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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 196 (1993), S. 494-501 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 45 (1997), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent studies have demonstrated the inhibitory effect of exogenous adenosine on TNF production. During inflammation endogenous adenosine levels are elevated and may be one of several anti-inflammatory mediators that reduce TNF synthesis. In the present study the authors investigated this role of adenosine in freshly isolated human PBMC. The effect of endogenous adenosine on TNF formation was studied by four different approaches. First, adenosine deaminase was added to LPS-stimulated mononuclear cells. This enzyme specifically deaminates extracellular adenosine to the inactive metabolite inosine. TNF production was augmented from baseline stimulation (LPS alone) of 3.5 ± 0.4 ng ml−1— 5.2 ± 0.9 ng ml−1 in the presence of 10 U ml−1 adenosine deaminase. Second, TNF production was determined after stimulation in the presence of dipyridamole, an inhibitor of cellular re-uptake of adenosine which increases extracellular concentrations. TNF synthesis was reduced dose-dependently from 3.1 ± 0.9 ng ml−1— 1.1 ± 0.2 ng ml−1 by 10 μm dipyridamole. Third, the adenosine A2 receptor antagonist 8-(3-chlorostyryl)caffeine (100 nm) enhanced TNF synthesis from a baseline of 3.7 ± 0.5 ng ml−1— 5.5 ± 0.9 ng ml−1. In contrast, no increase resulted from the addition of 100 nm of the specific A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. Finally, the authors were able to show that suppression of TNF formation by the specific type IV phosphodiesterase inhibitor rolipram can be completely reversed by adenosine deaminase or by the application of the A2 receptor antagonist. The authors conclude that endogenous adenosine controls TNF production. This effect of adenosine may not only have a physiological role but also appears to contribute to the pharmacological inhibition of TNF synthesis by exogenous agents such as the specific type IV phosphodiesterase inhibitor rolipram.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1439-0973
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In einer offenen kontrollierten Studie wurde bei 23 HIV-infizierten Patienten (CDC IV A–E) eine dokumentierte oropharyngeale Candidose mit 100 mg Fluconazol oral über 5 Tage behandelt (53 Episoden; 1–6 Episoden/Patient). Die Ergebnisse wurden mit einer Kontrollgruppe verglichen, in der 21 HIV-infizierte Patienten über 10–21 Tage mit 100 mg Fluconazol behandelt wurden. Von den Patienten wurden vor und nach jeder Therapie mit Fluconazol Candida-Isolate gewonnen, differenziert und einer Resistenztestung unterzogen (Mikro-Dilutionstechnik). Für die Resistenztestung wurden Inokulumgröße, pH des Mediums, Inkubationszeit und -temperatur standardisiert. Bis zu 85% der Patienten zeigten klinisch und mykologisch eine Heilung/Besserung.Candida albicans war der am häufigsten isolierte Hefepilz (86%) aus sämtlichen Proben, die mit Mundspülungen gewonnen wurden. 90% allerC. albicans-Isolate warenin vitro Fluconazol-empfindlich (MHK ≤ 1,56 mg/l). Eine Primärresistenz gegenüber Fluconazol wurde nicht beobachtet, aber in zwei Fällen trat sowohl klinisch als auchin vitro eine Fluconazol-Resistenz gegenüberC. albicans auf (MHK ≥ 25 mg/l). Eine Behandlung der Candidose mit 100 mg Fluconazol über 5 Tage führte zu einer vergleichbaren Heilungs-/Besserungsrate wie über 10–21 Tage, ohne daß die Rezidivrate wesentlich erhöht war. Eine therapiebedingte Selektion von Nicht-albicans-Arten(Candida krusei, Torulopsis glabrata) nach Fluconazol-Behandlung wurde selten beobachtet. Allerdings bestand bei einem Patienten der (klinische) Verdacht auf eine durchC. krusei unterhaltende orale Candidose, da nurC. krusei wiederholt nachgewiesen werden konnte.
    Notes: Summary In an open-label controlled study 23 HIV-infected patients (CDC IV A–E) with documented oropharyngeal candidosis were treated with 100 mg fluconazole orally over 5 days (53 episodes; 1–6 treatments/patient). Efficacy data were compared with a control group of 21 patients who received treatment for 10–21 days with 100 mg fluconazole for candidosis. Candida isolates were repeatedly recovered from patients before and after treatment with fluconazole and antifungal susceptibility testing (microbroth-dilution) was done. Inoculum size, medium pH, incubation time and temperature were standardized. Up to 85% of patients responded to therapy clinically and mycologically.Candida albicans was the most important yeast (86%) isolated from cultures of oral washings. In 90% ofC. albicans isolates MIC to fluconazole were low (≤1.56 mg/l). Primary resistance to fluconazole was not seen, but secondary resistance occurred in two cases clinically andin vitro (MIC≥25 mg/l). Short treatment for 5 days was as successful as for 10 to 21 days without leading to significantly more recurrences of oral candidosis in these patients. Selection ofCandida spp. other thanC. albicans (e. g.Candida krusei, Torulopsis glabrata) under repeated fluconazole treatment occurred rarely. One patient developed clinical signs of chronic recurrent candidiasis, where onlyC. krusei could be cultured repeatedly.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Der Internist 38 (1997), S. 466-469 
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Septischer Schock ; NO-Synthasehemmer ; Stickstoffmonoxid ; septischer Schock ; NO
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Beim septischen Schock wird vermehrt Stickstoffmonoxid (NO) gebildet, was zu Vasodilatation und Hypotension führt und zur bekannt hohen Mortalität dieses foudroyanten Krankheitsbildes beiträgt. Eine Hemmung der NO-Bildung zu therapeutischen Zwecken erscheint aus diesem Grunde wünschenswert. Von den verschiedenen Möglichkeiten, die vermehrte NO-Bildung zu verhindern, wird in dieser Arbeit über die therapeutische Gabe von NO-Synthaseinhibitoren (L-NMMA und L-NAME) beim septischen Schock berichtet.
    Type of Medium: Electronic Resource
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