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  • 1
    ISSN: 1520-4995
    Quelle: ACS Legacy Archives
    Thema: Biologie , Chemie und Pharmazie
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 256 (1975), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 253 (1975), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 308 (1978), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 5
    Digitale Medien
    Digitale Medien
    [s.l.] : Nature Publishing Group
    Nature 328 (1987), S. 724-726 
    ISSN: 1476-4687
    Quelle: Nature Archives 1869 - 2009
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Notizen: [Auszug] T and B spleen lymphocytes from CBA/J mice (H-2k haplotype) were enriched and analysed by cytofluorimetry after staining with monoclonal antibodies. The results are summarized in Table 1. After enrichment for T cells, at least 90% of the cells specifically bound the anti-Thy 1 antibody, and in the ...
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 6
    Digitale Medien
    Digitale Medien
    Springer
    Inflammation research 3 (1973), S. 370-379 
    ISSN: 1420-908X
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Selective release of inflammatory materials from leukocyte lysosomes may be regulated by antagonistic effects of cyclic 3′, 5′-adenosine monophosphate (cAMP) and cyclic 3′, 5′-guanosine monophosphate (cGMP). Lysosomal enzymes are released in the absence of phagocytosis when cytochalasin B (5 μg/ml) converts polymorphonuclear leukocytes (PMN) to secretory cells: lysosomes merge directly with the plasma membrane upon encounter of PMN with zymosan, and cells selectively extrude substantial proportions of lysosomal, but not cytoplasmic enzymes. β-Adrenergic stimulation (〉10−8 M isoproterenol or 10−7 M epinephrine) of human leukocytes produced a dose-related reduction in β-glucuronidase release (blocked by 10−6 M propranolol) whereas α-adrenergic stimulation (phenylephrine + propranolol) was ineffective. In contrast, the cholinergic agonist carbamylcholine chloride (〉10−8 M) enhanced enzyme secretion, an effect blocked by 10−6 M atropine. Incubation of cells with exogenous cAMP or with agents that increase endogenous cAMP levels (dibutyryl cAMP, prostaglandin E1, histamine) reduced extrusion of lysosomal enzymes; in contrast, exogenous cGMP increased β-glucuronidase release. Whereas colchicine (5×10−4 M), a drug which impairs microtubule integrity, reduced selective enzyme release, deuterium oxide, which favors microtubule assembly, enhanced selective release of lysosomal enzymes. The data suggest that granule movement and acid hydrolase release from leukocyte lysosomes requires intact microtubules and may be modulated by adrenergic and cholinergic agents which provoke changes in concentrations of cyclic nucleotides.
    Materialart: Digitale Medien
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  • 7
    ISSN: 1573-2576
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract In order to establish a model of lung disease in which the usefulness of potential antiinflammatory compounds can be evaluated, we have analyzed the biochemical and cellular responses of rabbits to zymosan deposition in their lungs. A suspension of zymosan particles was instilled into the lungs of rabbits using an intratracheal catheter. Because the influx of leukocytes and the transudation of plasma into affected lungs was expected to contribute to the total cellular enzyme and protein levels, lungs were homogenized and assayed after various time intervals for six cellular enzymes and for protein content. After one day, alkaline phosphatase and neutral protease levels were elevated by 90% and 50%, respectively, above normal values. After two and three days, all of the pulmonary enzymes assayed displayed maximal two- to fourfold increases in their levels of activity. After seven days, only the alkaline phosphatase and neutral protease levels remained slightly elevated by 50% and 30%, respectively. Histologic analysis revealed focal and diffuse intraalveolar, interstitial, peribronchiolar, and perivascular accumulations of macrophages, granulocytes, and lymphocytes. Severe pulmonary edema, evident microscopically after one to three days, correlated well with 100% increases in both the wet weight and protein content of the lungs. In control experiments, the intratracheal infusion of saline solution minus zymosan particles resulted in a variety of enzymatic changes in the lungs after three days, which could be distinguished both enzymatically and histologically from those following zymosan deposition; histopathologic analysis revealed a pattern of intravascular congestion with erythrocytes, edematous thickening of alveolar septa, and focal intraalveolar hemorrhages, but with no inflammatory infiltration. In summary, this study demonstrates the time course of an experimental model for acute and chronic lung inflammation, the extent of which may be quantitatively evaluated using cellular enzymatic markers.
    Materialart: Digitale Medien
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  • 8
    ISSN: 1573-2576
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Radiolabeled human peripheral blood monocytes released [3H]arachidonic acid upon challenge with the calcium ionophore A23187 (10ΜM), or f-Met-LeuPhe (FMLP, 1ΜM). Chromatographic analysis of [3H]arachidonic acid labeled phospholipids showed that stimulation by FMLP reduced the amount of labeled phosphatidylcholine exclusively. Treatment of the monocytes with 10−3 M dibutyryl cyclic AMP (d-cAMP) or 5×10−4 M isobutylmethylxanthine (IBMX) substantially inhibited [3H]arachidonic acid release (30%) and depletion from labeled phosphatidylcholine (PC) in FMLP—but not calcium ionophore—stimulated cells. Using the fluorescent probe Indo-1, the FMLP-induced cytosolic calcium increase was unaffected by 10−3 M dibutyryl cyclic AMP. The results suggest that FMLP-stimulated phospholipase activity is regulated by cyclic AMP, but not by depressing receptor-medicated increases in cytoplasmic free calcium.
    Materialart: Digitale Medien
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  • 9
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 131 (1987), S. 384-392 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Receptor-ligand interaction in mononuclear phagocytes is intimately linked to alterations in membrane phospholipids and release of arachidonic acid (AA). In addition, synthesis of bioactive lipids from released AA can result in further modification of cell responses. Upon challenge with opsonized zymosan, [3H]-arachidonic acid ([3H]-AA)-labeled human monocytes released 25 ± 2% of their incorporated radiolabel within 30 min. Pretreatment of the monocytes with 5 × 10-4 M isobutylmethylxanthine (IBMX) or 1 × 10-3 M dibutyrl cyclic AMP (d-cAMP) inhibited total [3H]-AA release in the presence of zymosan by 47% and 42%, respectively. Analysis of incorporated [3H]-AA in cellular phospholipid pools indicated that significant amounts of label were lost from both phosphatidylcholine (PC) and phosphatidylinositol (PI) during zymosan stimulation. Treatment with d-cAMP substantially inhibited the loss of label from PC, but had no affect on PI. HPLC analysis of cell supernatants from zymosan-treated cells indicated that 5-HETE was the predominant metabolite generated from [3H]-AA, and its production was depressed during treatment with d-cAMP. Phospholipase activity in human monocyte homogenates was not effected by d-cAMP or IBMX at the highest concentrations used, whether these were added directly to the homogenate or by pretreatment of whole cells, demonstrating that inhibition required an intact cell. These results suggest that human monocytes exposed to opsonized zymosan release AA via two mechanisms and that modulation by cAMP is indirectly effecting a phospholipase directed towards PC.
    Zusätzliches Material: 6 Ill.
    Materialart: Digitale Medien
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