Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Electronic Resource  (7)
Material
  • Electronic Resource  (7)
  • 1
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd.
    Journal of the European Academy of Dermatology and Venereology 17 (2003), S. 0 
    ISSN: 1468-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  As long-wave ultraviolet (UV) radiation penetrates the dermis, connective tissue cellular components and circulating blood cells can be possible targets for solar UVA. Basophils, involved in the effector phase of the inflammatory response, play a part in skin diseases such as chronic urticaria, psoriasis, atopic dermatitis, fixed drug eruption, allergic contact dermatitis, urticaria pigmentosa, systemic sclerosis and bullous pemphigoid.Objective  The evaluation of the in vitro effect of UVA on histamine release from human basophils.Methods  Basophils from healthy human volunteers were irradiated, respectively, with UVA at doses of 2.5, 5, 7.5, 10, 20 and 50 J/cm2 and then incubated with an anti-IgE serum. A fluorimetric technique was employed to determine histamine release from samples: (i) incubated with 2% HClO4 (complete lysis of basophils); (ii) irradiated with increasing doses of UVA; and (iii) unirradiated (controls).Results  Histamine release was: 100% for HClO4 incubated basophils, 30% for unirradiated and anti-IgE incubated cells (controls) and 27%, 24%, 34%, 41%, 60% and 70% for basophils irradiated with UVA doses, respectively, of 2.5, 5, 7.5, 10, 20 and 50 J/cm2 and incubated with anti-IgE. Histamine releasability from irradiated samples was statistically significant (P 〈 0.05), in comparison with controls, at UVA doses equal to 5, 10, 20 and 50 J/cm2.Conclusions  UVA exerts, at least in vitro, a biphasic dose-dependent action on histamine release from human basophils incubated with an anti-IgE serum: at the lowest irradiation doses (〈 5 J/cm2) it exerts an inhibitory effect and at the highest doses ( 10 J/cm2) histamine release increases significantly.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Basophils and mast cells play a major role in the pathogenesis of allergic disorders by releasing several proinflammatory mediators. Some histamine H1 receptor antagonists exert anti-inflammatory activities by modulating mediator release from basophils and mast cells.Objective To study the in vitro effects of mizolastine, an H1 receptor antagonist, on the release of eicosanoids, histamine and IL-4 from human basophils and lung mast cells.Methods and results Mizolastine (10−7–10−5 m) concentration-dependently inhibited the release of cysteinyl leukotriene C4 from anti-IgE-stimulated basophils (IC50: 3.85±0.28 μm) and mast cells (IC50: 3.92±0.41 μm). The same concentrations of mizolastine did not affect anti-IgE-induced prostaglandin D2 release from lung mast cells. In contrast, mizolastine enhanced up to 80% IgE-mediated histamine release (EC50: 4.63±0.14 μm) from basophils, but not from mast cells and it significantly potentiated IL-4 release from basophils induced by anti-IgE. Mizolastine did not affect histamine release from basophils induced by formyl peptide, whereas it inhibited cysteinyl leukotriene C4 release (IC50: 1.86±0.24 μm). Blockade of cytosolic phospholipase A2 and arachidonic acid mobilization by pyrrolidine-1 did not alter the effect of mizolastine on histamine release from basophils, thereby excluding accumulation of arachidonic acid metabolic intermediates as the cause of this effect. Mizolastine did not influence anti-IgE-induced activation of extracellular signal-regulated kinase-1 and -2 (ERK-1 and -2) in human basophils.Conclusions Mizolastine efficiently inhibits LTC4 synthesis in human basophils and mast cells presumably by interfering with 5-lipoxygenase. In contrast, it enhances histamine and IL-4 release only from anti-IgE-stimulated basophils. Therefore, mizolastine differentially regulates the production of mediators from basophils and mast cells in a cell- and stimulus-specific fashion.