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  • 1
    Electronic Resource
    Electronic Resource
    Amplification of the bradykinin response in rat uterus by pCMB-dextran T 10 (1975)
    Springer
    Inflammation research 5 (1975), S. 236-238 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract pCMB-Dextran T 10, a large, non-penetrating, SH-blocking reagent caused a reversible amplification of bradykinin sensitivity in the isolated rat uterus. High concentrations of this compound (1×10−3 M) can evoke spontaneous uterus contraction. pCMB-Dextran T 10 did not alter the biological activity of bradykinin. It is assumed that superficial membrane SH-groups are involved in the uterus contraction mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02026437
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  • 2
    Electronic Resource
    Electronic Resource
    β-Adrenergic receptor coupled-adenylate cyclase of human fat cell ghosts (1977)
    Springer
    Journal of molecular medicine 55 (1977), S. 625-628 
    Details
    ISSN: 1432-1440
    Keywords: Adenylat-Cyclase ; Katecholamine ; β-adrenerge Rezeptoren ; Menschliches Fettgewebe ; Adenylate Cyclase ; Catecholamines ; β-adrenergic receptor ; Human adipose tissue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of beta-adrenergic agonists such as isoproterenol, norepinephrine and epinephrine upon the adenylate cyclase activity of human fat cell ghosts were tested, each alone and in combination with the beta-blocking agent propranolol. Saturating concentrations of these agents showed a 2–6.5-fold increase of enzyme activity without addition of any artificial cofactors. Isoproterenol was more potent in stimulating the enzyme system than epinephrine and nor-epinephrine. Propranolol caused a dose-dependent rightward shift of the log-dose response curve of these beta-adrenergic agonists. The assay of human fat cell adenylate cyclase in vitro may provide a simple and convenient assay system for the screening of beta-adrenergic drugs of potential therapeutic importance.
    Notes: Zusammenfassung Die Wirkungen beta-adrenerger Substanzen wie Isoproterenol, Adrenalin und Noradrenalin wurden entweder allein oder zusammen mit Propranolol, einem Beta-Blocker, auf das Adenylat-Cyclase System aus menschlichem Unterhautfettgewebe untersucht. Einen Katecholamin-Sensitivität des menschlichen Enzymsystems ließ sich ohne Zusatz von künstlichen Kofaktoren nachweisen. Maximal-Konzentrationen von Isoproterenol, Adrenalin und Nor-Adrenalin führten zu einer 2–6,5fachen Zunahme der Enzym-Aktivität. Isoproterenol stimulierte deutlich stärker als die beiden Hormome. Propranolol führte zu einer kompetitiven Hemmung des stimulierenden Effektes der beta-adrenergen Agonisten. Es wird gefolgert, daß die in-vitro Messung der Adenylat-Cyclase Aktivität im menschlichem Fettgewebe eine einfache Möglichkeit zur Testung von Substanzen mit adrenerger Wirkung darstellt.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01482531
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  • 3
    Electronic Resource
    Electronic Resource
    Neue Aspekte der Katecholamin-Rezeptor Wechselwirkung. Ihre Bedeutung in Pathophysiologie und Klinik (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 635-639 
    Details
    ISSN: 1432-1440
    Keywords: Catecholamines ; adenylate cyclase ; -,β-receptors ; adrenergic drugs ; Katecholamine ; Adenylat Cyclase ; -,β-Rezeptoren ; adrenerge Pharmaka
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird ein Überblick über die molekularen Aspekte der Katecholaminwirkung und ihre klinischen Konsequenzen gegeben. Sowohl β- als auch (in einigen Geweben) α-Rezeptoren sind an das membrangebundene Adenylat-Cyclase System gekoppelt. Die adrenergen Rezeptoren sind separate Membranbestandteile. Ihre Anzahl und die Relation zwischen α- und β-Rezeptoren sind ständigen Änderungen unterworfen. Die Umwandlungsvorgänge auf Rezeptorebene werden gesteuerteinmal durch die Konzentration adrenerger Agonisten im Blut,zum anderen durch diätetische und endokrine Einflüsse. Erste klinische Untersuchungen weisen daraufhin, daß bei Langzeittherapie mit β2-adrenergen Agonisten mit einer Desensibilisierung der Zielorgane auf Rezeptorebene zu rechnen ist.
