The enigma of sepsis.
By N. Riedemann, R. Guo, P. Ward. Journal of Clinical Investigation, 2003
691 citations recorded by the source corpus.
Subfields: Critical Care and Intensive Care Medicine, Epidemiology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/5ed9e75b1fcd372749cdf577b99cb325e14595fe
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In Critical Care and Intensive Care Medicine
In Epidemiology
In Nutrition and Dietetics
Citations in the corpus
- Pathophysiology of ischemic acute kidney injury (2011, background): “Complement cascades are activated during sepsis, and C5a has been found to be elevated in rodent models of sepsis”
- Pre-B cell colony-enhancing factor inhibits neutrophil apoptosis in experimental inflammation and clinical sepsis. (2004, background): “Introduction Sepsis is a complex clinical syndrome that results from an activated systemic host inflammatory response to infection (1, 2).”
- Model organisms: Animal Models of sepsis: setting the stage (2005, positive): “However, more than 20 years of clinical trials have demonstrated that this approach was not overtly successfu”
- Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. (2004, neutral): “sepsis and multiple organ failure (30, 31).”
- NF-κB activation as a pathological mechanism of septic shock and inflammation (2006, neutral): “shock is the lack of the effective treatment (202).”
- Cytokine profiles as markers of disease severity in sepsis: a multiplex analysis (2007, background): “It is increasingly recognized that the inflammatory response and deregulated cytokine production play key roles in the development of multiple organ dysfunction [5].”
- MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis (2007, background): “It is well recognized that patients with sepsis are often immune suppressed, as illustrated by failure to eradicate their primary infections, a predisposition to develop secondary nosocomial infections, and an attenuated delayed-type hypersensitivity response (1, 2).”