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Loratadine, a novel histamine H1-receptor antagonist, is effective in the treatment of patients with seasonal and perennial rhinitis and some allergic skin disorders. Histamine and other chemical mediators are synthesized and immunologically released by human peripheral blood basophils and tissue mast cells (FcɛRI+ cells).Objective To evaluate the effects of loratadine and its main metabolite, desethoxylcarbonyl-loratadine (des-loratadine), on the immunological release of preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4: LTC4 and prostaglandin D2: PGD2) from human FcɛRI+ cells.Methods Human FcɛRI+ cells purified from peripheral blood and from skin (HSMC) and lung tissue (HLMC) were preincubated with loratadine and des-loratadine before immunological challenge with Der p 1 antigen or anti-FcɛRI. The release of preformed mediators (histamine and tryptase) and de novo synthesized eicosanoids was evaluated in the supernatants of human FcRI+ cells.Results Preincubation (15m in, 37°C) of purified (36–74%) basophils with loratadine (3 × 10–6–10–4M) and des-loratadine before Der p 1 antigen or anti-FcɛRI challenge concentration-dependency (5–40%) inhibited the release of histamine and LTC4. Loratadine (3 × 10–6–l0–4M) and des-loratadine also inhibited (10–40%) histamine, LTC4, and PGD2 release from purified HLMC (16–68%) activated by anti-FcɛRI. Loratadine (3 × 10–6–10–4M) and des-loratadine caused concentration-dependent inhibition (10–40%) of histamine, tryptase. LTC4, and PGD2 release from purified HSMC (24– 72%) immunologically challenged with anti-FcɛRI.Conclusion These results indicate that loratadine and its main metabolite have anti- inflammatory activity by inhibiting the release of preformed and de novo synthesized mediators from human FcɛRI+ cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 32 (2002), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated thein vitro effects of increasing concentrations (10−5–10−3 M) of four muscle relaxants (succinylcholine, d-tubocurarine, vecuronium and atracurium) on histamine release (HR) from human peripheral blood basophils and mast cells isolated from lung parenchyma (HLMC) and skin tissues (HSMC). Basophils released less than 5% of their histamine content when incubated with any one of the muscle relaxants. In contrast, mast cells showed a marked heterogeneity in their response. Succinylcholine did not induce HR from any type of mast cell, and only high concentrations of d-tubocurarine (10−3 M) caused HR from HSMC and HLMC. Vecuronium concentration-dependently induced HR from HLMC and HSMC. Atracurium concentration-dependently caused marked HR from HLMC and HSMC up to a maximum of 46.2±15.1% and 30.6±6.0%, respectively. From both HLMC and HSMC HR caused by atracurium and vecuronium was extremely rapid (t1/2〈1 min). The releasing activity of atracurium and vecuronium on HLMC and HSMC was reduced, but not abolished, by lowering the temperature of the incubation buffer to 22°C and 4°C. These results confirm that there are functional differences between human basophils and mast cells and among mast cells isolated from different anatomical sites in response to the muscle relaxants tested.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that physiological concentrations of zinc (≃7×10−6 M) inhibit the release of histamine from human basophil leukocytes (Maroneet al., J. Pharmacol. Exp. Ther. 217: 292, 1981). In these experiments we compared the effect of zinc chloride on the release of chemical mediators from human basophils and mast cells isolated from human lung. Preincubation (5 min, 37°C) of human basophils and lung mast cells with zinc chloride (10−6–3×10−5 M) caused dose-related inhibition of histamine and peptide leukotriene C4 (LTC4) release induced by anti-IgE. Increase Ca2+ concentrations (0.3 to 6 mM) in the extracellular medium completely reversed the inhibitory effect of zinc on anti-IgE-mediated histamine secretion. Zinc chloride was a competitive antagonist of the action of Ca2+ in histamine secretion induced by anti-IgE with a dissociation constant (Kd) of about 10−5 M in both the basophil and mast cell systems. Thus physiological concentrations of zinc inhibit the release of histamine from human basophils and lung mast cells, presumably by blocking Ca2+ uptake induced by anti-IgE activation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...