J
James J. Collins
Researcher at Massachusetts Institute of Technology
Publications - 700
Citations - 105255
James J. Collins is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Synthetic biology & Population. The author has an hindex of 151, co-authored 669 publications receiving 89476 citations. Previous affiliations of James J. Collins include Baylor College of Medicine & University at Albany, SUNY.
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Incomplete follow-up in the National Cancer Institute's formaldehyde worker study and the impact on subsequent reanalyses and causal evaluations.
TL;DR: Reanalyses of the National Cancer Institute cohort study on nasopharyngeal cancer (NPC) risk among formaldehyde exposed workers (Hauptmann et al., 2004) are performed and readers are asked for a prompt corrigendum of the 2004 publication.
A role for the bacterial GATC methylome in antibiotic stress survival
Christian A. Ross,Peter Belenky,Hu Li,Nadia Cohen,Saloni R. Jain,Rebecca S. Shapiro,Arnaud Gutierrez,James J. Collins +7 more
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Intervention effectiveness evaluation criteria: promoting competitions and raising the bar.
Ted Scharf,Larry J. Chapman,James J. Collins,Julia Limanowski,Catherine A. Heaney,Linda M. Goldenhar +5 more
TL;DR: The development of the criteria used to evaluate manuscripts is described, with respect to improving the science of evaluation methodology, promoting the highest ethical standards in intervention evaluation, and using the current criteria as a starting point for continuing to raise the bar for evaluation methodology.
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Identification of Simplified Microbial Communities That Inhibit Clostridioides difficile Infection through Dilution/Extinction.
TL;DR: An experimental platform to simplify complex communities of fecal bacteria through dilution and rapidly screen for their ability to resist C. difficile colonization resistance is developed and four new simplified communities of microbes with potential for development of new therapies to treat C.difficile disease are identified.
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Modulating the evolutionary trajectory of tolerance using antibiotics with different metabolic dependencies
Erica J. Zheng,Ian W. Andrews,Alexandra T Grote,Abigail L. Manson,Miguel A. Alcantar,Ashlee M. Earl,James J. Collins +6 more
TL;DR: In this article , the authors identify a mechanism of tolerance evolution in E. coli involving deletion of the sodium-proton antiporter gene nhaA, which results in downregulated metabolism and upregulated stress responses, and find that cycling of antibiotics with different metabolic dependencies interrupts evolution of tolerance in vitro, increasing the lifetime of treatment efficacy.