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Jungnam Joo

Researcher at National Institutes of Health

Publications -  21
Citations -  513

Jungnam Joo is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Genetic model & Genome-wide association study. The author has an hindex of 10, co-authored 21 publications receiving 446 citations.

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Testing association for markers on the X chromosome.

TL;DR: Performance of several approaches for testing association on the X chromosome are compared, and how departure from Hardy‐Weinberg equilibrium would affect type I error and power of these association tests using X‐linked SNPs is examined.
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Statistical design of personalized medicine interventions: The Clarification of Optimal Anticoagulation through Genetics (COAG) trial

TL;DR: In a personalized medicine intervention, the minimum detectable difference used in sample size calculations is not a known quantity, but rather an unknown quantity that depends on the genetic makeup of the subjects enrolled, and it is recommended that they be monitored during the conduct of a personalized Medicine intervention.
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Conditional linkage and genome-wide association studies identify UGT1A1 as a major gene for anti-atherogenic serum bilirubin levels – The Framingham Heart Study

TL;DR: The studies suggest that UGT1A1 may be the major gene with strong effects on bilirubin levels and the TA-repeat polymorphism might be the key polymorphism within the gene controlling bilirUBin levels.
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Rationale and study design of the CardioGene Study: genomics of in-stent restenosis.

TL;DR: The CardioGene Study is an ongoing study of restenosis in bare mental stents (BMS) for the treatment of coronary artery disease to understand the genetic determinants of the responses to vascular injury that result in the development of restanosis in some patients but not in others.
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Differences in the Phenotype, Cytokine Gene Expression Profiles, and In Vivo Alloreactivity of T Cells Mobilized with Plerixafor Compared with G-CSF

TL;DR: Preclinical data show plerixafor, in contrast with G-CSF, does not alter the phenotype and cytokine polarization of T cells, which raises the possibility that T cell–mediated immune sequelae of allogeneic transplantation in humans may differ when donor allografts are mobilized with plerxafor compared with G.CSF.