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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of physical chemistry 〈Washington, DC〉 94 (1990), S. 194-199 
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 14 (1984), S. 76-81 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cellular origin and kinetics of TXB2 and 6-keto PGF1α in carrageenan-induced pleurisy has been studied. Maximum levels of these prostanoids occurred 1 hour after induction of pleurisy. Mononuclear cells initially present in the pleural cavity synthesized TXB2 and 6-keto PGF1α from (14C) arachidonic acid. By contrast, PMN cells harvested 6 hours after the induction of inflammation did not produce 6-keto-PGF1α. Selective inhibition of thromboxane synthetase with drugsin vitro andin vivo increased the formation of 6-keto-PGF1α, the stable breakdown product of PGI2. This metabolic effect was parallel to an increase in the volume of exudate and in PMN migration. These results suggest that TXA2 seems to be implicated not only as a chemotactic agent but also as an antagonist of PGI2 vasodilator effects.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract By using a clearly defined model of acute inflammation in rats, CaPP-induced pleurisy, we compared the evolution of four APR levels (Hp, HpX, α2M, SAP) at a local and peripheral site. At the same time we studied thromboxane and prostacyclin concentrations in pleural exudate. The levels of APR have shown a progressive increase up to 24 h. For α2M, Hp, HpX the increase in serum concentration was more rapid than in exudate, whereas the evolution of SAP level was parallel in the intra and extra-vascular compartments. On the other hand the levels of albumin and transferrin which are not APR remained constant in serum and also in exudate from 6 h to 24 h. Thromboxane and prostacyclin levels reached a peak during the first two hours of the inflammatory reaction followed by a rapid decrease. These prostanoids may be considered as early and transient mediators of acute inflammation, whereas the acute phase proteins studied have a more prolonged role in the inflammatory reaction.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The chemiluminescent (CL) response of peritoneal macrophages was suppressed by induction 4 h earlier of an inflammatory reaction in the pleural cavity which was negated by prior administration of indomethacin, ketoprofen and BW 755C. These changes were accompanied by a concomitant rise in peritoneal PGI2 levels which was abolished by drug pretreatment.In vitro treatment of normal peritoneal macrophages with PGI2 inhibited their subsequent CL response. Indomethacin and ketoprofen produced elevated CL of macrophages obtained from untreated controlsin vitro which was blocked by the lipoxygenase inhibitor NDGA. BW 755C and NDGAin vitro strongly inhibited macrophage CL and partially inhibited CL in a cell-free system. Use of these drugsin vivo demonstrated that indomethacin and ketoprofen augmented the CL response of peritoneal macrophages while BW 755C had no effect. These results suggest the inflammatory processper se can modulate the functions of macrophages in parts of the body remote from the inflammatory site. Moreover this modulation may be under the control of the prostanoid system.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 12 (1982), S. 353-359 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have studied the effect of immunomodulating agents on polymorphonuclear leucocyte chemotaxis and their relation to the modification of cyclic nucleotide levels. The tested drugs (levamisole, tuftsin, azimexon, muramyl dipeptide, isoprinosine) inhibited the chemotaxis of ‘normal’ cells but restored the impaired chemotactic responsiveness of inflammatory cells. None of these drugs had any significant effect on cyclic nucleotide levels in ‘normal’ cells. All the drugs, except isoprinosine, produced an increase in the cGMP levels in inflammatory cells. These results suggest that immunomodulators are able to modify PMN chemotaxis. This effect cannot, however, be related to modification of the cyclic nucleotide levels.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The first phase of the healing process is characterized by the development of an inflammatory reaction involving migration of inflammatory cells and release of inflammatory mediators. In a previous study, we have demonstrated that the water soluble tetrachlorodecaoxygen complex (TCDO), first synthetized to promote wound healing, inhibits polymorphonuclear (PMN) migration. The aim of the present study was to investigate the activity of TCDO on the progression of an acute non-specific inflammatory reaction, on the release of 6-keto-PGF1α and PGE2 and on PMN oxidative metabolism in the rat. Injected in the pleural cavity, TCDO (15 μmoles/rat) significantly decreased the number of exudative cells while 1.5 μmoles/rat inhibited PMN oxidative metabolismex vivo (assessed by chemiluminescent assay and measurement of O 2 − generation) after stimulation of the cells by opsonized zymosan. Similar observations were madein vitro after incubation of PMNs with various concentrations of TCDO (300 to 3 μM). The effect was dose-related and highly significant up to the concentration of 3 μM. In parallel, TCDO decreased the amounts of 6-keto-PGF1α and PGE2 in exudates harvested 1 hour after the intrapleural injection of isologous serum. Effects were significantly different from control levels, from 1.5 to 0.03 μmoles/rat for 6-keto-PGF1α and from 1.5 to 0.01 μmoles/rat for PGE2. This effect was observed when TCDO was injected at the same time or 1 hour before the isologous serum but not later. TCDO also inhibited LTB4 generationin vitro after PMN stimulation by calcium ionophore A23187, at concentrations up to 150 μM. The effects of TCDOin vivo andin vitro on rat PMN functions and inflammatory mediator release mimic certain activities of anti-inflammatory drugs. These properties may be beneficial in the very early stages of the wound healing process.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1420-908X
