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John Bartels

Researcher at University of Pittsburgh

Publications -  27
Citations -  1285

John Bartels is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Inflammation & Systems biology. The author has an hindex of 13, co-authored 25 publications receiving 1233 citations. Previous affiliations of John Bartels include University of Pennsylvania.

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Translational Systems Biology of Inflammation

TL;DR: The efforts to use translational systems biology to develop an integrated framework to gain insight into the problem of acute inflammation are described, highlighting the promise of this multidisciplinary field.
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The acute inflammatory response in diverse shock states.

TL;DR: A mathematical model incorporating major elements of the acute inflammatory response in C57Bl/6 mice was developed and found that a single model with different initiators including the autonomic system could describe the response to various insults.
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In silico design of clinical trials: a method coming of age.

TL;DR: The construction of an in silico clinical trial could provide profound insight into the design of clinical trials of immunomodulatory therapies, ranging from optimal patient selection to individualized dosage and duration of proposed therapeutic interventions.
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In silico models of acute inflammation in animals

TL;DR: A mathematical model is constructed using ordinary differential equations that encompass the dynamics of cells and cytokines of the acute inflammatory response, as well as global tissue dysfunction and may provide insights into the complex dynamics of acute inflammation in a manner that can be tested in vivo using many fewer animals than has been possible previously.
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The role of initial trauma in the host's response to injury and hemorrhage: insights from a correlation of mathematical simulations and hepatic transcriptomic analysis.

TL;DR: A mathematical model encompassing the dynamics of the acute inflammatory response that incorporates the intertwined effects of inflammation and global tissue damage was constructed and demonstrated that ST alone accounts for a substantial proportion of the observed phenotypic and genetic/molecular changes versus untreated animals.