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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cutaneous pathology 16 (1989), S. 0 
    ISSN: 1600-0560
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Thirty plantar warts were analyzed for the presence of HPV-1 type-specific and PV genus-specific capsid antigens by immunofluorescence (IF) using monoclonal and polyclonal antibodies and type-specific HPV-1 DNA employing in situ hybridization methods. Fifteen of 30 plantar warts were positive by IF for PV genus-specific structural viral antigens. Thirteen of the 15 productively infected plantar warts expressed intranuclear HPV-1 type-specific capsid antigens and viral DNA, which were detected in the same distribution in each individual wart. The 2 productively infected plantar warts that did not react with HPV-1 type-specific MoAbs did not react with HPV-1 type-specific DNA by in situ hybridization. Thus, serotyping of HPV-1 capsid antigens by monoclonal antibodies is concordant with genotyping of HPV-1 viral DNA by in situ hybridization in productively infected plantar warts.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 28-31 
    ISSN: 1432-1912
    Keywords: B-HT 920 ; B-HT 958 ; Presynaptic dopamine autoreceptors ; Dopamine release ; Nucleus accumbens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of two thiazoloazepine derivatives, B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]azepine) and B-HT 958 (2-amino-6-(p-chloro-benzyl)-4H-5,6,7,8-tetrahydrothiazolo[5,4-d]azepine) on electrically evoked overflow of 3H-dopamine were studied. Slices from nucleus accumbens of the rat were preincubated with 3H-dopamine and superfused at 23°C or 37°C. Electrical field stimulation was applied using frequencies of 0.5 or 5 Hz. 1. At 37°C/5 Hz, B-HT 920 markedly and dose-dependently (0.01–0.1 μmol/l) reduced the stimulation evoked overflow of tritium. Its dose-response curve was shifted to the right at 23°C/0.5 Hz and 23°C/5 Hz, respectively. A similar result was obtained with the dopamine receptor agonist, apomorphine (1 μmol/l). 2. B-HT 958 (0.1–10 μmol/l) also reduced electrically induced overflow of tritium at 37°C/5 Hz, had no effect at 23°C/0.5 Hz, and facilitated tritium overflow at 23°C/5 Hz. 3. Sulpiride (10 μmol/l) completely prevented the effects of B-HT 920 (1 μmol/l) or B-HT 958 (1 μmol/l) at 37°C/ 5 Hz, whereas phentolamine (1 μmol/l) had no effect on the actions of the two drugs under these experimental conditions. 4. From the patterns of effects obtained under the different experimental conditions it is concluded that B-HT 920 acts as full agonist at presynaptic dopamine autoreceptors whereas B-HT 958 acts as partial agonist.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 613-617 
    ISSN: 1432-1912
    Keywords: B-HT 920 ; B-HT 933 ; B-HT 958 ; Presynaptic α2-auto-receptor ; Noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the three azepine compounds, B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]azepine), B-HT 933 [2-amino-6-ethyl-5, 6, 7, 8-tetrahydro-4H-oxazolo [4,5-d]azepine; azepexole] and B-HT 958 (2-amino-6-(p-chloro-benzyl)-4H-5, 6, 7, 8-tetrahydrothiazolo[5,4-d]azepine) on electrically evoked overflow of 3H-noradrenaline were studied. Slices from parietal cortex (Cξ) or nucleus anterior hypothalami (nah) were incubated with 3H-noradrenaline, superfused at 23°C or 37°C in the presence of the noradrenaline uptake inhibitor desipramine (3 μmol/l) and field stimulated at frequencies of 0.3 or 3 Hz. 1. At 37°C/0.3 Hz, B-HT 920 and B-HT 933 concentration-dependently decreased the evoked overflow of tritium in both regions studied, whereas B-HT 958 had no effect. 2. In a second set of experiments each drug was tested under three additional experimental conditions, i. e. 37°C/3 Hz, 23°C/ 0.3 Hz and 23°C/3 Hz. Increasing the stimulation frequency to 3 Hz or lowering the superfusion temperature to 23°C reduced the effects of B-HT 920 (1 μmol/l) and B-HT 933 (10 μmol/l) as compared to the effects at 37°C/0.3 Hz. When tested at 23°C/3 Hz, both drugs did not significantly affect the evoked overflow of tritium in the Cx or the nah. In contrast, B-HT 958 (10 μmol/l), caused a facilitation of evoked overflow in both regions when the higher stimulation frequency or the lower superfusion temperature was used. Its release-enhancing action was most pronounced at 23°C/3 Hz. 3. Idazoxan (0.1 μmol/l) antagonized the effects of BHT 920 (10 μmol/l) and B-HT 933 (10 gmmol/l) in the Cx at 37°C/0.3 Hz. The ineffectiveness of B-HT 958 under these experimental conditions was not changed in the presence of idazoxan. Sulpiride (10 μmol/l) did not affect the action of any of the three compounds. 4. From the patterns of effects obtained under the different experimental conditions it is concluded that B-HT 920 and B-HT 933 act as agonists at prejunctional α2-adrenoceptors, whereas B-HT 958 acts as a weak antagonist at these sites. Send offprint requests to E. A. Singer at the above address
