Institution
Memorial University of Newfoundland
Education•St. 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.
Topics: Population, Context (language use), Health care, Gadus, Computer science
Papers published on a yearly basis
Papers
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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
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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
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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
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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
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The Centre for Applied Genomics1, Google2, University of Toronto3, McGill University4, University of Alberta5, McMaster University6, Dalhousie University7, Queen's University8, University of Western Ontario9, Autism Speaks10, University of Illinois at Chicago11, University of Washington12, Trinity College, Dublin13, Vanderbilt University14, Newcastle University15, Boston Children's Hospital16, Utrecht University17, University of California, San Diego18, Memorial University of Newfoundland19, Children's Hospital of Eastern Ontario20, Stanford University21, Centre for Addiction and Mental Health22, Drexel University23
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
Name | H-index | Papers | Citations |
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Daniel Levy | 212 | 933 | 194778 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Martin G. Larson | 171 | 620 | 117708 |
Peter B. Jones | 145 | 1857 | 94641 |
Dafna D. Gladman | 129 | 1036 | 75273 |
Guoyao Wu | 122 | 764 | 56270 |
Fereidoon Shahidi | 119 | 951 | 57796 |
David Harvey | 115 | 738 | 94678 |
Robert C. Haddon | 112 | 577 | 52712 |
Se-Kwon Kim | 102 | 763 | 39344 |
John E. Dowling | 94 | 305 | 28116 |
Mark J. Sarnak | 94 | 393 | 42485 |
William T. Greenough | 93 | 200 | 29230 |
Soottawat Benjakul | 92 | 891 | 34336 |