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Institution

Memorial University of Newfoundland

EducationSt. John's, Newfoundland and Labrador, Canada
About: Memorial University of Newfoundland is a education organization based out in St. John's, Newfoundland and Labrador, Canada. It is known for research contribution in the topics: Population & Context (language use). The organization has 13818 authors who have published 27785 publications receiving 743594 citations. The organization is also known as: Memorial University & Memorial University of Newfoundland and Labrador.


Papers
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Journal ArticleDOI
TL;DR: It is suggested that strategic alliances serve an important legitimating function for firms and that this role, mediated by alliance governance structure and partner selection preferences, has a significant influence on firm and alliance performance.
Abstract: Drawing on an institutional perspective, this paper suggests that strategic alliances serve an important legitimating function for firms and that this role, mediated by alliance governance structure and partner selection preferences, has a significant influence on firm and alliance performance. A theoretical framework is proposed that identifies five types of legitimacy associated with strategic alliances and the specific conditions under which legitimation may be an important outcome of strategic alliances. Propositions are developed to explain when firms are most likely to enter into alliances for legitimacy purposes and how the legitimating role of strategic alliances contributes to firm and alliance performance. The paper concludes with a summary and implications of a legitimacy-based view of alliances. Copyright © 2007 John Wiley & Sons, Ltd.

659 citations

Journal ArticleDOI
TL;DR: More studies are needed to definitively conclude that vitamin D can offer preventive and therapeutic benefits across a wide range of physiological states and chronic nonskeletal disorders.
Abstract: Significant controversy has emerged over the last decade concerning the effects of vitamin D on skeletal and nonskeletal tissues. The demonstration that the vitamin D receptor is expressed in virtually all cells of the body and the growing body of observational data supporting a relationship of serum 25-hydroxyvitamin D to chronic metabolic, cardiovascular, and neoplastic diseases have led to widespread utilization of vitamin D supplementation for the prevention and treatment of numerous disorders. In this paper, we review both the basic and clinical aspects of vitamin D in relation to nonskeletal organ systems. We begin by focusing on the molecular aspects of vitamin D, primarily by examining the structure and function of the vitamin D receptor. This is followed by a systematic review according to tissue type of the inherent biological plausibility, the strength of the observational data, and the levels of evidence that support or refute an association between vitamin D levels or supplementation and maternal/child health as well as various disease states. Although observational studies support a strong case for an association between vitamin D and musculoskeletal, cardiovascular, neoplastic, and metabolic disorders, there remains a paucity of large-scale and long-term randomized clinical trials. Thus, at this time, more studies are needed to definitively conclude that vitamin D can offer preventive and therapeutic benefits across a wide range of physiological states and chronic nonskeletal disorders.

650 citations

Journal Article
TL;DR: The involvement of mismatch repair deficiency in the premalignant stage of tumorigenesis in HNPCC cases is suggested, and it is suggested that mismatch repair genes (MSH2 or others) are defective in the germline of nearly all these patients.
Abstract: A replication error (RER) phenotype has been documented both in sporadic colorectal tumors and in tumors from patients with hereditary nonpolyposis colorectal cancer (HNPCC). In the current study 8 of 49 (16%) sporadic colorectal cancers (CRCs) and 25 of 29 (86%) CRCs from HNPCC patients were found to be RER+. All 9 (100%) CRCs from HNPCC patients with germline mutations of the mismatch repair gene MSH2 were found to be RER+, while 16 of 20 CRCs from HNPCC kindreds unlinked or not studied for linkage to MSH2 were RER+. Corresponding analysis in colorectal adenomas revealed that only 1 of 33 (3%) sporadic tumors but 8 of 14 (57%) HNPCC tumors were RER+. Moreover, RER was found in all 6 extracolonic cancers (endometrium, 2; kidney, 1; stomach, 1; duodenum, 1; and ovary, 1) derived from members of HNPCC families. These data suggest the involvement of mismatch repair deficiency in the premalignant stage of tumorigenesis in HNPCC cases, and suggest that mismatch repair genes (MSH2 or others) are defective in the germline of nearly all these patients.

647 citations

Journal ArticleDOI
TL;DR: In this article, the power of inductively coupled plasma-mass spectrometry (ICP-MS) is demonstrated for petrogenetic studies using a simple HF-HNO3 dissolution in screwtop Teflon® bombs.

