The combination of palytoxin and 1-oleoyl-2-acetyl-glycerol (OAG) synergistically stimulates production of 6-keto-PGF1 alpha and PGF2 alpha by rat liver cells (the C-9 cell line). In contrast, the combination of 12-O-tetradecanoylphorbol-13-acetate (TPA)-type tumor promoters (TPA, dihydroteleocidin B, aplysiatoxin, phorbol-12,13-didecanoate) and OAG does not. Production of 6-keto-PGF1 alpha by palytoxin added with recombinant murine interleukin-1 (IL-1) or with insulin is also greater than the sum of the two effects taken independently. Palytoxin and OAG individually stimulate the release of radiolabeled compounds from the rat liver cells pre-labeled with [3H]arachidonic acid and also act synergistically to release labeled metabolites. After separation by h.p.l.c., these materials co-chromatograph with authentic 6-keto-PGF1 alpha and arachidonic acid. The synergistic stimulation by palytoxin and OAG is biphasic; a rapid synergistic production of 6-keto-PGF1 alpha or release of radiolabel from [3H]arachidonic acid prelabeled cells is followed, after approximately 2-4 h, by a prolonged synergistic response.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Extraction of 40 Hz EEG bursts for chaos analysis of brain function.

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Biomedical Engineering↗

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Chronic hypoxia and developmental regulation of cytochrome c expression in rats.

OBJECTIVE: To test the hypothesis that chronic hypoxia upregulates cytochrome c expression in heart, brain, and liver of fetal and maternal rats. METHODS: Time-dated pregnant Sprague-Dawley rats were divided into normoxic and hypoxic (48 hours of 10.5% oxygen from days 19 to 21) groups, and were killed on day 21. Tissue levels of cytochrome c in heart, brain, and liver were determined by using monoclonal antiserum for cytochrome c. RESULTS: Chronic hypoxia caused a decrease in fetal body weight (5.3 +/- 0.1 to 4.7 +/- 0.1 g) and an increase in heart/body weight ratio (0.0048 +/- 0.0001 to 0.0061 +/- 0.0002). Cytochrome c levels were 4-, 2.6-, and 13-fold higher in heart, liver, and brain, respectively, of the mother than of the fetus. Chronic hypoxia did not change cytochrome c levels in maternal tissues but caused a 70% increase and 54% decrease in cytochrome c levels in the fetal heart and liver, respectively. No difference was observed in the fetal brain. CONCLUSIONS: The results suggest that expression of cytochrome c is tissue specific and developmentally regulated. Chronic hypoxia showed differential regulation of cytochrome c levels both developmentally and tissue specifically. The increased sensitivity of cytochrome c in fetal tissue to chronic hypoxia is likely to represent a fetal adaptive mechanism to the stress of chronic hypoxia.

Animals↗