1993
DOI: 10.1097/00003246-199310001-00004
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Tumor necrosis factor and the therapeutic potential of anti-tumor necrosis factor antibodies

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Cited by 37 publications
(15 citation statements)
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“…TNF-α is especially notable for its involvement in the development of various types of organ failure, which probably occur through similar mechanisms (Okajima 2001). Previous studies have also shown that pretreatment with anti-TNF-α antibodies may significantly attenuate the effects of hyperoxia-induced lung injury (Wherry et al 1993). The present study extends upon previous work by demonstrating that after 95% oxygen exposure over the course of 14 days, a number of factors are influenced in neonatal rat pups, including reduced body weight gain, decreased survival rate, and increased total protein level in BAL and leukocyte counts both in blood and BAL.…”
Section: Discussionmentioning
confidence: 99%
“…TNF-α is especially notable for its involvement in the development of various types of organ failure, which probably occur through similar mechanisms (Okajima 2001). Previous studies have also shown that pretreatment with anti-TNF-α antibodies may significantly attenuate the effects of hyperoxia-induced lung injury (Wherry et al 1993). The present study extends upon previous work by demonstrating that after 95% oxygen exposure over the course of 14 days, a number of factors are influenced in neonatal rat pups, including reduced body weight gain, decreased survival rate, and increased total protein level in BAL and leukocyte counts both in blood and BAL.…”
Section: Discussionmentioning
confidence: 99%
“…Elevation of TNF-α represents one of the first pulmonary responses to hyperoxia. Treatment of animals with antibodies directed against TNF-α reduces hyperoxia-induced lung injury, strongly suggesting a causal relationship between TNF-α and hyperoxic lung injury [9].…”
Section: Introductionmentioning
confidence: 99%
“…TNF received notice in the early 1990s for its role as an endogenous mediator of endotoxic shock [15,16]. The relatively sudden, massive release of TNF characteristic of the sepsis syndrome disrupts the endothelium's inherent anticoagulant properties, activates neutrophils, and induces the release of a host of additional inflammatory cytokines, culminating in cardiovascular collapse.…”
Section: Introductionmentioning
confidence: 99%
“…Two basic approaches to TNF inhibition were employed in the sepsis syndrome [15][16][17][18][19]: (1) monoclonal antibodies to TNF, and (2) soluble TNF receptor fusion proteins. These two approaches met with similarly disappointing results in sepsis, failing to demonstrate convincing evidence of efficacy despite the conduct of large studies.…”
Section: Introductionmentioning
confidence: 99%