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  • 1
    ISSN: 1662-8985
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: The industrial application of stainless steels is of high importance because of their highcorrosion resistance and forming behaviour. The evolution of martensite during the deep drawingprocesses leads to an increasing strain hardening of the material. In the collaborative research centre675 “Erzeugung hochfester metallischer Strukturen und Verbindungen durch gezieltes Einstellenlokaler Eigenschaften” (Creation of high strength metallic structures and joints by setting up scaledlocal material properties), metal forming processes is being researched. Emphasis on this part of theproject is the stress-induced formation of martensite in sheet metal and bulk metal components inmetastable austenitic steel. The aim of the investigations is to develop partial structure fields ofmartensite in sheet metal components in order to construct a lightweight structure. Therefore,components are divided into stretched and non-stretched parts. This leads to a defined buckling ofcomponents, for example in case of a crash. Furthermore, the effect of the transformation inducedformation of martensite in metastable austenitic steel should be utilised on bulk metal formingcomponents. Thereby special load adapted components with locally optimized properties areproducible, like austenitic ductile regions and martensitic high-strength areas
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background Lupus erythematosus tumidus (LET), a photosensitive skin disorder with characteristic clinical and histological features, has not been generally accepted as a subset of cutaneous lupus erythematosus (CLE). Objectives To analyse the expression of epidermal surface molecules in skin biopsy specimens from patients with LET and to relate the results to other variants of CLE, such as discoid lupus erythematosus (DLE) and subacute CLE (SCLE). Methods In total, 45 patients with different subtypes of CLE were included in the study, and cryostat sections from primary and ultraviolet (UV) A- and UVB-induced skin lesions were investigated using immunohistochemical methods. Results In contrast to healthy controls, skin lesions of LET showed upregulation of intercellular adhesion molecule-1 (ICAM-1) and histocompatibility class II molecules (HLA-DR), with an expression pattern resembling that seen in DLE and SCLE. Furthermore, staining with a monoclonal antibody against 27E10, a distinct marker for cell activation and differentiation, revealed intense focal or band-like labelling of all epidermal layers independent of the type of lesion. Conclusions Expression of epidermal surface molecules such as ICAM-1, HLA-DR and 27E10 is equally upregulated in primary and UV-induced lesions of patients with LET, DLE and SCLE. These results support our recent clinical findings that LET represents a distinct subset of CLE with a similar immunopathomechanism rather than a different disease.
    Type of Medium: Electronic Resource
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  • 3
    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: Long-term treatment with interferon alpha (IFN-α) has recently been shown to reduce the bone marrow infiltrate and cutaneous lesions in systemic mast cell disease. We therefore administered this cytokine to six patients with urticaria pigmentosa for up to 12 months, using subcutaneous injections of 5×106U, initially five times, and subsequently three times a week. The generally well-tolerated therapy resulted in marked improvement of the cutaneous symptoms, especially in three of the patients who suffered from very severe pruritus. Two of the patients with bone marrow infiltration showed normal findings after treatment. However, in none of the patients was there any change in the skin lesions, or decrease in the degree of cutaneous mast cell infiltration, as evidenced by light and electron microscopic examination. These findings indicate that IFN-α is highly effective in the control of symptoms, but otherwise does not influence the cutaneous lesions of urticaria pigmentosa.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 132 (1995), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We report a 55-year-old man with severe inflammatory epidermolysis bullosa acquisita. The skin lesions did not respond to various immunosuppressive treatments. The combined administration of prednisone, azathioprine, dapsone and colchicine resulted only in a transient and incomplete resolution of the lesions. The bullae and increased skin fragility were successfully controlled by the addition of high-dose intravenous immunoglobulin therapy.