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 118-121 
    ISSN: 1432-1912
    Keywords: Presynaptic receptors ; α2-Adrenoceptors ; Noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Slices prepared from rat cerebral cortex were labelled with 3H-noradrenaline and superfused. Electrical field stimulation was carried out 15 min (S1) and 45 min (S2) after the start of collection of 5-min samples using 4 pulses delivered at 100 Hz. Drugs acting at α2-adrenoceptors were added 20 min before S2, and their effects were evaluated using the S2/S1-ratio. The α2-adrenoceptor antagonists idazoxan (1 μmol/l) and rauwolscine (1 μmol/l) failed to increase stimulation-evoked overflow of radioactivity in the absence or presence of the noradrenaline reuptake inhibitor desipramine (1 gmol/l). This indicates that the duration of electrical stimulation was too short to allow development of α2-adrenoceptor-mediated auto-inhibition by released noradrenaline. The effect of clonidine (3–1000 nmol/l) on stimulation-evoked overflow of radioactivity was tested in the absence and presence of three different reuptake inhibitors (desipramine, 1 μol/l; maprotiline, 1 μol/l; cocaine, 10 μmol/l). The analysis yielded identical concentration-response curves under all conditions. These results argue against an action of inhibitors of neuronal reuptake of noradrenaline at the presynaptic α2-adrenoceptor and against the concept of a functional link between uptake site and receptor.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; Presynaptic α-adrenoceptor ; α2-Adrenoceptor ; Clonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of clonidine on the stimulation-evoked overflow of tritium was studied in brain slices preincubated with3H-noradrenaline. The slices were prepared from parietal cortex (Cx), nucleus anterior hypothalami (nah) and nucleus tractus solitarii (nts). After preincubation, the tissues were superfused at 23°C or 37°C with a medium containing the noradrenaline uptake inhibitor desipramine. Electrical field stimulation was applied using stimulation frequencies of 0.3–10 Hz. 1. At 23°C/0.3 Hz, clonidine concentration-dependently inhibited the evoked overflow of tritium in all three brain regions. In contrast, at 23°C/3 Hz the inhibitory effect of the drug in the Cx was abolished and a facilitation was observed in the nah and nts. When tested at increasing frequencies of stimulation in the nts at 23°C, clonidine exerted a dual action, characterized by a reduction of electrically evoked responses at frequencies below 1 Hz and a facilitation at frequencies above 1 Hz. 2. At 37°C, clonidine concentration-dependently decreased the evoked overflow in all brain regions studied, this effect being more pronounced at 0.3 Hz than at 3 Hz. 3. The apparent lack of an effect of clonidine on the stimulation-evoked overflow of tritium in the Cx at 23°C/3 Hz was turned to a facilitation when noradrenaline (0.01 μmol/l) was included in the superfusion medium. Conversely, an inhibitory effect of clonidine was seen when the uptake blocker desipramine (as well as noradrenaline) was omitted from the superfusion medium. 4. The facilitation by clonidine of the stimulus-induced release in the nah at 23°C/3 Hz was reversed to inhibition when the noradrenaline content of the slices was reduced to about 60% by exposure to a medium containing 50 mmol/l potassium before preincubation with3H-noradrenaline. 5. A marked difference regarding the two superfusion temperatures was noted at the ultrastructural level: the superfusion of slices resulted in a widening of extracellular spaces, dissociation of synaptic clefts with preservation of presynaptic terminals, and intracytoplasmatic uptake of horseradish peroxidase. These changes were more pronounced after superfusion at 37°C than at 23°C. In accordance with these observations, the retention of3H-polyethyleneglycol in slices superfused at 37°C was greater than in slices superfused at 23°C. 6. It is concluded that in superfusion/stimulation experiments with brain slices temperature-dependent changes at the ultrastructural level may have an influence on the concentration of noradrenaline in the synaptic cleft. The results emphasize the role of the biophase concentration of noradrenaline with regard to the magnitude and the direction of the presynaptic effect of clonidine.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 338 (1988), S. 62-67 
    ISSN: 1432-1912
