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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 117 (1987), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In 13 patients with delayed pressure urticaria (DPU) and in seven patients with chronic recurrent urticaria (CRU), prick tests were performed with a large battery of common allergens, including food extracts. Seven patients with DPU and all patients with CRU had positive early cutaneous reactions (15 min) (ECR), while six of the DPU and only one of the CRU patients had positive late cutaneous reactions (6h) (LCR). In the CRU patients, food allergens caused a positive ECR in one and no LCR in any of the cases, while two DPU patients had ECR and four had LCR to food allergens. The one patient with CRU and a positive LCR reacted to fungi, while of the DPU patients, five had LCRs to fungi, two to other inhalants, three to NaCl and one to histamine. None of the DPU patients lost their delayed pressure reactivity while on a diet lacking the food allergens to which they gave positive reactions.These results show that DPU patients have more frequent LCR than do CRU patients. They do not, however, confirm earlier reports claiming that the majority of DPU patients are allergic to food allergens and that their disease can be cured by elimination of the offending agents from their diet.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 13 (1981), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Low molecular weight eosinophil chemotactic factor (ECF), which has previously been demonstrated in mast cells, basophils, neutrophils and eosinophils, was shown to be released by several types of mononuclear phagocytes. Highly purified rat peritoneal macrophages and human monocytes produced ECK on stimulation with the calcium ionophore A23187 (Ion) and with phagocytic stimuli in a time-dependent fashion, whereas lymphocyte- or mast cell-specific stimuli were ineffective. Two murine macrophage lines and a fibroblast cell line (L cells) also generated and secreted ECF with the different stimuli. ECF from macrophages was similar to that from neutrophils in its target cell specificity (eosinophils and neutrophils) and its elution profile on Sephadex G-Hl columns (300–500 dalton). ECF secretion from monocytes was not affected by mitomycin C or cycloheximide, whereas indomethacin enhanced and a phospholipase A inhibitor decreased its production. These in vitro findings suggest that, through LCF, mononuclear phagocytes may potentially regulate eosinophil and neutrophil influx to sites of inflammatory reactions.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 15 (1982), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Purified mature rat peritoneal mast cells, on exposure to zymosan or latex beads, phagocytize these particles, although less efficiently than macrophages. During phagocytosis, histamine, β-glucuronidase, and eosinophil chemotactic factor are released from mast cells in a time-, temperature- and dose-dependent fashion. Complement components, cytochalasin B (5 μg/m1, and indomethacin (10-6m). enhanced mediator release, whereas compound BW 755C (20 μg/ml), a cyclooxygenasc and lipoxygenase inhibitor of arachidonate metabolism, totally abolished this process. Phagocytosis of mast cells thus activates imracellular mechanisms that closely resemble those observed with other phagocytic cells. These observations add a new perspective to the role of mast cells in inflammatory events.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 2 (1993), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Langerhans cells in the skin have recently been shown to bind IgE molecules via a high-affinity IgE receptor. Using two specific antibodies, 29C6 and 6F7, against the α-chain of the high-affinity IgE receptor we here demonstrate that Langerhans cells express this receptor in oral mucosa. A specific antibody. Tül, against the low-affinity IgE receptor showed only low expression of this receptor. High-affinity binding for IgE may be important for induction and support of Langerhans cell-dependent transepithelial IgE-mediated allergic reactions and inflammation.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 5 (1996), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Following the activation of specific receptors, phospholipase C has been shown to cleave the membrane phospholipid phosphatidylinositol bisphosphate into the 2nd messengers inositol 1,4,5-trisphosphate and di-acylgiycerol. Both 2nd messengers contribute to the regulation of cellular proliferation. The receptor for bradykinin is coupled to this pathway in keratinocytes, but knowledge about other activators of phospholipase C is limited. Additional mediators and agents were therefore examined regarding their ability to activate phospholipase C in HaCaT keratinocytes. Analysis for 3H-inositol phosphates was performed by anion-exchange HPLC. Thrombin and melittin induced a time- and dose-dependent release of inositol 1,4,5-trisphosphate. Several other mediators examined such as angiotension II, neurotensin, C3a, pituitary adenylate cyclase activating peptide, phenylephrin, and prostaglandin E2, did not induce the formation of inositol phosphates. In view of the mitogenic activity and the increased formation of thrombin after tissue injury, the coupling of the thrombin receptor to phospholipase C in HaCaT keratinocytes suggests a rôle of this protease in epidermal wound healing.