    Type of Medium: Electronic Resource
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  • 5
    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: Schnitzler's syndrome is a distinct disease entity characterized by the association of chronic urticaria, intermittent fever, arthralgia, elevated erythrocyte sedimentation rate and IgM macroglobulin-aemia. We report a patient with the same symptoms, but a monoclonal IgG instead of IgM gammopathy. Histological examination of the urticarial lesions showed signs of mild leucocyto-clastic vasculitis. Except for the different class of the monoclonal immunoglobulin, the clinical symptoms, laboratory findings and histology in this patient were identical with those in classical Schnitzler's syndrome. IgG and IgM paraproteins may be equivalent with regard to the putative pathophysiology of the disease process in Schnitzler's syndrome. We therefore suggest that the spectrum of Schnitzler's syndrome is expanded to include patients with chronic urticaria and monoclonal IgG gammopathy, as a closely related variant.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background Ultraviolet (UV)-B irradiation has been shown to be an inducer of vascular endothelial growth factor (VEGF) in primary keratinocytes and epidermal cell lines in vitro. Objectives To determine the expression pattern and the causal role of VEGF in the UVB-mediated angiogenic response in vivo in human skin and in a mouse model. Methods Skin biopsies or epidermal lysates thereof were studied for VEGF expression following UVB irradiation at a dose of 50 or 60 mJ cm−2, respectively, using immunostaining and a VEGF-specific highly sensitive sandwich enzyme-linked immunosorbent assay. The VEGF-dependent increase in vessels upon repetitive UVB irradiation was studied in skh-1 hairless mice using immunostaining for factor VIII-related antigen (FVIII RAG) in the presence and absence of intraperitoneally injected neutralizing VEGF antibodies. Results VEGF was found to be induced in the epidermis following UVB irradiation of human and mouse skin. Repetitive UVB irradiation of skh-1 hairless mice resulted in an increase in FVIII RAG positive vessels in the skin. UVB-induced angiogenic response could be partly abrogated by neutralizing antibodies against VEGF, while isotype-matched IgG control antibodies did not reveal any suppressive effect. Conclusions Our results support previous in vitro data and show the in vivo relevance of VEGF as a paracrine inducer of cutaneous vessels after UVB irradiation.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Contact dermatitis (CD) is a frequent dermatological disease with a high socioeconomical impact characterized by acute to chronic inflammation of the skin, often leading to therapy-resistent eczema. Proteinase-activated receptor-2 (PAR-2), a G-protein-coupled receptor for certain serine proteases, is localized on keratinocytes, endothelial cells, and nerve fibers and has been demonstrated to play a role during inflammation of several tissues. However, the precise role of PAR-2 and the underlying mechanism of PAR-2-induced regulation of inflammation are still fragmentary. Therefore, we were interested in whether or not PAR-2 is involved in cutaneous inflammation using a model of experimentally induced allergic (ACD) and irritant (ICD) contact dermatitis. In wild-type (PAR-2+/+) mice, PAR-2 agonists induced an increased intradermal edema and enhanced plasma extravasation with a maximum between 3 and 24 h. These inflammatory responses were significantly diminished in PAR-2-deficient (PAR2–/–) mice and controls (vehicle). Morphological analysis revealed a dramatic increase of spongiosis and intradermal edema along with enhanced infiltration of neutrophils and monocytes in PAR-2+/+ mice as compared with PAR-2–/– mice. Interestingly, nitric oxide (NOS) inhibitors significantly diminished these effects, indicating a role of NO in PAR-2-induced inflammatory responses of the skin. Functional studies at the RNA and protein level further revealed PAR-2-induced upregulation of the cell adhesion molecules ICAM-1 and E-selectin by dermal microvascular endothelial cells during inflammation, suggesting that PAR-2 directly regulates cell adhesion molecule function during skin inflammation. PAR-2 agonists also stimulated upregulation of mediators involved in cutaneous inflammatory responses such as IL-6 and NO in murine and human (dermal) endothelial cells. Together, these results strongly suggest a proinflammatory role of PAR-2 during CD and probably other inflammatory dermatoses, especially during the early phase characterized by edema, plasma extravasation, and recruitment of inflammatory cells to the site of inflammation. Thus, PAR-2 antagonists may be therapeutic tools for the treatment of inflammatory skin disorders such as contact dermatitis and atopic eczema.