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Institution

Harvard University

EducationCambridge, Massachusetts, United States
About: Harvard University is a education organization based out in Cambridge, Massachusetts, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 208150 authors who have published 530388 publications receiving 38152182 citations. The organization is also known as: Harvard & University of Harvard.
Topics: Population, Cancer, Health care, Galaxy, Medicine


Papers
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Journal Article
TL;DR: Porter as discussed by the authors argues that the Internet is not disruptive to most existing industries and established companies and, contrary to recent thought, the Internet itself will be neutralized as a source of advantage.
Abstract: Many of the pioneers of Internet business, both dot-coms and established companies, have competed in ways that violate nearly every precept of good strategy. Rather than focus on profits, they have chased customers indiscriminately through discounting, channel incentives, and advertising. Rather than concentrate on delivering value that earns an attractive price from customers, they have pursued indirect revenues such as advertising and click-through fees. Rather than make trade-offs, they have rushed to offer every conceivable product or service. It did not have to be this way--and it does not have to be in the future. When it comes to reinforcing a distinctive strategy, Michael Porter argues, the Internet provides a better technological platform than previous generations of IT. Gaining competitive advantage does not require a radically new approach to business; it requires building on the proven principles of effective strategy. Porter argues that, contrary to recent thought, the Internet is not disruptive to most existing industries and established companies. It rarely nullifies important sources of competitive advantage in an industry; it often makes them even more valuable. And as all companies embrace Internet technology, the Internet itself will be neutralized as a source of advantage. Robust competitive advantages will arise instead from traditional strengths such as unique products, proprietary content, and distinctive physical activities. Internet technology may be able to fortify those advantages, but it is unlikely to supplant them. Porter debunks such Internet myths as first-mover advantage, the power of virtual companies, and the multiplying rewards of network effects. He disentangles the distorted signals from the marketplace, explains why the Internet complements rather than cannibalizes existing ways of doing business, and outlines strategic imperatives for dot-coms and traditional companies.

3,558 citations

Journal ArticleDOI
TL;DR: The Pool Lecture as mentioned in this paper was founded by Ithiel de Sola Pool, a brilliant, broad-gauged scholar whose interests ranged from the Nazi elite to direct satellite broadcasting, from the first rigorous computer simulation of electoral behavior to the development of network theory.
Abstract: It is a daunting honor to deliver the inaugural Pool Lecture. Ithiel de Sola Pool was a brilliant, broad-gauged scholar whose interests ranged from the Nazi elite to direct satellite broadcasting, from the first rigorous computer simulation of electoral behavior to the development of network theory, from which he invented "small world" research. He helped found the field of political communications. A graduate of the University of Chicago's political science department during its classic golden age, and first chair of the MIT political science department, Pool must also have been a remarkable teacher, for his students continue to contribute to our understanding of technology, communications, and political behavior. When I accepted this honor, I did not guess how close my own inquiry would lead me to Pool's own professional turf. I shall return to the contemporary relevance of Pool's insights at the conclusion of this talk.

3,554 citations

Journal ArticleDOI
TL;DR: Data support the involvement of ApoE ϵ4 in the pathogenesis of late-onset familial and sporadic AD and suggest it may operate as a susceptibility gene (risk factor) for the clinical expression of AD.
Abstract: Apolipoprotein E, type epsilon 4 allele (APOE epsilon 4), is associated with late-onset familial Alzheimer's disease (AD). There is high avidity and specific binding of amyloid beta-peptide with the protein ApoE. To test the hypothesis that late-onset familial AD may represent the clustering of sporadic AD in families large enough to be studied, we extended the analyses of APOE alleles to several series of sporadic AD patients. APOE epsilon 4 is significantly associated with a series of probable sporadic AD patients (0.36 +/- 0.042, AD, versus 0.16 +/- 0.027, controls [allele frequency estimate +/- standard error], p = 0.00031). Spouse controls did not differ from CEPH grandparent controls from the Centre d'Etude du Polymorphisme Humain (CEPH) or from literature controls. A large combined series of autopsy-documented sporadic AD patients also demonstrated highly significant association with the APOE epsilon 4 allele (0.40 +/- 0.026, p < or = 0.00001). These data support the involvement of ApoE epsilon 4 in the pathogenesis of late-onset familial and sporadic AD. ApoE isoforms may play an important role in the metabolism of beta-peptide, and APOE epsilon 4 may operate as a susceptibility gene (risk factor) for the clinical expression of AD.

3,551 citations

Journal ArticleDOI
05 Jan 1973-Science
TL;DR: Theory and data suggest that a male in good condition at the end of the period of parental investment is expected to outreproduce a sister in similar condition, while she is expectedto outre produce him if both are in poor condition, and natural selection should favor parental ability to adjust the sex ratio of offspring produced according to parental able to invest.
Abstract: Theory and data suggest that a male in good condition at the end of the period of parental investment is expected to outreproduce a sister in similar condition, while she is expected to outreproduce him if both are in poor condition. Accordingly, natural selection should favor parental ability to adjust the sex ratio of offspring produced according to parental ability to invest. Data from mammals support the model: As maternal condition declines, the adult female tends to produce a lower ratio of males to females.

3,547 citations

Journal ArticleDOI
09 Jun 2000-Science
TL;DR: Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
Abstract: We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.

3,543 citations


Authors

Showing all 209304 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Eric S. Lander301826525976
Robert Langer2812324326306
Meir J. Stampfer2771414283776
Ronald C. Kessler2741332328983
JoAnn E. Manson2701819258509
Albert Hofman2672530321405
Graham A. Colditz2611542256034
Frank B. Hu2501675253464
Bert Vogelstein247757332094
George M. Whitesides2401739269833
Paul M. Ridker2331242245097
Richard A. Flavell2311328205119
Eugene Braunwald2301711264576
Ralph B. D'Agostino2261287229636
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
2023358
20221,907
202130,528
202029,818
201926,011