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Jonathan L. Haines

Researcher at Case Western Reserve University

Publications -  463
Citations -  44478

Jonathan L. Haines is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Genome-wide association study & Single-nucleotide polymorphism. The author has an hindex of 100, co-authored 463 publications receiving 40225 citations. Previous affiliations of Jonathan L. Haines include John P. Hussman Institute for Human Genomics & Bascom Palmer Eye Institute.

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Design and anticipated outcomes of the eMERGE-PGx project: a multicenter pilot for preemptive pharmacogenomics in electronic health record systems.

Laura J. Rasmussen-Torvik, +56 more
TL;DR: The design and initial implementation of the eMERGE‐PGx project is described, including site‐specific project implementation and anticipated products, including genetic variant and phenotype data repositories, novel variant association studies, clinical decision support modules, clinical and process outcomes, approaches to managing incidental findings, and patient and clinician education methods.
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Incorporating language phenotypes strengthens evidence of linkage to autism

TL;DR: It is tentatively concluded that there may be more than one autism susceptibility locus related to language development, and the linkage signals obtained are mainly attributable to the subgroup of families in which both probands had language delay.
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Functional Candidate Genes in Age-Related Macular Degeneration: Significant Association with VEGF, VLDLR, and LRP6

TL;DR: Test results suggest that LRP6, VEGF, and VLDLR may play a role in the risk of developing AMD, and genetic variation in five of these genes (IL1A, CKB, A2M, MGST1, and DCP1) is unlikely to explain a significant fraction of the risk
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Evidence for a role of the rare p.A152T variant in MAPT in increasing the risk for FTD-spectrum and Alzheimer's diseases

Giovanni Coppola, +211 more
TL;DR: These data provide the first genetic evidence and functional studies supporting the role of MAPT p.A152T as a rare risk factor for both FTD-s and AD and the concept that rare variants can increase the risk for relatively common, complex neurodegenerative diseases is suggested.