sources. —Forty research teams contributed data onAPOEgenotype, sex, age at disease onset, and ethnic background for 5930 patients who met criteria for probable or definite AD and 8607 controls without dementia who were recruited from clinical, community, and brain bank sources. Main Outcome Measures. —Odds ratios (ORs) and 95% confidence intervals (Cls) for AD, adjusted for age and study and stratified by major ethnic group (Caucasian, African American, Hispanic, and Japanese) and source, were computed forAPOEgenotypes ∈2/∈2,∈2/∈3,∈2/∈4,∈3/∈4 and ∈4/∈4 relative to the ∈3/∈3 group. The influence of age and sex on the OR for each genotype was assessed using logistic regression procedures. Results. —Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes ∈2/∈4 (OR=2.6, 95% Cl=1.6-4.0), ∈3/∈4 (OR=3.2, 95% Cl=2.8-3.8), and ∈4/∈4 (OR=14.9, 95% CI=10.8-20.6); whereas, the ORs were decreased for people with genotypes ∈2/∈2 (OR=0.6, 95% Cl=0.2-2.0) and ∈2/∈3 (OR=0.6, 95% Cl=0.5-0.8). TheAPOE∈4-AD association was weaker among African Americans and Hispanics, but there was significant heterogeneity in ORs among studies of African Americans (P Conclusions. —TheAPOE∈4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women. The association betweenAPOE∈4 and AD in African Americans requires clarification, and the attenuated effect ofAPOE∈4 in Hispanics should be investigated further.

3,825 citations

Journal ArticleDOI
Y. Fukuda1, T. Hayakawa1, E. Ichihara1, Kunio Inoue1, K. Ishihara1, H. Ishino1, Yoshitaka Itow1, Takaaki Kajita1, J. Kameda1, S. Kasuga1, Ken-ichiro Kobayashi1, Yohei Kobayashi1, Yusuke Koshio1, M. Miura1, Masayuki Nakahata1, S. Nakayama1, A. Okada1, Ko Okumura1, N. Sakurai1, Masato Shiozawa1, Yoshihiro Suzuki1, Y. Takeuchi1, Y. Totsuka1, Shinya Yamada1, M. Earl2, Alec Habig2, E. Kearns2, M. D. Messier2, Kate Scholberg2, J. L. Stone2, Lawrence Sulak2, C. W. Walter2, M. Goldhaber3, T. Barszczxak4, D. Casper4, W. Gajewski4, P. G. Halverson4, J. Hsu4, W. R. Kropp4, L. R. Price4, Frederick Reines4, Michael B. Smy4, Henry W. Sobel4, Mark R. Vagins4, K. S. Ganezer5, W. E. Keig5, R. W. Ellsworth6, S. Tasaka7, J. W. Flanagan8, A. Kibayashi8, John G. Learned8, S. Matsuno8, V. J. Stenger8, D. Takemori8, T. Ishii, Junichi Kanzaki, T. Kobayashi, S. Mine, K. Nakamura, K. Nishikawa, Yuichi Oyama, A. Sakai, Makoto Sakuda, Osamu Sasaki, S. Echigo9, M. Kohama9, A. T. Suzuki9, Todd Haines10, Todd Haines4, E. Blaufuss11, B. K. Kim11, R. Sanford11, R. Svoboda11, M. L. Chen12, Z. Conner12, Z. Conner13, J. A. Goodman12, G. W. Sullivan12, J. Hill14, C. K. Jung14, K. Martens14, C. Mauger14, C. McGrew14, E. Sharkey14, B. Viren14, C. Yanagisawa14, W. Doki15, Kazumasa Miyano15, H. Okazawa15, C. Saji15, M. Takahata15, Y. Nagashima16, M. Takita16, Takashi Yamaguchi16, Minoru Yoshida16, Soo-Bong Kim17, M. Etoh18, K. Fujita18, Akira Hasegawa18, Takehisa Hasegawa18, S. Hatakeyama18, T. Iwamoto18, M. Koga18, Tomoyuki Maruyama18, Hiroshi Ogawa18, J. Shirai18, A. Suzuki18, F. Tsushima18, Masatoshi Koshiba1, M. Nemoto19, Kyoshi Nishijima19, T. Futagami20, Y. Hayato20, Y. Kanaya20, K. Kaneyuki20, Y. Watanabe20, D. Kielczewska21, D. Kielczewska4, R. A. Doyle22, J. S. George22, A. L. Stachyra22, L. Wai23, L. Wai22, R. J. Wilkes22, K. K. Young22 
Abstract: We present an analysis of atmospheric neutrino data from a 33.0 kton yr (535-day) exposure of the Super-Kamiokande detector. The data exhibit a zenith angle dependent deficit of muon neutrinos which is inconsistent with expectations based on calculations of the atmospheric neutrino flux. Experimental biases and uncertainties in the prediction of neutrino fluxes and cross sections are unable to explain our observation. The data are consistent, however, with two-flavor ${\ensuremath{ u}}_{\ensuremath{\mu}}\ensuremath{\leftrightarrow}{\ensuremath{ u}}_{\ensuremath{\tau}}$ oscillations with ${sin}^{2}2\ensuremath{\theta}g0.82$ and $5\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}4}l\ensuremath{\Delta}{m}^{2}l6\ifmmode\times\else\texttimes\fi{}1{0}^{\ensuremath{-}3}\mathrm{eV}{}^{2}$ at 90% confidence level.

