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  • 2000-2004
  • 1980-1984  (3)
  • 1970-1974
  • striatum  (2)
  • 6-mercaptopurine  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Acantholysis producedin vitro with pemphigus serum: Hydrocortisone inhibits acantholysis, while dapsone and 6-mercaptopurine do not inhibit acantholysis (1984)
    Springer
    Journal of clinical immunology 4 (1984), S. 359-363 
    Details
    ISSN: 1573-2592
    Keywords: Pemphigus ; steroid ; hydrocortisone ; dapsone ; 6-mercaptopurine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Many studies have shown that human skin in organ cultures containing pemphigus antibody undergoes acantholysis, the histologic hallmark of pemphigus vulgaris. Thisin vitro organ culture system provides a good model to determine if drugs used to treat pemphigus inhibit the effect of pemphigus antibody after it is produced. In this study we determined if hydrocortisone, dapsone, and 6-mercaptopurine (6-MP) could inhibit acantholysis observed in human skin organ cultures containing high constant levels of pemphigus plasma. In six experiments we demonstrated that hydrocortisone (10−3 and 5×10−4 M) present at the start of organ culture inhibited acantholysis induced by pemphigus sera. Thus, this study raises the possibility that the large doses of steroids used to treat acute pemphigus could act directly on the skin, inhibiting acantholysis in the presence of high titers of pemphigus antibody. Other effective immunosuppressive drugs, such as dapsone and 6-MP, probably do not act directly on the skin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00917138
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of adenosine analogues (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 193-204 
    Details
    ISSN: 1573-6830
    Keywords: adenosine ; catecholamines ; neurotransmission ; calcium ; brain ; striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Adenosine analogues inhibit calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical and hippocampal vesicular preparations. Inhibition requires high concentrations (100µM) of the adenosine analogues and is abolished in the presence of high concentrations (2 mM) of calcium ions. The inhibitory effect of 2-chloroadenosine is blocked by theophylline. The structure activity profile (N 6-d-phenylisopropyladenosine ≥N 6-l-phenylisopropyladenosine ≥ 2-chloroadenosine 〉N 6-cyclohexyladenosine, adenosine 5′-cyclopropylcar-boxamide) is not that expected of either A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 2. Calcium-dependent K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations is inhibited by apomorphine. However, only 2-chloroadenoine causes an inhibition of K+-evoked release of [3H]dopamine. Other adenosine analogues such asd- andl-phenylisopropyladenosine and adenosine 5′-cyclopropylcar-boxamide cause a facilitation of K+-evoked release. The facilitation is abolished or reduced in the presence of high concentrations (2 mM) of calcium ions. The sites of action of adenosine analogues do not appear to have structural requirements identical to those expected of A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 3. The results indicate that adenosine analogues can have either inhibitory or facilitory effects on K+-evoked release of catecholamines from central synaptic terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711147
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Release of norepinephrine and dopamine from brain vesicular preparations: Effects of calcium antagonists (1982)
    Springer
    Cellular and molecular neurobiology 2 (1982), S. 205-213 
    Details
    ISSN: 1573-6830
    Keywords: calcium ; catecholamines ; neurotransmission ; brain ; striatum ; calcium antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The calcium antagonists D-600 (1–10µM) and diltiazem (10–25µM) inhibit K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical vesicular preparations. The inhibition of release is partially reversed by increasing concentrations of calcium to 2 mM. Diltiazem at 100µM has no effect on K+-evoked release of [3H]norepinephrine at 0.15 mM calcium but does inhibit release at 2.0 mM calcium. 2. The calcium antagonist nifedipine and dantrolene, an agent purported to antagonize release of calcium from intracellular storage sites, have no effect on K+-evoked release of [3H]norepinephrine. 3. The calcium antagonists D-600 (1µM) and diltiazem (10µM) inhibit K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations. Higher concentrations of drug, namely, 10µM for D-600 and 100µM for diltiazem, cause a potentiation rather than an inhibition of K+-evoked release. The potentiation is reduced in magnitude upon raising the extracellular calcium to 2.0 mM. Indeed, 10µM D-600 then inhibits K+-evoked release of [3H]dopamine. 4. The results indicate that putative calcium antagonists can have both inhibitory and facilitory effects on calcium-dependent K+-evoked release of catecholamines from central synaptic endings. Furthermore, certain peripheral calcium antagonists such as nifedipine and dantrolene may prove ineffective in central systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711148
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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