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  • 1
    Electronic Resource
    Electronic Resource
    High-coercivity magnetic hard disks using glass substrates (1990)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 67 (1990), S. 4701-4703 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: A new structure for sputtered thin-film high-density longitudinal magnetic recording media using glass substrates has been proposed. The coercivity of Co alloy films is increased considerably by depositing a thin Ti layer between the Cr underlayer and the glass substrates. X-ray diffraction analysis indicates a change in the preferred orientation of the Cr layer. Transmission electron microscopy reveals that there is a significant change in the microstructure of the columnar Cr layer when Ti coating is used. It is proposed that the Ti film prevents oxygen from the glass substrates from reacting with the Cr and Co alloy magnetic layers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.346070
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  • 2
    Electronic Resource
    Electronic Resource
    Immunolocalization of target autoantigens in IgA pemphigus (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical and experimental dermatology 29 (2004), S. 0 
    Details
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: IgA pemphigus is a rare autoimmune bullous disease characterized by IgA deposition at keratinocyte cell surfaces. Clinically and histologically, IgA pemphigus is divided into two major subtypes: subcorneal pustular dermatosis (SPD) type and intraepidermal neutrophilic IgA dermatosis (IEN) type. Using cDNA transfection and living cell immunofluorescence, we previously showed that desmocollin 1, one of the desmosomal cadherins, is the autoantigen in SPD-type IgA pemphigus, but the autoantigen in IEN type is still unclear. In the present study we investigated antigen localization by postembedding immunoelectron microscopy. We examined three sera each of SPD-type and IEN-type IgA pemphigus. In SPD-type, gold particles were observed predominantly in the extracellular spaces between keratinocytes at desmosomes, although a few particles were observed in the intracellular domain at the desmosomal attachment plaques. In IEN type, the gold particles were observed mainly in the intercellular spaces in nondesmosomal areas. These results provide evidence that the IgA in the sera of SPD-type IgA pemphigus reacts with the extracellular domain of desmocollins. In contrast, the autoantigen for IEN type may in fact not be a component of desmosomes. IEN-type IgA pemphigus may be the first member of the pemphigus group of autoimmune bullous dermatoses that reacts with a nondesmosomal transmembranous protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2230.2004.01436.x
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  • 3
    Electronic Resource
    Electronic Resource
    A case of cold abscess due to disseminated tuberculosis in an AIDS patient (2000)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 142 (2000), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2000.03323.x
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  • 4
    Electronic Resource
    Electronic Resource
    Familial cluster of cutaneous Mycobacterium avium infection resulting from use of a circulating, constantly heated bath water system (2000)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 142 (2000), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We describe familial cases of cutaneous infection caused by Mycobacterium avium. A 45-year-old father, his 14-year-old son and 11-year-old daughter, among five persons in a family, presented with a 2-month history of inflammatory subcutaneous nodules and ulcerations. Histology of skin biopsy specimens showed granulomatous inflammation, and mycobacterial colonies isolated from the skin of each patient were identified as M. avium by DNA hybridization analysis. The patients were all treated successfully with combined drug therapy consisting of rifampicin, isoniazid and clarithromycin. Their lesions were purely cutaneous M. avium infection, without any visceral involvement. Neither systemic disease nor immunological impairment was detected in the family. However, they all used a circulating, constantly heated bath water system. The bath water was continuously heated to about 40 °C without changing the water for a few months, and M. avium was isolated from the filter of the bath tub heating unit. It is considered that this unusual familial cluster of cutaneous M. avium infection in healthy persons may have resulted from the use of contaminated bath water.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2000.03428.x
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  • 5
    Electronic Resource
    Electronic Resource
    Suppression of tumour necrosis factor-α expression in leprosy skin lesions during treatment for leprosy (1997)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 136 (1997), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The expression of tumour necrosis factor (TNF)-α in leprosy skin lesions was examined before and during successful treatment in a patient with borderline lepromatous leprosy. Before treatment, immunohistochemical staining of a skin biopsy specimen showed diffuse TNF-α deposits in granulomas and significant TNF-α deposits on infiltrated mononuclear cells. After 1 year's treatment, the skin lesions exhibited a reduction in granulomas, and a concomitant reduction in deposits of TNF-α.Furthermore, the level of expression of TNF-α messenger RNA. as examined using a reverse transcriptase-polymerase chain reaction method, was reduced markedly after treatment. These findings provide evidence for a correlation between the expression of TNF-α and disease activity suggesting that TNF-α is a useful prognostic indicator for inflammation in leprosy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.1997.d01-1208.x
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  • 6
    Electronic Resource