3,784 citations

Journal ArticleDOI
TL;DR: In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
Abstract: Eleven susceptibility loci for late-onset Alzheimer's disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer's disease cases and 37,154 controls. In stage 2, 11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer's disease cases and 11,312 controls. In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.

3,726 citations

Journal ArticleDOI
TL;DR: The author discusses the pros and cons of implementing an enterprise system, showing how a system can produce unintended and highly disruptive consequences and cautions against shifting responsibility for its adoption to technologists.
Abstract: Enterprise systems present a new model of corporate computing. They allow companies to replace their existing information systems, which are often incompatible with one another, with a single, integrated system. By streamlining data flows throughout an organization, these commercial software packages, offered by vendors like SAP, promise dramatic gains in a company's efficiency and bottom line. It's no wonder that businesses are rushing to jump on the ES bandwagon. But while these systems offer tremendous rewards, the risks they carry are equally great. Not only are the systems expensive and difficult to implement, they can also tie the hands of managers. Unlike computer systems of the past, which were typically developed in-house with a company's specific requirements in mind, enterprise systems are off-the-shelf solutions. They impose their own logic on a company's strategy, culture, and organization, often forcing companies to change the way they do business. Managers would do well to heed the horror stories of failed implementations. FoxMeyer Drug, for example, claims that its system helped drive it into bankruptcy. Drawing on examples of both successful and unsuccessful ES projects, the author discusses the pros and cons of implementing an enterprise system, showing how a system can produce unintended and highly disruptive consequences. Because of an ES's profound business implications, he cautions against shifting responsibility for its adoption to technologists. Only a general manager will be able to mediate between the imperatives of the system and the imperatives of the business.

3,681 citations

Journal ArticleDOI
15 Apr 2010-Nature
TL;DR: In this paper, the authors develop a framework for understanding the robustness of interacting networks subject to cascading failures and present exact analytical solutions for the critical fraction of nodes that, on removal, will lead to a failure cascade and to a complete fragmentation of two interdependent networks.
Abstract: Complex networks have been studied intensively for a decade, but research still focuses on the limited case of a single, non-interacting network. Modern systems are coupled together and therefore should be modelled as interdependent networks. A fundamental property of interdependent networks is that failure of nodes in one network may lead to failure of dependent nodes in other networks. This may happen recursively and can lead to a cascade of failures. In fact, a failure of a very small fraction of nodes in one network may lead to the complete fragmentation of a system of several interdependent networks. A dramatic real-world example of a cascade of failures ('concurrent malfunction') is the electrical blackout that affected much of Italy on 28 September 2003: the shutdown of power stations directly led to the failure of nodes in the Internet communication network, which in turn caused further breakdown of power stations. Here we develop a framework for understanding the robustness of interacting networks subject to such cascading failures. We present exact analytical solutions for the critical fraction of nodes that, on removal, will lead to a failure cascade and to a complete fragmentation of two interdependent networks. Surprisingly, a broader degree distribution increases the vulnerability of interdependent networks to random failure, which is opposite to how a single network behaves. Our findings highlight the need to consider interdependent network properties in designing robust networks.

3,651 citations


Authors

Showing all 49233 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Robert Langer2812324326306
Meir J. Stampfer2771414283776
Ronald C. Kessler2741332328983
JoAnn E. Manson2701819258509
Albert Hofman2672530321405
George M. Whitesides2401739269833
Paul M. Ridker2331242245097
Eugene Braunwald2301711264576
Ralph B. D'Agostino2261287229636
David J. Hunter2131836207050
Daniel Levy212933194778
Christopher J L Murray209754310329
Tamara B. Harris2011143163979
André G. Uitterlinden1991229156747
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023223
2022810
20216,943
20206,837
20196,120
20185,593