    Keywords: Rabbit brain cortex ; Noradrenaline release ; Single pulse stimulation ; Presynaptic receptor interactions ; α2-Autoreceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were carried out in rabbit cerebrocortical slices in order to find out whether the attenuation by presynaptic α2-autoreceptors of effects mediated by presynaptic opioid κ- and adenosine A1-receptors requires activation of the α2-receptors. The slices were preincubated with 3H-noradrenaline and then superfused with medium containing desipramine 1 μmol/l. They were stimulated electrically either with single pulses or with trains of 32 pulses at 1 Hz. The overflow of tritium elicited by a single pulse amounted to 0.21% of the tritium content of the tissue. It was Ca2+-dependent and tetrodotoxin-sensitive and not changed by rauwolscine 1 μmol/l or yohimbine 0.3 μmol/l. Ethylketocyclazocine (EK; 0.1–10 nmol/l) and R-(−)-N6-phenylisopropyladenosine (PIA; 1–1,000 nmol/1) potently inhibited the overflow evoked by a single pulse, and their effects were not changed by yohimbine. — The overflow of tritium elicited by trains of 32 pulses at 1 Hz amounted to 0.92% of the tritium content of the tissue and was increased approximately fourfold by yohimbine 0.3 μmol/l. EK and PIA were less potent inhibitors than in the one pulse experiments. Yohimbine greatly enhanced the effects of EK and PIA. The enhancement was even more pronounced when the Ca2+ concentration in the medium was reduced in order to obtain a control tritium overflow similar to that evoked by 32 pulses in the absence of yohimbine. The results demonstrate that there is no α2-adrenergic autoinhibition when noradrenaline release is elicited by a single pulse. Under these conditions, the non-activated presynaptic α2-adrenoceptor does not interfere with presynaptic opioid κ- and adenosine A1-receptor mechanisms. It is only when the autoreceptor is activated by released noradrenaline that it attenuates neighbouring presynaptic receptor mechanisms, and this attenuation is removed by α2-adrenoceptor antagonists.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1912
    Keywords: Presynaptic α2-autoreceptors ; Rabbit brain cortex ; Rat brain cortex ; Noradrenaline release ; pA2 value determination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An attempt was made to determinepA2 values of antagonists at the presynaptic, release-inhibiting α2-autoreceptorsof rabbit and rat brain cortex under conditions when there was very little released noradrenaline in the autoreceptor biophase and, hence,pA2 values were not distorted by endogenous autoinhibition. Cortex slices were preincubated with3H-noradrenaline and then superfused and stimulated by trains of 4 pulses delivered at 100 Hz or, in a few cases, by trains of 36 pulses at 3 Hz. The α-adrenoceptor agonists clonidine, noradrenaline, and α-methylnoradren-aline concentration-dependently decreased the stimulation-evoked overflow of tritium. The a-adrenoceptor antagonists yohimbine, rauwolscine and idazoxan did not increase the overflow of tritium elicited by 4 pulses/100 Hz in rabbit brain slices and increased it only slightly in rat brain slices. In contrast, the antagonists increased markedly the overflow at 36 pulses/3 Hz. All antagonists caused parallel shifts to the right of the concentration-response curves of clonidine, noradrenaline, and α-methylnoradrenaline.pA2 values were calculated either from linear regression of log [agonist concentration ratio − 1] on log [antagonist concentration] or from sigmoid curve fitting. The slopes of the linear regression lines were close to unity, and thepA2 values calculated by the two methods agreed well. There was no consistent preferential antagonism of any antagonist to any agonist.pA2 values determined with stimulation by 4 pulses/100 Hz were by 0.53–0.80 log units higher than those determined with stimulation by 36 pulses/3 Hz. ThepA2 values (4 pulses/100 Hz) of yohimbine and rauwolscine in rabbit brain slices (approximately 7.9 and 8.2, respectively), were slightly higher than in rat brain slices (approximately 7.6 and 7.7, respectively), whereas thepA2 value of idazoxan in the rabbit. (about 7.1) was lower than itspA2 value in the rat (about 8.0). The experiments confirm thatpA2 values determined under conditions of autoinhibition are too low. Stimulation with short (30 ms) bursts of pulses permits the estimation ofpA2 values at presynaptic a2-autoreceptors without (rabbit) or almost without (rat) the complication of autoinhibition. The values suggest that α2-adrenoceptors in rabbit brain cortex differ slightly from those in rat brain cortex.
    Type of Medium: Electronic Resource
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