Massive Majorana neutrinos in prebounce supernovae.
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Biomedical subjects
Publications and source records attributed to A Raychaudhuri.
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Injection of 2.5 mg of lambda-carrageenan into the rat pleural cavity resulted in a time-dependent increase in pleural exudate substance P (SP) levels up to 24 hr. Synergistic increases in the exudate formation were observed when a sub-optimal quantity of carrageenan was injected with SP. Pre-treatment of rats with capsaicin at 50 and 100 mg/kg s.c. daily for one week prior to the induction of pleurisy blocked the increase in exudate volume and SP levels when compared to that normally detected after carrageenan injection. These results suggest that inhibition of SP production may improve inflammatory conditions.
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1. CGS 8515 selectively inhibited 5-LO (IC50 = 0.1 microM) with negligible effect on CO, 12-LO, 15-LO and TxS at concentrations up to 100 microM. 2. CGS 8515 selectively inhibited A23187-induced formation of 5-LO products in rat and human whole blood with a 20-70 fold separation of effects over the formation of CO products. 3. Ex vivo and in vivo studies with rats showed that CGS 8515, at an oral dose of 2-50 mg/kg, significantly inhibited A23187-induced formation of LTs in whole blood and in the lung. The effect persisted for at least 6 h in the ex vivo blood model. 4. CGS 8515, at oral doses as low as 5 mg/kg, significantly suppressed exudate volume and leukocyte migration in the carrageenan-induced pleurisy and sponge models in the rat.
CGS 8515 inhibited 5-hydroxyeicosatetraenoic acid (5-HETE) and leukotriene B4 synthesis in guinea pig leukocytes (IC50 = 0.1 microM). The compound did not appreciably affect cyclooxygenase (sheep seminal vesicles), 12-lipoxygenase (human platelets), 15-lipoxygenase (human leukocytes) and thromboxane synthetase (human platelets) at concentrations up to 100 microM. CGS 8515 inhibited A23187-induced formation of leukotriene products in whole blood (IC50 values of 0.8 and 4 microM, respectively, for human and rat) and in isolated rat lung (IC50 less than 1 microM) in vitro. The selectivity of the compound as a 5-lipoxygenase inhibitor was confirmed in rat whole blood by the 20-70-fold separation of inhibitory effects on the formation of leukotriene from prostaglandin products. Ex vivo and in vivo studies with rats showed that CGS 8515, at an oral dose of 2-50 mg/kg, significantly inhibited A23187-induced production of leukotrienes in whole blood and in the lung. The effect persisted for at least 6 h in the ex vivo whole blood model. CGS 8515, at oral doses as low as 5 mg/kg, significantly suppressed exudate volume and leukocyte migration in the carrageenan-induced pleurisy and sponge models in the rat. Inhibitory effects of the compound on inflammatory responses and leukotriene production in leukocytes and target organs are important parameters suggestive of its therapeutic potential in asthma, psoriasis and inflammatory conditions.
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The immunopharmacology of RMI 9563 - bis[3-(diethylamino)propyl]fluoranthene-3,9-dicarboxylate dihydrochloride--has been described. The compound, when given parenterally, inhibited several cell-mediated immune responses (EAE, tuberculin skin reaction, adjuvant arthritis) in rats, enhanced IgM and IgG antibody-producing cells in mice, and displayed anti-inflammatory activity in several models (carrageenan paw edema, adjuvant arthritis, direct passive Arthus reaction--a model of inflammation that is immunologically induced and complement-dependent). RMI 9563 suppressed the activation of complement in vitro by the selective inhibition of C1 esterase.
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Tilorone suppressed inflammation induced by immune (direct passive Arthus reaction) as well as by non-immune agents (carrageenam-induced paw edema and abscess formation), if the compound is given 24 hr prior to the proinflammatory agonists. The non-immune anti-inflammatory effect is independent of the adrenals. A surprising findings was that total serum hemolytic complement is markedly elevated 24 hr after a single dose of tilorone.
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