J
John J. Arcaroli
Researcher at University of Colorado Denver
Publications - 79
Citations - 5712
John J. Arcaroli is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Lung injury & Cancer. The author has an hindex of 35, co-authored 79 publications receiving 5186 citations. Previous affiliations of John J. Arcaroli include University of Colorado Hospital & Anschutz Medical Campus.
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Patient-derived tumour xenografts as models for oncology drug development
John J. Tentler,Aik Choon Tan,Colin D. Weekes,Antonio Jimeno,Stephen Leong,Todd M. Pitts,John J. Arcaroli,Wells A. Messersmith,S. Gail Eckhardt +8 more
TL;DR: This Review will discuss specific PDTX disease examples illustrating an overview of the opportunities and limitations of these models in cancer drug development, and describe concepts regarding predictive biomarker development and future applications.
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HMG-1 as a mediator of acute lung inflammation.
TL;DR: In endotoxin-induced acute lung inflammation, administration of anti-HMG-1 Abs either before or after endotoxin exposure decreased the migration of neutrophils to the lungs as well as lung edema, indicating that H MG-1 is a distal mediator of acute inflammatory lung injury.
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Activation of gene expression in human neutrophils by high mobility group box 1 protein
Jong Sung Park,John J. Arcaroli,Ho Kee Yum,Huan Yang,Haichao Wang,Kuang Yao Yang,Kang Hyeon Choe,Derek Strassheim,Todd M. Pitts,Kevin J. Tracey,Edward Abraham +10 more
TL;DR: It is demonstrated that HMGB1 increases the nuclear translocation of NF-kappaB and enhances the expression of proinflammatory cytokines in human neutrophils and is an effective stimulus of neutrophil activation that can contribute to development of a proinflammatory phenotype in diseases characterized by excessively high levels ofHMGB1.
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Neutrophils as early immunologic effectors in hemorrhage- or endotoxemia-induced acute lung injury
TL;DR: It is shown that neutrophils play a central role in initiating acute inflammatory responses and causing injury in the lungs after hemorrhage or endotoxemia and Neutropenia was associated with significant reductions in IL-1beta and MIP-2 but not in TNF-alpha expression in the lung after endotoxia.
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Genetic polymorphisms and sepsis.
TL;DR: Future therapeutic trials as well as actual treatment regimens for patients with sepsis are likely to be designed to target specific genotypes and associated cellular responses, maximizing clinical response and patient safety.