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Stuart D. Tyner

Researcher at Walter Reed Army Institute of Research

Publications -  46
Citations -  3101

Stuart D. Tyner is an academic researcher from Walter Reed Army Institute of Research. The author has contributed to research in topics: Plasmodium falciparum & Artesunate. The author has an hindex of 20, co-authored 43 publications receiving 2831 citations. Previous affiliations of Stuart D. Tyner include Medical Corps & San Antonio Military Medical Center.

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p53 mutant mice that display early ageing-associated phenotypes

TL;DR: It is suggested that p53 has a role in regulating organismal ageing by generating mice with a deletion mutation in the first six exons of the p53 gene that express a truncated RNA capable of encoding a carboxy-terminal p53 fragment.
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Independent Emergence of Artemisinin Resistance Mutations Among Plasmodium falciparum in Southeast Asia

TL;DR: While there was some evidence of spreading resistance, there was no evidence of resistance moving westward from Cambodia into Myanmar, and K13 appears to be a major determinant of artemisinin resistance throughout Southeast Asia.
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Genetic loci associated with delayed clearance of Plasmodium falciparum following artemisinin treatment in Southeast Asia

TL;DR: Replication and validation studies are needed to refine the location of loci responsible for artemisinin resistance and to understand the mechanism behind it; however, two SNPs on chromosomes 10 and 13 may be useful markers of delayed parasite clearance in surveillance for artesunate resistance in Southeast Asia.
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Tranexamic acid administration to pediatric trauma patients in a combat setting: the pediatric trauma and tranexamic acid study (PED-TRAX).

TL;DR: TXA was used in approximately 10% of pediatric combat trauma patients, typically in the setting of severe abdominal or extremity trauma and metabolic acidosis and suggested significant improvements in discharge neurologic status as well as decreased ventilator dependence.
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Is p53 haploinsufficient for tumor suppression? Implications for the p53+/- mouse model in carcinogenicity testing.

TL;DR: It is hypothesized that the reduced p53 dosage in the p53+/- cells provides an environment more conducive to the development of further oncogenic lesions and the initiation of a tumor, and to support the idea that p53 is indeed a haploinsufficient tumor suppressor, it is shown here that normal p 53+/-cells exhibit reduced parameters of growth control and stress response compared to their p53-/- counterparts.