Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

3
88
0
1

Year Published

1996
1996
2012
2012

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 161 publications
(92 citation statements)
references
References 28 publications
3
88
0
1
Order By: Relevance
“…59 Because antibodies against CD11b and CD18 prevented the oxidant stress and protected in the Gal/ET model, 8 it can be concluded that neutrophils after adherence to hepatocytes are the main source of this oxidant stress. Hepatocellular mitochondria, which may generate reactive oxygen after prolonged exposure to high levels of TNF-␣ in vitro, 60 appeared not to be a relevant source of reactive oxygen after Gal/ET administration in vivo. This conclusion is based on the observation that the increase in tissue GSSG levels did not correlate with TNF-␣ formation, e.g., a similar TNF-␣ generation but no neutrophil-mediated injury after treatment with ET alone did not result in higher tissue GSSG levels (Dr. H. Jaeschke, unpublished observation June, 1998).…”
Section: Discussionmentioning
confidence: 88%
“…59 Because antibodies against CD11b and CD18 prevented the oxidant stress and protected in the Gal/ET model, 8 it can be concluded that neutrophils after adherence to hepatocytes are the main source of this oxidant stress. Hepatocellular mitochondria, which may generate reactive oxygen after prolonged exposure to high levels of TNF-␣ in vitro, 60 appeared not to be a relevant source of reactive oxygen after Gal/ET administration in vivo. This conclusion is based on the observation that the increase in tissue GSSG levels did not correlate with TNF-␣ formation, e.g., a similar TNF-␣ generation but no neutrophil-mediated injury after treatment with ET alone did not result in higher tissue GSSG levels (Dr. H. Jaeschke, unpublished observation June, 1998).…”
Section: Discussionmentioning
confidence: 88%
“…The molecular basis for obesityrelated sensitization remains uncertain but might reflect, at least in part, relative overexpression of IFNg after LPS exposure. IFN-g is known to augment TNF toxicity in isolated mouse hepatocytes (28) and is increased in many experimental models of TNFrelated liver injury (29). Our observation that cellular production of IFN-g is increased in obese children with liver injury is provocative because it suggests that early in life intrinsic obesity-related alterations of immune function might provide an important mechanism for obesity-related liver damage.…”
Section: Discussionmentioning
confidence: 89%
“…13,15,25 In compromised hepatocytes, for example, either due to the administration of a transcriptional inhibitor (e.g., GalN or actinomycin D) or oxidative stress, TNF-␣ is a strong inducer of hepatocyte apoptosis. 11,19,21,26 However, it is important to note that the effect of the sole administration of TNF-␣ on healthy hepatocytes, either in vivo or in vitro, is beneficial in many biological situations. 11,19 For example, following partial hepatectomy in mice and in culture of primary hepatocytes, TNF-␣ potentiates hepatocyte proliferation.…”
Section: Discussionmentioning
confidence: 99%