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A network-based analysis of systemic inflammation in humans
Oligonucleotide and complementary DNA microarrays are being used to subclassify histologically similar tumours, monitor disease progress, and individualize treatment regimens. However, extracting newExpand
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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia
Bacterial infection of the mammalian bloodstream can lead to overwhelming sepsis, a potentially fatal syndrome of irreversible cardiovascular collapse (shock) and critical organ failure. Cachectin,Expand
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A genomic storm in critically injured humans
Critical injury in humans induces a genomic storm with simultaneous changes in expression of innate and adaptive immunity genes.
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Genomic responses in mouse models poorly mimic human inflammatory diseases
A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry newExpand
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Inflammatory cytokines and cell response in surgery.
The systemic inflammatory response as mediated by the cytokine network is undoubtedly complex. While inflammatory cytokines are indispensable in wound healing and the restoration of homeostasis, itExpand
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Shock and tissue injury induced by recombinant human cachectin.
Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin.Expand
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Treatment of septic shock with the tumor necrosis factor receptor:Fc fusion protein. The Soluble TNF Receptor Sepsis Study Group.
BACKGROUND A recombinant, soluble fusion protein that is a dimer of an extracellular portion of the human tumor necrosis factor (TNF) receptor and the Fc portion of IgG1 (TNFR:Fc) binds andExpand
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Acute Inflammatory Response to Endotoxin in Mice and Humans
ABSTRACT Endotoxin injection has been widely used to study the acute inflammatory response. In this study, we directly compared the inflammatory responses to endotoxin in mice and humans. EscherichiaExpand
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Epinephrine inhibits tumor necrosis factor-alpha and potentiates interleukin 10 production during human endotoxemia.
Short-term preexposure of mononuclear cells to epinephrine inhibits LPS-induced production of TNF, whereas preexposure for 24 h results in increased TNF production. To assess the effects ofExpand
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Tumor necrosis factor soluble receptors circulate during experimental and clinical inflammation and can protect against excessive tumor necrosis factor alpha in vitro and in vivo.
Tumor necrosis factor alpha (TNF alpha), a primary mediator of systemic responses to sepsis and infection, can be injurious to the organism when present in excessive quantities. Here we report thatExpand
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