Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
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Target Concepts:
Gene/Protein
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Query: UMLS:C0020672 (
hypothermia
)
17,327
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. Intravenous (I.V.) injection of human recombinant interleukin-1 alpha (
IL-1 alpha
) produced dose-dependent monophasic fevers in rats. Moreover, the I.V. injection of
IL-1 alpha
produced dose-dependent rises in the plasma concentrations of adrenocorticotrophic hormone (ACTH) 30 min after injections with dosages of 5 micrograms/kg and 15 micrograms/kg of
IL-1 alpha
. 2. The febrile responses induced by the I.V. injection of
IL-1 alpha
(15 micrograms/kg) were completely abolished, and conversely
hypothermia
occurred, when the animals were pre-treated with a cyclo-oxygenase inhibitor, indomethacin (INDO). Pre-treatment with INDO also inhibited the increase in the plasma concentrations of ACTH induced by I.V. injection of
IL-1 alpha
(15 micrograms/kg), indicating that enhancement of plasma concentrations of ACTH induced by I.V. injection of
IL-1 alpha
is processed through the action of prostaglandins. 3. Intrapreoptic injection of prostaglandin E2 produced a dose-dependent fever with a rapid onset at doses of 25 and 100 ng. Moreover, the intrapreoptic injection of prostaglandin E2 increased the plasma concentrations of ACTH in a dose-dependent manner 30 min after injections. 4. The intrapreoptic injection of
IL-1 alpha
(20 ng) caused slow monophasic fever. However, no significant elevation of plasma concentrations of ACTH was observed 30, 90 and 180 min after the intrapreoptic injection of
IL-1 alpha
, as compared with the ACTH levels at each time in the control group which received an intrapreoptic injection of saline. 5. These results suggest that intrapreoptic prostaglandin E plays an important role in the ACTH response by inducing the release of corticotrophin-releasing factor (CRF).
...
PMID:Possible involvement of prostaglandin E in development of ACTH response in rats induced by human recombinant interleukin-1. 255 95
Ischemic-reperfusion injury (IRI) can affect many organ systems. Examples include strokes, coronary occlusion, accidental
hypothermia
, compartment syndrome and neonatal hypoxia. To date no mechanism has been fully accepted to explain acute inflammation associated with IRI. There is circumstantial evidence from animal and human ex-vivo cardiac experiments to support the hypothesis that acute inflammation associated with IRI is in part caused by IL-1 beta and/or
IL-1 alpha
secretion. Danger signal formation, such as uric acid/calcium pyrophosphate crystallization and other cellular stresses, may occur in IRI. These in turn may stimulate innate immune pathways (i.e. cryopyrin-inflammasome; and/ or toll-like receptors 2 and 4) to secrete IL-1 beta. Most IL-1 targeted therapy studies have focused on chronic human diseases and hopefully this discussion will create a framework to encourage use of this therapy in acute inflammation associated with IRI.
...
PMID:Ischemic-reperfusion syndromes: biochemical and immunologic rationale for IL-1 targeted therapy. 1847 71
