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  • 1
    Online Resource
    Online Resource
    Berlin [u.a.] : Springer
    Person(s): Hertel, Peter
    Keywords: Mathematik ; Lehrbuch ; Mathematik
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource
    ISBN: 9783540890430 , 9783540890447
    Series Statement: Springer-Lehrbuch
    RVK:
    Language: German
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  • 2
    Online Resource
    Online Resource
    Berlin [u.a.] : Springer
    Person(s): Hertel, Peter
    Keywords: Mathematik ; Aufgabensammlung ; Mathematik
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource
    ISBN: 9783642177880 , 3642177883 , 9783642177897
    Series Statement: Springer-Lehrbuch
    RVK:
    Language: German
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  • 3
    Online Resource
    Online Resource
    Berlin [u.a.] : Springer
    Person(s): Hertel, Peter
    Keywords: Theoretische Physik ; Lehrbuch ; Theoretische Physik
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource
    ISBN: 9783540366447 , 354036644X , 9783540366454
    Series Statement: Springer-Lehrbuch
    DDC: 530.1
    RVK:
    RVK:
    Language: German
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  • 4
    Book
    Book
    Berlin [u.a.] : Springer
    Person(s): Hertel, Peter
    Keywords: Theoretische Physik ; Theoretische Physik - Lehrbuch ; Lehrbuch ; Theoretische Physik
    Type of Medium: Book
    Pages: XIII, 379 S. , graph. Darst.
    ISBN: 9783540366447 , 354036644X
    Series Statement: Springer-Lehrbuch
    DDC: 530
    RVK:
    RVK:
    Language: German
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Trauma und Berufskrankheit 2 (2000), S. S199 
    ISSN: 1436-6274
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    The European physical journal 186 (1965), S. 288-298 
    ISSN: 1434-601X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract A distinction is made between bound states which can be calculated by a many channel method and those which can already be obtained parameter free by an inelastic single channel calculation. Two many channel models are investigated and it is shown that in some cases an inelastic single channel calculation needs additional parameters which are furnished by the many channel treatment only. The results may have some bearance on the problem whether the nucleon is a bound state.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    The European physical journal 211 (1968), S. 491-494 
    ISSN: 1434-601X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The lifetime of a hypotheticalκ meson with low mass, introduced byGlashow andWeinberg in a model for simultaneous breaking ofSU(3) and chiral symmetry, is calculated. The coupling constant of theκ toKπ is obtained by assuming that the divergence of the strangeness changing vector current is dominated by theκ pole.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Communications in mathematical physics 28 (1972), S. 159-176 
    ISSN: 1432-0916
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics , Physics
    Notes: Abstract The energy as function of entropy and the free energy as function of temperature is calculated rigorously for nonrelativistic fermions with interactions. It is shown that in the appropriate thermodynamic limit the corresponding Thomas-Fermi equation becomes exact.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1432-1912
    Keywords: 5-HT1A receptor antagonist ; Citalopram ; Antidepressant ; Electrophysiology ; Dorsal raphe nucleus ; (S)-UH-301 ; (+)-WAY100135
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this study we have examined the acute effects of systemic administration of the selective serotonin reuptake inhibitor (SSRI), citalopram, in combination with either of the two selective 5-HT1A receptor antagonists, (S)-5-fluoro-8-hydroxy-2-(dipropylamino)-tetralin [(S)-UH-301] or (+)-N-tertbutyl 3-(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenylpropionamide dihydrochloride [(+)-WAY100135], on the activity of single 5-HT neurons in the dorsal raphe nucleus (DRN) of anesthetized rats using extracellular recording techniques. Acute administration of citalopram (0.3 mg/kg i.v.) significantly decreased the firing rate of DRN-5-HT cells most likely as a result of indirect stimulation of inhibitory somatodendritic 5-HT1A autoreceptors located on 5-HT cells in the DRN. This effect of citalopram was completely reversed by (S)-UH-301 (0.5 mg/kg i.v.) and partly by (+)WAY100135 (0.5 mg/kg i.v.). Furthermore, the inhibitory effect of citalopram on the activity of 5-HT neurons