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Mast cells and basophils are central effector cells of allergic reactions and are involved in inflammatory diseases. These cell types produce an array of mediators including a broad spectrum of cytokines. In order to examine whether antiallergic drugs modulate the release of these mediators, we have investigated the influence of dexamethasone and decarboethoxy-loratadine (DEL), the active metabolite of the H1-blocking agent loratadine, on the release of IL-6 and IL-8 by the human mast cell line HMC-1 and the human basophilic cell line KU812 by ELISA. Dexamethasone (10−6-10−11 M) or Del (10−5-10−14 M) were added to the cells either 1 h prior to or simultaneously with PMA and Ca-ionophore A23187. When preincubated with the cells, DEL dose-dependently suppressed IL-6 release by up to 40% and IL-8 release by up to 50%. Dexamethasone potently suppressed secretion of both cytokines if simultaneously added to the cells with the stimuli by up to 60% and after preincubalion by up to 80%. Since both antihistamines and glucocorticoids are used for treatment of allergic diseases, the findings reported here indicate that these drugs may modulate allergic reactions via inhibition of cytokine release from mast cells and basophils.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 130 (1994), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Despite the fact that several cell types residing in or travelling through the skin are targets and/or sources of nerve growth factor (NGF), little is known about the role of NGF in skin development, physiology and disease. Employing a previously defined skin organ culture assay for studying the proliferation of murine keratinocytes in their natural tissue environment, we have assessed the effect of murine NGF (7S) on keratinocyte proliferation in intact skin derived from two defined stages of the murine hair cycle. We found that 10–200 ng/ml NGF stimulated epidermal keratinocyte proliferation in organ-cultured C57 BL-6 mouse skin in the telogen phase of the hair cycle. Follicle keratinocyte proliferation was stimulated by 100 ng/ml NGF in telogen skin organ culture, but this concentration of NGF inhibited both epidermal and follicle keratinocyte proliferation in organ culture of anagen skin. The latter inhibitory effect of NGF was abrogated by co-incubation with neutralizing anti-NGF antibodies or with the protein kinase C inhibitor staurosporine. The proliferation-modulatory effects of NGF were associated with the induction of significant mast cell degranulation, and were inhibited by cromoglycate co-administration. This is the first report of a modulatory, hair cycle-dependent effect of NGF on keratinocyte proliferation in situ, which may require the presence of mast cells. Our study supports the notion of auto- and paracrine functions of NGF in murine skin physiology, which can be further assessed in the physiologically relevant mouse model delineated here.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 133 (1995), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: As urticarial lesions involve tissue invasion by inflammatory cells, and as β2-integrins play a central part in adhesion of leucocytes to endothelia, allowing their migration into the tissues, we have explored the distribution and sequential expression of these molecules in tissue sections from different forms of urticaria.Prick test weals (of 10 min duration) to common inhalant allergens showed only a minor increase of CD18, whereas in a case of cold urticaria CD11b and CD18 molecules were increasingly upregulated within the first 30 min after elicitation of the lesions. Skin test sites in delayed pressure urticaria, and urticarial esions (〉 6 h duration) of acute and chronic recurrent urticaria also showed marked upregulation of CD11b and CD18, and to a lesser extent of CD11a, but this did not strongly correlate with the intensity of the mixed cellular infiltrate. Non-lesional skin showed expression of β2-integrins in chronic urticaria, delayed pressure urticaria, and less so in acute urticaria, suggesting generalized leucocyte activation. This analysis of integrins thus suggests an early and extensive involvement of these molecules in the pathological events associated with the evolution of urticarial lesions.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 51 (1996), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In order to clarify the pathogenetic role of basophils and mast cells in chronic urticaria, histamine and leukotriene (LT)C4 release was examined in washed mixed leukocytes (n= 8) and skin mast cells (n= 5) from patients with chronic urticaria and compared with the same cells from normal controls (n= 9). Anti-IgE-stimulated basophil histamine release was significantly reduced in urticaria patients (median 2.9%vs 15.1% in normal controls), whereas histamine release to A23187. FMLP, and PAF, as well as anti-IgE-induced LTC4 release, showed no differences in both groups. In contrast, anti-IgE-stimulated skin mast cells from urticaria patients reacted similarly to those of controls (median histamine release 11.4%vs 14.2% in normal controls). Pretreatment of the cells with interleukin (IL)-3 upregulated responsiveness of basophil histamine release to anti-IgE in urticaria patients (median histamine release 14.3%), but pretreatment with the H2-antagonist cimetidine showed no effect. These data show that reduced basophil histamine releasability in chronic urticaria is not H2 mediated. It is a stimulus, mediator-, and cell type-restricted phenomenon that can, at least partially, be reversed in the presence of the cytokine IL-3.
    Type of Medium: Electronic Resource
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