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 10 (2001), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: To investigate the pathomechanisms of leukocytoclastic vasculitis (LcV) we compared mouse models of LcV with non-vasculitic irritant contact dermatitis (ICD). Criteria for LcV as met by the immune complex-mediated Arthus reaction (Art-r) were also fulfilled by the localized Shwartzman reaction (Shw-r) and by cutaneous Loxoscelism (Lox) (injection of venom from Loxosceles reclusa containing sphingomyelinase D). After depletion of PMN (by γ-irradiation) vessel damage could not be elicited in these models, distinguishing them from models of direct endothelial insult (necrotizing ICD). Depletion of complement could only delay, but not inhibit the Art-r, and did not change ICD, Lox or the Shw-r. The Shw-r exclusively revealed a sustained local expression of vascular adhesion molecules for 24 h in the preparatory phase (LPS s.c.), not observed in the Art-r, in Lox or ICD. Subsequent challenge with LPS i.p. was associated with upregulation of Mac-1 and ICAM-1 on PMN, but not of VLA-4 or LFA-1 (FACS analysis). Cytokines which were able to replace LPS in priming for LcV in the Shw-r (TNF-α and IL-1β) also induced sustained expression of adhesion molecules, whereas IL-12 and IFN-γ did neither. Neutralizing IL-12 or IFN-γ also inhibited neither LcV nor sustained expression of adhesion molecules, whereas anti-TNF-α inhibited both. Anti-TNF-α had no marked inhibitory effects in the Art-r, in Lox or ICD. Combined (but not separate) neutralization of both E-selectin and VCAM-1 by antibodies suppressed LcV independent from reducing influx of PMN, proving that their sustained expression is decisive for the Shw-r and interferes with normal diapedesis. Since Loxosceles venom is known to dysregulate diapedesis and degranulation of PMN in vitro, since adherent immune complexes activate PMN at the vessel wall, and since adhesion molecules are dysregulated in the Shw-r, we suggest that LcV develops when activation of PMN coincides with vascular alterations which interfere with normal diapedesis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract VCAM-1 (vascular cell adhesion molecule-1) is a cytokine-in-ducible adhesion molecule which is known to mediate adhesion of mononuclear cells to endothelial cells in vitro via binding to the integrin VLA-4 (very late antigen-4). To further elucidate the role and regulation of VCAM-1 in vivo, we compared in vitro and in vivo expression of VCAM-1 in response to cytokines and investigated immunohistochemically the expression of VCAM-1 in three murine models of experimental inflammation. These models differed with regard to the pathogenetic mechanism and the subsequent infiltrate: allergic contact dermatitis (ACD) to DNFB as a T cell-controlled, DTH type of inflammation, cutaneous infection with Leishmania major as a chronic granulomatous inflammation and the cauterized cornea as a model for acute inflammation. VCAM-1 was found to be markedly enhanced on vascular endothelia in all types of inflammation and after subcutaneous administration of LPS and TNF-a. Administration of IL-4, however, failed to induce VCAM-1 both in vivo and in vitro. The increased VCAM-1 expression in the inflammatory models correlated with the appearance of infiltrating monocytes/ macrophages. A concomitant influx of CD4-positive/CD8-positive lymphocytes was only observed in ACD and Leishmaniasis.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1173
    Keywords: Key words Acquired — C1-inhibitor deficiency — Angioneurotic oedema — Paraprotein — Livedo reticularis ; Schlüsselwörter Erworbener C1-Inhibitor-Mangel — Angioödem — Paraprotein — Livedo racemosa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A 61-year-old patient with life-threatening angioneurotic oedema was found to have an acquired C1-inhibitor (C1-INH) deficiency. In addition to lowered serum levels of C1-INH (both protein concentration and enzymatic activity), C2, C4 and CH50, which are characteristic for the hereditary form of angioneurotic oedema, markedly lowered C1q was found, which is typical for the acquired form. There were no antibodies against C1-INH. Repeated thorough examinations disclosed no neoplasm, though the presence of neoplasm has often been reported to be associated with the acquired C1-INH deficiency. However, the patient showed persistent paraproteinaemia and paraproteinuria and developed livedo reticularis. Treatment with danazol resulted in a rise in the complement fraction levels and cessation of angioneurotic oedema. Paraproteinaemia and livedo reticularis persisted unchanged.
    Notes: Zusammenfassung Wir berichten über einen 61jährigen Patienten mit lebensbedrohlichen Angioödemen, bei dem wir ursächlich einen erworbenen C1-Inhibitor-(INH)-Mangel feststellten. Neben erniedrigten Werten für C1-INH (Proteinkonzentration und enzymatische Aktivität), C2, C4 und CH50, wie sie auch für das hereditäre angioneurotische Ödem charakteristisch wären, wies unser Patient gleichzeitig eine ausgeprägte C1q-Verminderung auf. Dieser Befund ist diagnostisch wegweisend für die erworbene Form des Angioödems. Antikörper gegen C1-INH lagen nicht vor. Bei wiederholten Durchuntersuchungen fand sich kein Anhalt für ein Neoplasma, welches häufig mit einem akquirierten Angioödem assoziiert ist. Allerdings lagen eine Paraproteinämie und Paraproteinurie ohne den Nachweis eines Plasmozytoms vor. Im weiteren Verlauf entwickelte der Patient eine Livedo racemosa. Unter Danazoltherapie (Winobanin) kam es zu einem Anstieg bzw. zu einer Normalisierung der Komplementfraktionen und einem Ausbleiben der Angioödeme. Paraproteinämie und Livedo racemosa blieben unverändert bestehen.
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