    Notes: Summary The molecular aspects of catecholamine-receptor interactions are reviewed with respect to their clinical implications. β- and in some tissues α-adrenergic receptors are coupled to the membrane-bound adenylate cyclase. The adrenergic receptor sites are distinct membrane constituents. Their number and the ratio α- to β-receptor sites depend on the plasma concentration of catecholamines and are affected by diet and endocrinological factors. Recent clinical studies suggest that long-term treatment with β-adrenergic agonists may induces desensitization of target tissues due to changes in the adrenergic receptor moieties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477016
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  • 4
    Electronic Resource
    Electronic Resource
    cAMP-System und bakterielle Toxine (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 1109-1114 
    Details
    ISSN: 1432-1440
    Keywords: Bacterial toxins ; Infectious disease Adenylate cyclase ; Adenosine diphosphate-ribosyltransferases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of cytotoxic proteinaceous bacterial toxins on the adenylate cyclase cyclic adenosine monophosphate (cAMP) system of host cells are reviewed. Bacterial exotoxins affecting intracellular cAMP levels of host cells can be classified into two subgroups: (1) adenosine diphosphate (ADP)-ribosyl-transferases and, (2) invasive adenylate cyclases. Among the ADP-ribosylating toxins are the enterotoxins of Vibrio cholerae, of Escherichia coli and one of the pertussis toxins termed “islet-activating protein”. Toxins within this class share several structural and functional features. The three toxins consist of two functionally distinct parts: an A-component that is active enzymatically and a B-component that binds to surface receptors on cells or, if added in isolation blocks, the action of the complete toxin. The complete toxin shows little or no activity in broken cell preparations. When these toxins act on whole cells the contact is made initially through component B and then component A,but not B enters the cell and catalyzes the ADP-ribosylation of nucleotide regulatory components within the adenylate cyclase complex. The activities of the A-subunits of cholera toxin and heat-labile coli enterotoxin are directed against the stimulatory nucleotide-binding protein of adenylate cyclase whereas islet-activating protein probably alters the inhibitory coupling protein of host cells. Only recently two bacterial adenylate cyclases from Bacillus anthracis and Bordetella pertussis were described which are capable of invading mammalian cells. These invasive adenylate cyclases, like ADP-ribosylating toxins, require the presence of specific proteins for binding and are activated by calmodulin which is not present in bacteria. The role of this newly discovered class of bacterial exotoxins in infectious disease remains to be defined. Preliminary evidence, however, indicates that invasive bacterial cyclases may serve to suppress defense mechanisms in the host and thereby contribute to longer survival of parasitic bacteria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01530837
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  • 5
    Electronic Resource
    Electronic Resource
    Präadipozyten: Ein neues Modell in der Fettsuchtforschung (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 853-857 
    Details
    ISSN: 1432-1440
    Keywords: Preadipocytes ; Differentiation ; Adipose tissue ; Obesity ; Präadipozyten ; Differenzierung ; Fettgewebe ; Fettsucht
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Fettzellen entstehen aus differenzierungsfähigen Vorläuferzellen (Präadipozyten). Präadipozyten entsprechen morphologisch und funktionell Fibroblasten. Der Differenzierungsvorgang ist gekennzeichnet durch die Ausbildung des typischen sphärischen Erscheinungsbildes der reifen Fettzelle und durch die koordinierte Induktion von Schlüsselenzymen der Lipolyse und der Lipogenese, sowie den Erwerb der charakteristischen Hormonempfindlichkeit der reifen Fettzelle. Der Differenzierungsvorgang wird durch einen bisher nicht charakterisierten Serumfaktor ausgelöst und durch Insulin, Steroide, Prolactin, Prostaglandin F2α sowie Methylxanthine beschleunigt; er wird durch Cocarcinogene und Prostaglandin E1 gehemmt. Erste pathophysiologische Untersuchungen mit Präadipozyten von genetisch fettsüchtigen Mäusen lassen vermuten, daß sich eine genetische Prädisposition zur Obesitas schon auf Präadipozytenebene manifestiert. Regionale Differenzen in der hormonalen Regulation des Differenzierungsprozesses könnten zu den typischen, geschlechtspezifischen Unterschieden in der Verteilung der Körperfettmasse beitragen.
