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James Morris

Bio: James Morris is an academic researcher from Clemson University. The author has contributed to research in topics: Trypanosoma brucei & Hexokinase. The author has an hindex of 56, co-authored 240 publications receiving 18654 citations. Previous affiliations of James Morris include University of Cincinnati & Durham University.


Papers
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Journal ArticleDOI
TL;DR: An algorithm is presented which finds all occurrences of one given string within another, in running time proportional to the sum of the lengths of the strings, showing that the set of concatenations of even palindromes, i.e., the language $\{\alpha \alpha ^R\}^*$, can be recognized in linear time.
Abstract: An algorithm is presented which finds all occurrences of one given string within another, in running time proportional to the sum of the lengths of the strings. The constant of proportionality is low enough to make this algorithm of practical use, and the procedure can also be extended to deal with some more general pattern-matching problems. A theoretical application of the algorithm shows that the set of concatenations of even palindromes, i.e., the language $\{\alpha \alpha ^R\}^*$, can be recognized in linear time. Other algorithms which run even faster on the average are also considered.

3,156 citations

Journal ArticleDOI
17 Feb 2012-Science
TL;DR: Functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies are described.
Abstract: Genome-sequencing studies indicate that all humans carry many genetic variants predicted to cause loss of function (LoF) of protein-coding genes, suggesting unexpected redundancy in the human genome. Here we apply stringent filters to 2951 putative LoF variants obtained from 185 human genomes to determine their true prevalence and properties. We estimate that human genomes typically contain ~100 genuine LoF variants with ~20 genes completely inactivated. We identify rare and likely deleterious LoF alleles, including 26 known and 21 predicted severe disease-causing variants, as well as common LoF variants in nonessential genes. We describe functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies.

1,186 citations

01 Jan 2015
TL;DR: The contribution of rare and low-frequency variants to human traits is largely unexplored as mentioned in this paper, but the contribution of these variants to the human traits has not yet been fully explored.
Abstract: The contribution of rare and low-frequency variants to human traits is largely unexplored. Here we describe insights from sequencing whole genomes (low read depth, 7×) or exomes (high read depth, 80×) of nearly 10,000 individuals from population-based and disease collections. In extensively phenotyped cohorts we characterize over 24 million novel sequence variants, generate a highly accurate imputation reference panel and identify novel alleles associated with levels of triglycerides (APOB), adiponectin (ADIPOQ) and low-density lipoprotein cholesterol (LDLR and RGAG1) from single-marker and rare variant aggregation tests. We describe population structure and functional annotation of rare and low-frequency variants, use the data to estimate the benefits of sequencing for association studies, and summarize lessons from disease-specific collections. Finally, we make available an extensive resource, including individual-level genetic and phenotypic data and web-based tools to facilitate the exploration of association results.

824 citations

Journal ArticleDOI
TL;DR: The origins of Andrew are traced, its goals and strategies are discussed, and an overview of the current status of its implementation and usage is given.
Abstract: The Information Technology Center (ITC), a collaborative effort between IBM and Carnegie-Mellon University, is in the process of creating Andrew, a prototype computing and communication system for universities. This article traces the origins of Andrew, discusses its goals and strategies, and gives an overview of the current status of its implementation and usage.

701 citations

Journal ArticleDOI
TL;DR: In this paper, a model of client involvement stages is proposed, role definition and control for clients in complex service creation are discussed, and attention to issues that emerge from this discussion is encouraged.
Abstract: Clients of service organizations have important roles to perform in creating services. Yet, comparatively little attention has been directed at the participation of clients in complex and demanding client performance domains. In this paper, clients are viewed as “partial” employees and (1) a model of client involvement stages is proposed, (2) role definition and control for clients in complex service creation are discussed, and (3) attention to issues that emerge from this discussion is encouraged.

685 citations


Cited by
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28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations

Journal ArticleDOI
Adam Auton1, Gonçalo R. Abecasis2, David Altshuler3, Richard Durbin4  +514 moreInstitutions (90)
01 Oct 2015-Nature
TL;DR: The 1000 Genomes Project set out to provide a comprehensive description of common human genetic variation by applying whole-genome sequencing to a diverse set of individuals from multiple populations, and has reconstructed the genomes of 2,504 individuals from 26 populations using a combination of low-coverage whole-generation sequencing, deep exome sequencing, and dense microarray genotyping.
Abstract: The 1000 Genomes Project set out to provide a comprehensive description of common human genetic variation by applying whole-genome sequencing to a diverse set of individuals from multiple populations. Here we report completion of the project, having reconstructed the genomes of 2,504 individuals from 26 populations using a combination of low-coverage whole-genome sequencing, deep exome sequencing, and dense microarray genotyping. We characterized a broad spectrum of genetic variation, in total over 88 million variants (84.7 million single nucleotide polymorphisms (SNPs), 3.6 million short insertions/deletions (indels), and 60,000 structural variants), all phased onto high-quality haplotypes. This resource includes >99% of SNP variants with a frequency of >1% for a variety of ancestries. We describe the distribution of genetic variation across the global sample, and discuss the implications for common disease studies.