was significantly attenuated by pretreatment with (S)-UH-301 (0.25 mg/kg i.v.) or (+)-WAY100135 (0.25 mg/kg i.v.). We have also studied the effects of (S)-UH-301 (0.03–0.50 mg/kg i.v.) on the firing rate of single DRN5-HT cells in rats chronically treated with citalopram (20 mg/kg/day i.p. × 14 days). Administration of (S)UH-301 significantly and dose-dependently increased the activity of 5-HT cells in citalopram-treated rats, but did not affect these neurons in saline-treated (1 m1/kg/day i.p. × 14 days), control rats. Our results thus suggest that 5-HT1A receptor antagonists can augment both the acute and chronic effects of citalopram on central serotonergic neurotransmission. Since the antidepressant effect of SSRIs is critically linked to the availability of 5-HT, these findings support the notion that 5-HT1A receptor antagonists may not only shorten the latency of onset of SSRIs in the treatment of depression, but also increase their efficacy.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1432-1912
    Keywords: Key words Antidepressant ; Citalopram ; Frontalcortex ; Microdialysis ; Serotonin ; 5-HT1Areceptor antagonist ; (S)-UH-301
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In a recent study, utilizing single cell recording techniques, we have shown that administration of 5-HT1A receptor antagonists, e.g. (S)-UH-301, to rats concomitantly treated, acute or chronically, with the selective serotonin reuptake inhibitor (SSRI) citalopram significantly increases the activity of 5-hydroxytryptamine (5-HT) containing neurons in the dorsal raphe nucleus (DRN). Here we report correlative experiments using microdialysis in freely moving animals to measure extracellular levels of 5-HT and its metabolite 5-hydroxyindole acetic acid (5-HIAA) in the frontal cortex, a major projection area for DRN-5-HT neurons. Acute administration of (S)-UH-301 (2.5 mg/ kg s.c.) or citalopram (2.0 mg/kg s.c.) increased 5-HT concentrations with a maximum of about 70% and 185%, respectively, above baseline. However, when (S)-UH-301 was administered 30 min before citalopram the maximal increase in 5-HT levels was approximately 400%. In rats chronically treated with citalopram (20 mg/kg/day i.p. for 14 days) basal 5-HT concentrations in the frontal cortex were significantly increased and 5-HIAA concentrations were decreased when measured 10–12 h, but not 18–20 h, after the last injection of citalopram, as compared to basal 5-HT and 5-HIAA concentrations in chronic saline-treated rats. When (S)-UH-301 (2.5 mg/kg s.c.) was administered 12 h, but not 20 h, after the last dose of citalopram it produced a significantly larger increase in extracellular concentrations of 5-HT than in control rats. However, in rats pretreated with a single, very high dose of citalopram, 20 mg/kg i.p., administration of (S)-UH-301 at 12 h after citalopram did not increase 5-HT levels. The augmentation by (S)-UH-301 of the increase in brain 5-HT output produced by acute administration of citalopram is probably due to antagonism of the citalopram induced feedback inhibition of 5-HT cells in the DRN, as previously suggested. However, the capacity of (S)-UH-301 to further increase the already elevated extracellular concentrations of 5-HT in brain in animals maintained on a chronic citalopram regimen, in which significant tolerance to the initial feedback inhibition of DRN-5-HT cells had developed, represents a novel finding. Generally, the reduced feedback inhibition of 5-HT neurons obtained with chronic citalopram treatment, and the associated elevation of brain 5-HT concentrations, may be related to functional desensitization of somatodendritic 5-HT1A autoreceptors in the DRN. This phenomenon may also largely explain the larger increase in 5-HT output produced by (S)-UH-301 in chronic citalopram treated animals as compared to its effect in control animals. Yet, a contributory factor may be a slight, remaining feedback inhibition of the 5-HT cells caused by residual citalopram at 12, but not 20 h after its last administration.  Previous clinical studies suggest that addition of a 5-HT1A receptor antagonist to an SSRI in the treatment of depression may accelerate the onset of clinical effects. Moreover, in therapy-resistant cases maintained on SSRI treatment, addition of a 5-HT1A receptor antagonist may improve clinical efficacy. Since the therapeutic effect of SSRIs in depression has been found to be critically linked to the availability of 5-HT in brain, our experimental results support, in principle, both of the above clinically based notions.
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