(WFRF:(Molina PE))
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 02632naa a2200457 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:1940502 | |
| 003 | SwePub | |
| 008 | 240701s1999 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:19405022 URI |
| 024 | 7 | a https://doi.org/10.1126/science.285.5425.2482 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Wang, HC4 aut |
| 245 | 1 0 | a HMG-1 as a late mediator of endotoxin lethality in mice |
| 264 | 1 | b American Association for the Advancement of Science (AAAS),c 1999 |
| 520 | a Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group–1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target. | |
| 700 | 1 | a Bloom, O4 aut |
| 700 | 1 | a Zhang, MH4 aut |
| 700 | 1 | a Vishnubhakat, JM4 aut |
| 700 | 1 | a Ombrellino, M4 aut |
| 700 | 1 | a Che, JT4 aut |
| 700 | 1 | a Frazier, A4 aut |
| 700 | 1 | a Yang, H4 aut |
| 700 | 1 | a Ivanova, S4 aut |
| 700 | 1 | a Borovikova, L4 aut |
| 700 | 1 | a Manogue, KR4 aut |
| 700 | 1 | a Faist, E4 aut |
| 700 | 1 | a Abraham, E4 aut |
| 700 | 1 | a Andersson, Ju Karolinska Institutet4 aut |
| 700 | 1 | a Andersson, Uu Karolinska Institutet4 aut |
| 700 | 1 | a Molina, PE4 aut |
| 700 | 1 | a Abumrad, NN4 aut |
| 700 | 1 | a Sama, A4 aut |
| 700 | 1 | a Tracey, KJ4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t Science (New York, N.Y.)d : American Association for the Advancement of Science (AAAS)g 285:5425, s. 248-251q 285:5425<248-251x 0036-8075x 1095-9203 |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:1940502 |
| 856 | 4 8 | u https://doi.org/10.1126/science.285.5425.248 |
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