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Institution

Indiana University

EducationBloomington, Indiana, United States
About: Indiana University is a education organization based out in Bloomington, Indiana, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 64480 authors who have published 150058 publications receiving 6392902 citations. The organization is also known as: Indiana University system & indiana.edu.


Papers
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Journal ArticleDOI
TL;DR: In this article, the authors examined the relative impact of organizational citizenship behaviors and objective sales productivity on sales managers' evaluations of the performance of the company's products. But, the research objective was not to examine the impact of OCBs on the performance evaluation of the product.
Abstract: The research objective was to examine the relative impact of “organizational citizenship behaviors” (OCBs) and objective sales productivity on sales managers’ evaluations of the performance of thei...

718 citations

Journal ArticleDOI
TL;DR: A new computational model, MutPred, is developed that is based upon protein sequence, and which models changes of structural features and functional sites between wild-type and mutant sequences and can provide insight into the specific molecular mechanism responsible for the disease state.
Abstract: Motivation: Advances in high-throughput genotyping and next generation sequencing have generated a vast amount of human genetic variation data. Single nucleotide substitutions within protein coding regions are of particular importance owing to their potential to give rise to amino acid substitutions that affect protein structure and function which may ultimately lead to a disease state. Over the last decade, a number of computational methods have been developed to predict whether such amino acid substitutions result in an altered phenotype. Although these methods are useful in practice, and accurate for their intended purpose, they are not well suited for providing probabilistic estimates of the underlying disease mechanism. Results: We have developed a new computational model, MutPred, that is based upon protein sequence, and which models changes of structural features and functional sites between wild-type and mutant sequences. These changes, expressed as probabilities of gain or loss of structure and function, can provide insight into the specific molecular mechanism responsible for the disease state. MutPred also builds on the established SIFT method but offers improved classification accuracy with respect to human disease mutations. Given conservative thresholds on the predicted disruption of molecular function, we propose that MutPred can generate accurate and reliable hypotheses on the molecular basis of disease for ~11% of known inherited disease-causing mutations. We also note that the proportion of changes of functionally relevant residues in the sets of cancer-associated somatic mutations is higher than for the inherited lesions in the Human Gene Mutation Database which are instead predicted to be characterized by disruptions of protein structure. Availability: http://mutdb.org/mutpred Contact:predrag@indiana.edu; smooney@buckinstitute.org

718 citations

Book
Albert Cohen1
01 Mar 1971

717 citations

Journal ArticleDOI
TL;DR: This article found that the most influential level of social information is drawn from the 90th to 95th percentile of previous contributions and that social information increases contributions by 12% for new members but not for renewing members.
Abstract: We study the effect of social information on the voluntary provision of public goods. Competing theories predict that others’ contributions might be either substitutes or complements to one's own. We demonstrate a positive social information effect on individual contributions, supporting theories of complementarities. We find the most influential level of social information is drawn from the 90th to 95th percentile of previous contributions. We furthermore find the effect to be significant for new members but not for renewing members. In the most effective condition, social information increases contributions by 12% ($13). These increased contributions do not crowd out future contributions.

717 citations

Journal ArticleDOI
Michael Lynch1
TL;DR: A consideration of the long-term consequences of current human behavior for deleterious-mutation accumulation leads to the conclusion that a substantial reduction in human fitness can be expected over the next few centuries in industrialized societies unless novel means of genetic intervention are developed.
Abstract: Although mutation provides the fuel for phenotypic evolution, it also imposes a substantial burden on fitness through the production of predominantly deleterious alleles, a matter of concern from a human-health perspective. Here, recently established databases on de novo mutations for monogenic disorders are used to estimate the rate and molecular spectrum of spontaneously arising mutations and to derive a number of inferences with respect to eukaryotic genome evolution. Although the human per-generation mutation rate is exceptionally high, on a per-cell division basis, the human germline mutation rate is lower than that recorded for any other species. Comparison with data from other species demonstrates a universal mutational bias toward A/T composition, and leads to the hypothesis that genome-wide nucleotide composition generally evolves to the point at which the power of selection in favor of G/C is approximately balanced by the power of random genetic drift, such that variation in equilibrium genome-wide nucleotide composition is largely defined by variation in mutation biases. Quantification of the hazards associated with introns reveals that mutations at key splice-site residues are a major source of human mortality. Finally, a consideration of the long-term consequences of current human behavior for deleterious-mutation accumulation leads to the conclusion that a substantial reduction in human fitness can be expected over the next few centuries in industrialized societies unless novel means of genetic intervention are developed.

716 citations


Authors

Showing all 64884 results

NameH-indexPapersCitations
Frank B. Hu2501675253464
Stuart H. Orkin186715112182
Bruce M. Spiegelman179434158009
David R. Williams1782034138789
D. M. Strom1763167194314
Markus Antonietti1761068127235
Lei Jiang1702244135205
Brenda W.J.H. Penninx1701139119082
Nahum Sonenberg167647104053
Carl W. Cotman165809105323
Yang Yang1642704144071
Jaakko Kaprio1631532126320
Ralph A. DeFronzo160759132993
Gavin Davies1592036149835
Tyler Jacks158463115172
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023127
2022694
20217,273
20207,310
20196,943
20186,496