    Notes: Summary The present knowledge about the differentiation of preadipocytes into adipocytes is reviewed. The adipose conversion is initiated by an as yet unknown serum factor and is enhanced by various hormones including insulin, prostaglandin F2α, steroids, and prolactin; prostaglandin E1 and phorbol diesters are inhibitors of differentiation. Adipose conversion of fibroblasts (preadipocytes) is associated with the coordinate induction of key enzymes of the lipogenetic and lipolytic pathways and is accompanied by profound changes in hormone responsiveness. Pathophysiological studies with preadipocytes of genetically obese mice show differences between adipocyte precursors of obese animals and lean controls which may be causually related to obesity. Regional differences in the hormonal regulation of fibroblast conversion might be important for the sexdifferences of fat deposition in human beings.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476995
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  • 6
    Electronic Resource
    Electronic Resource
    Activation of human large bowel adenylate cyclase by methylated prostaglandin E2 analogues (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 417-419 
    Details
    ISSN: 1432-1440
    Keywords: Menschliche Kolonschleimhaut ; Adenylat-Cyclase ; Methylierte Prostaglandin-Analoga ; Durchfälle ; Kolonsekretion ; Human colonic mucosa ; Adenylate cyclase ; Methylated prostaglandin analogues ; Diarrhea ; Colonic secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of methylated analogues of prostaglandin E 2 upon the adenylate cyclase system in human colonic mucosa were tested. 16,16-dimethyl-prostaglandin E2 and 15-(S)-methyl-prostaglandin E2 increased the cyclase system in a dose-related manner. Maximal stimulation (about 250%) of enzyme activity occurred at a prostaglandin analogue concentration of 0.1 g/l. Diarrhea seen in patients treated with these orally effective prostaglandin analogues might in part be explained by activation of large bowel adenylate cyclase which is supposed to play a key role in the secretory process in this organ.
    Notes: Zusammenfassung Es wurden die Wirkungen der methylierten Prostaglandin-Analoga auf das menschliche Kolon-Adenylat Cyclase-System untersucht. 16,16-Dimethyl-Prostaglandin E2 und 15-(S)-Methyl-Prostaglandin E2 stimulierten das menschliche Enzymsystem dosis-abhängig und in etwa gleichem Ausmaß. Maximaleffekte (ca. 250%-Stimulierung) wurden bei einer Prostaglandin-Konzentration von 0.1 g/l beobachtet. Bei der Therapie mit den oral wirksamen Prostaglandin-Analogen werden als Nebenwirkungen häufig Durchfälle registriert. Das Adenylat Cyclase System spielt eine Schlüsselrolle im Sekretionsprozeß des Dickdarms. Unsere Ergebnisse machen wahrscheinlich, daß das gehäufte Auftreten von Durchfällen bei Prostaglandin-Therapie zumindest zum Teil durch eine Aktivierung des Kolon-Adenylat-Cyclase-Systems zu erklären ist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01480481
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  • 7
    Electronic Resource
    Electronic Resource
    Chemiluminescent determination of adenosine, inosine, and hypoxanthine/xanthine
    Amsterdam : Elsevier
    Analytical Biochemistry 163 (1987), S. 45-51 
    Details
    ISSN: 0003-2697
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0003-2697(87)90091-1
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  • 8
    Electronic Resource
    Electronic Resource
    Bioluminescent determination of free fatty acids
    Amsterdam : Elsevier
    Analytical Biochemistry 140 (1984), S. 349-353 
    Details
    ISSN: 0003-2697
    Keywords: NADH-linked luciferase system ; acyl-CoA synthetase ; free fatty acids ; isolated rat adipocytes ; serum
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0003-2697(84)90176-3
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  • 9
    Electronic Resource
    Electronic Resource
    Catecholamine-sensitive adenylate cyclase of human fat cell ghosts characteristics of the GMP(PNP)-liganded state
    Amsterdam : Elsevier
    Clinica Chimica Acta 73 (1976), S. 497-504 
    Details
    ISSN: 0009-8981
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0009-8981(76)90153-4
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  • 10
    Electronic Resource
    Electronic Resource
    Microdetermination of glycerol using bacterial NADH-linked luciferase
    Amsterdam : Elsevier
    Clinica Chimica Acta 120 (1982), S. 295-300 
    Details
    ISSN: 0009-8981
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0009-8981(82)90370-9
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