646 citations

Journal ArticleDOI
Ryan K. C. Yuen1, Daniele Merico1, Matt Bookman2, Jennifer L. Howe1, Bhooma Thiruvahindrapuram1, Rohan V. Patel1, Joe Whitney1, Nicole A. Deflaux2, Jonathan Bingham2, Zhuozhi Wang1, Giovanna Pellecchia1, Janet A. Buchanan1, Susan Walker1, Christian R. Marshall1, Mohammed Uddin1, Mehdi Zarrei1, Eric Deneault1, Lia D’Abate3, Lia D’Abate1, Ada J.S. Chan1, Ada J.S. Chan3, Stephanie Koyanagi1, Tara Paton1, Sergio L. Pereira1, Ny Hoang1, Worrawat Engchuan1, Edward J Higginbotham1, Karen Ho1, Sylvia Lamoureux1, Weili Li1, Jeffrey R. MacDonald1, Thomas Nalpathamkalam1, Wilson W L Sung1, Fiona Tsoi1, John Wei1, Lizhen Xu1, Anne Marie Tassé4, Emily Kirby4, William Van Etten, Simon N. Twigger, Wendy Roberts, Irene Drmic1, Sanne Jilderda1, Bonnie Mackinnon Modi1, Barbara Kellam1, Michael J. Szego1, Michael J. Szego3, Cheryl Cytrynbaum, Rosanna Weksberg3, Lonnie Zwaigenbaum5, Marc Woodbury-Smith6, Marc Woodbury-Smith1, Jessica Brian3, Lili Senman3, Alana Iaboni3, Krissy A.R. Doyle-Thomas3, Ann Thompson6, Christina Chrysler6, Jonathan Leef3, Tal Savion-Lemieux4, Isabel M. Smith7, Xudong Liu8, Rob Nicolson9, Vicki Seifer10, Angie Fedele10, Edwin H. Cook11, Stephen R. Dager12, Annette Estes12, Louise Gallagher13, Beth A. Malow14, Jeremy R. Parr15, Sarah J. Spence16, Jacob A. S. Vorstman17, Brendan J. Frey3, James T. Robinson18, Lisa J. Strug3, Lisa J. Strug1, Bridget A. Fernandez19, Mayada Elsabbagh4, Melissa T. Carter20, Joachim Hallmayer21, Bartha Maria Knoppers4, Evdokia Anagnostou3, Peter Szatmari3, Peter Szatmari22, Robert H. Ring23, David Glazer2, Mathew T. Pletcher10, Stephen W. Scherer1, Stephen W. Scherer3 
TL;DR: Se sequencing of 5,205 samples from families with ASD, accompanied by clinical information, creating a database accessible on a cloud platform and through a controlled-access internet portal that identified 18 new candidate ASD-risk genes and found that participants bearing mutations in susceptibility genes had significantly lower adaptive ability.
Abstract: We are performing whole-genome sequencing of families with autism spectrum disorder (ASD) to build a resource (MSSNG) for subcategorizing the phenotypes and underlying genetic factors involved. Here we report sequencing of 5,205 samples from families with ASD, accompanied by clinical information, creating a database accessible on a cloud platform and through a controlled-access internet portal. We found an average of 73.8 de novo single nucleotide variants and 12.6 de novo insertions and deletions or copy number variations per ASD subject. We identified 18 new candidate ASD-risk genes and found that participants bearing mutations in susceptibility genes had significantly lower adaptive ability (P = 6 × 10-4). In 294 of 2,620 (11.2%) of ASD cases, a molecular basis could be determined and 7.2% of these carried copy number variations and/or chromosomal abnormalities, emphasizing the importance of detecting all forms of genetic variation as diagnostic and therapeutic targets in ASD.

641 citations


Authors

Showing all 13990 results

NameH-indexPapersCitations
Daniel Levy212933194778
Rakesh K. Jain2001467177727
Peter W.F. Wilson181680139852
Martin G. Larson171620117708
Peter B. Jones145185794641
Dafna D. Gladman129103675273
Guoyao Wu12276456270
Fereidoon Shahidi11995157796
David Harvey11573894678
Robert C. Haddon11257752712
Se-Kwon Kim10276339344
John E. Dowling9430528116
Mark J. Sarnak9439342485
William T. Greenough9320029230
Soottawat Benjakul9289134336
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202386
2022269
20211,808
20201,749
20191,568
20181,516