    Keywords: Cetirizine ; Anti H1 ; PGE2 ; IL-1 ; Monocyte/macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cetirizine was first described as a specific anti-H1 molecule displaying potent antiallergic activity. It was later found that its pharmacological properties extended to cellular actions as on eosinophil recruitment at inflammatory sites in allergic patients. Monocytes and macrophages participate in allergic mechanisms, particularly through high affinity H1 and H2 membrane receptors and generation of pro- and anti-inflammatory agents; among them histamine-induced factors, IL-1 and prostanoids are of importance. The aim of this work was to investigate the effect exerted by various concentrations of cetirizine (0.1–10 μg/ml) appliedin vitro to human monocytes and peritoneal rat macrophages cultured for 24 h. Peritoneal macrophages were collected either from normal or experimentally inflamed rats. Human monocytes, isolated from peripheral blood, were studied either in a resting state or after stimulation by LPS fromEscherichia coli (1 and 10 μg/ml). Cetirizine (10 μg/ml) significantly enhanced IL-1 release by human monocytes stimulated by a weak LPS concentration (1 μg/ml) but could not modify the maximal increase of IL-1 release induced by 10 μg/ml of LPS. It did not exert any effect on resting cells. Cetirizine (0.1–10 μg/ml) enhanced PGE2 release by resting human monocytes. Concentrations of 1 and 10 μg/ml enhanced PGE2 release by LPS-stimulated monocytes, and by healthy and inflamed rat macrophages. This effect was concentration-dependent. Our findings point to an anti-inflammatory action of cetirizine via PGE2 release and histamine H2 interactions. Cetirizine did not directly modify IL-1 generation by resting monocytes but the IL-1 production observed after LPS stimulation could promote the mechanisms by which PGE2 is released.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 31 (1975), S. 672-674 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Résumé Une injection à des rats d'α-méthyl-para-tyrosine (α-MPT), d'α-MpT-méthyl ester ou d'α-méthyl-méta-tyrosine (α-MmT), aux doses de 200 mg/kg, produit une augmentatio rapide et importante de l'excrétion urinaire de l'adrénaline et de la noradrénaline, ainsi que de l'acide vanyl-mandélique. La surrénalectomie ne modifie pas l'augmentation de l'excrétion urinaire de noradrénaline produite après injection d'α-MpT-méthyl ester. L'élévation des taux des catécholamines urinaires résulte vraisemblablement de leur libération tissulaire, sous l'action de l'α-MpT ou de l'α-MmT.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The development of adjuvant arthritis induced important modifications in intracellular levels of cyclic AMP and GMP in primary and secondary lymphoid organs: a continuous decrease in cyclic AMP and a biphasic increase in the level of cyclic GMP which correlate well with the onset of the acute phase and the systemization of the disease.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Thermal injury in rats leads to an impairment of polymorphonuclear leukocyte (PMN) functions, particularly oxidative metabolism and phosphoinositide turnover. As prostaglandin E2, which has immunosuppressive properties, is released in high levels after burn trauma, we investigated the in vitro and in vivo effects of a nonsteroidal antiinflammatory drug, niflumic acid, on oxidative and phosphoinositide metabolism in PMNs from healthy and burned rats. Given the role of fluoride ions on PMN, the influence of niflumic acid was compared with that of sodium fluoride (NaF) at equivalent doses of F−. In vitro, niflumic acid and sodium fluoride had no effect on oxidative metabolism in stimulated by formyl methionyl-leucyl-phenylalanine (FMLP) or opsonized zymosan (OZ) or nonstimulated PMNs from healthy and burned rats. Niflumic acid slightly increased the production of inositol phosphate by nonstimulated PMNs from healthy and burned rats. Niflumic acid and NaF partly restored the stimulating effect of FMLP on inositol phosphate production by PMNs from burned rats. In vivo treatment with niflumic acid and NaF increased the oxidative metabolism of PMNs from burned rats but not healthy rats. Niflumic acid, more than NaF, restored the activity of both stimulants on phosphoinositide metabolism in PMNs from burned rats. In conclusion, at non-antiinflammatory doses, while inhibiting cyclooxygenase activity, niflumic acid exerts a complex effect on the burn-induced depression of PMN functions. The fluoride anion induces similar but generally weaker effects and seems to be involved in the restoring effects of niflumic acid on PMN functions in burned rats.
    Type of Medium: Electronic Resource
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