12,661 citations

Journal Article
Fumio Tajima1
30 Oct 1989-Genomics
TL;DR: It is suggested that the natural selection against large insertion/deletion is so weak that a large amount of variation is maintained in a population.

11,521 citations

Journal ArticleDOI
TL;DR: In this paper, the authors go beyond the existing distinction between attitudinal and behavioral commitment and argue that commitment, as a psychological state, has at least three separable components reflecting a desire (affective commitment), a need (continuance commitment), and an obligation (normative commitment) to maintain employment in an organization.

9,212 citations

Journal ArticleDOI
Monkol Lek, Konrad J. Karczewski1, Konrad J. Karczewski2, Eric Vallabh Minikel1, Eric Vallabh Minikel2, Kaitlin E. Samocha, Eric Banks1, Timothy Fennell1, Anne H. O’Donnell-Luria3, Anne H. O’Donnell-Luria2, Anne H. O’Donnell-Luria1, James S. Ware, Andrew J. Hill1, Andrew J. Hill2, Andrew J. Hill4, Beryl B. Cummings1, Beryl B. Cummings2, Taru Tukiainen1, Taru Tukiainen2, Daniel P. Birnbaum1, Jack A. Kosmicki, Laramie E. Duncan2, Laramie E. Duncan1, Karol Estrada1, Karol Estrada2, Fengmei Zhao1, Fengmei Zhao2, James Zou1, Emma Pierce-Hoffman1, Emma Pierce-Hoffman2, Joanne Berghout5, David Neil Cooper6, Nicole A. Deflaux7, Mark A. DePristo1, Ron Do, Jason Flannick2, Jason Flannick1, Menachem Fromer, Laura D. Gauthier1, Jackie Goldstein2, Jackie Goldstein1, Namrata Gupta1, Daniel P. Howrigan1, Daniel P. Howrigan2, Adam Kiezun1, Mitja I. Kurki1, Mitja I. Kurki2, Ami Levy Moonshine1, Pradeep Natarajan, Lorena Orozco, Gina M. Peloso1, Gina M. Peloso2, Ryan Poplin1, Manuel A. Rivas1, Valentin Ruano-Rubio1, Samuel A. Rose1, Douglas M. Ruderfer8, Khalid Shakir1, Peter D. Stenson6, Christine Stevens1, Brett Thomas1, Brett Thomas2, Grace Tiao1, María Teresa Tusié-Luna, Ben Weisburd1, Hong-Hee Won9, Dongmei Yu, David Altshuler1, David Altshuler10, Diego Ardissino, Michael Boehnke11, John Danesh12, Stacey Donnelly1, Roberto Elosua, Jose C. Florez1, Jose C. Florez2, Stacey Gabriel1, Gad Getz1, Gad Getz2, Stephen J. Glatt13, Christina M. Hultman14, Sekar Kathiresan, Markku Laakso15, Steven A. McCarroll2, Steven A. McCarroll1, Mark I. McCarthy16, Mark I. McCarthy17, Dermot P.B. McGovern18, Ruth McPherson19, Benjamin M. Neale2, Benjamin M. Neale1, Aarno Palotie, Shaun Purcell8, Danish Saleheen20, Jeremiah M. Scharf, Pamela Sklar, Patrick F. Sullivan21, Patrick F. Sullivan14, Jaakko Tuomilehto22, Ming T. Tsuang23, Hugh Watkins17, Hugh Watkins16, James G. Wilson24, Mark J. Daly1, Mark J. Daly2, Daniel G. MacArthur2, Daniel G. MacArthur1 
18 Aug 2016-Nature
TL;DR: The aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC) provides direct evidence for the presence of widespread mutational recurrence.
Abstract: Large-scale reference data sets of human genetic variation are critical for the medical and functional interpretation of DNA sequence changes. Here we describe the aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC). This catalogue of human genetic diversity contains an average of one variant every eight bases of the exome, and provides direct evidence for the presence of widespread mutational recurrence. We have used this catalogue to calculate objective metrics of pathogenicity for sequence variants, and to identify genes subject to strong selection against various classes of mutation; identifying 3,230 genes with near-complete depletion of predicted protein-truncating variants, with 72% of these genes having no currently established human disease phenotype. Finally, we demonstrate that these data can be used for the efficient filtering of candidate disease-causing variants, and for the discovery of human 'knockout' variants in protein-coding genes.

8,758 citations