    Electronic Resource
    Requirement of CD80 and CD86 Molecules for Antigen Presentation by Eosinophils (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 44 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors analysed the antigen-presenting ability of eosinophils purified from peritoneal exudate cells of interleukin-5 (IL-5) transgenic mice. The granulocyte-macrophage colony-stimulating factor (GM-CSF)-treated eosinophils induced proliferative responses of primed lymph node T cells and thymus T cells to staphylococcal enterotoxin B (SEB), while untreated eosinophils induced little or no response. GM-CSF-treated eosinophils also induced proliferation of ovalbumin (OVA)-primed lymph node T cells to OVA. Although untreated eosinophils expressed no MHC class II molecule on the surface the eosinophils could be induced to express major histocompatibility complex (MHC) class II molecules when treated with GM-CSF. In the present study, anti-I-Ak monoclonal antibodies (MoAbs) strongly inhibited proliferation of thymus T cells and proliferation of OVA-primed lymph node T cells in response to OVA, but weakly inhibited proliferation of primed T cells in response to SEB. Furthermore, CD80 (B7-1) and CD86 (B7-2) were expressed on the surfaces of untreated eosinophils. The expression of those two molecules on the eosinophils was increased by incubation with GM-CSF. Moreover, anti-CD80 or anti-CD86 MoAbs blocked proliferative responses of primed lymph node T cells and thymus T cells to SEB, and also blocked responses of primed lymph node T cells to OVA. Thus, CD80 and CD86 play an important role in stimulation of T cells by eosinophils.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-303.x
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  • 7
    Electronic Resource
    Electronic Resource
    The role of LFA-1 in osteoclast development induced by co-cultures of mouse bone marrow cells and MC3T3-G2/PA6 cells (2002)
    Oxford, UK : Munksgaard International Publishers
    Journal of periodontal research 37 (2002), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Interactions between leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM−1) influence the development of osteoclasts. However, little is known about how these adhesion molecules are involved in the process of osteoclast development. This study evaluated the role of LFA-1 and its ligands in osteoclast development and bone resorption. Co-cultures of bone marrow cells from LFA-1-deficient mice and MC3T3-G2/PA6 (PA6) cells were cultured in the presence of 1α,25(OH)2D3 and dexamethasone for 7 days. The number of TRAP-positive cells that were generated by bone marrow cells from LFA-1-deficient mice was smaller than that generated by bone marrow cells from wild-type mice. In addition, the bone-resorbing activity of osteoclast-like cells that were generated from LFA-1-deficient mice was lower than that generated by osteoclast-like cells from wild-type mice. Immunofluorescence flow cytometry showed that osteoclast stromal PA6 cells expressed the cell adhesion molecules, ICAM-1 and VCAM-1. When monoclonal antibodies to mice VCAM-1, CD11b or CD18 were added separately to the co-culture system, the number of TRAP-positive cells that were generated from LFA-1-deficient mice was 20–30% smaller than that generated from wild-type mice. The formation of TRAP-positive cells from both LFA-1 deficient and wild-type mice was especially inhibited by anti-CD18 antibody, in comparison to the addition of normal IgG serum. These results suggest that LFA-1 adhesion molecules play a role in osteoclast development by affecting adhesion between stromal cells and osteoclast progenitors before the occurrence of ODF-ODF receptor signaling. CD18 appears to be a key adhesion molecule in cell-to-cell contacts during the early stage of osteoclast development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0765.2002.00610.x
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  • 8
    Electronic Resource
    Electronic Resource
    Role of the Ek Molecule in the Generation of Suppressor T Cells in Response to LDHB (1982)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 16 (1982), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The role of the Ek (EαEβk) molecule in the generation of suppressor T (Ts) cells specific for lactate dehydrogenase B (LDHB) was studied using different approaches. First, lymph node cells from LDHB-primed B1O.A(2R) (AkEk) nonresponder mice were shown to suppress the LDHB-specific and Ak-restricted proliferative response of T cells from the congenic responder strain B10.A(4R), which does not express E molecules (AkEo). Similarly, lymph node cells from primed CBA (AkEk) mice suppressed the anti-LDHB response of Lyt-1+Lyt-2- T celfs (depleted of Lyt-2-bearing TS cells) from the same mice. Second, in vitro priming of 2R (AkEk) T cells with LDHB-pulsed 4R (AkEo) antigen-presenting cells (APC) generated T-cell proliferation but not suppression. Third, nonresponder 2R mice were turned into responders by injecting them with LDHB-pulsed 4R APC or monoclonal Ia.m7 antibody that blocks the Ek molecule. The data demonstrate that expression of Ek molecules by the APC is necessary to generate LDHB-specific Ts cells, which in turn prevent the proliferation of Lyt-l+Lyt-2- (probably helper) cells recognizing the same antigen in the context of the Ak molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1982.tb00695.x
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  • 9
    Electronic Resource
    Electronic Resource
    Histopathological study of focal dermal hypoplasia (Goltz syndrome) (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental dermatology 17 (1992), S. 0 
    Details
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We report a case of focal dermal hypoplasia, or Goltz syndrome in a 13-year-old girl. The patient presented with a variety of cutaneous defects, including atrophy-like depressions, striations, a verrucous papilloma, and lipomas. Histopathological examination showed deposits of fat cells or adipose tissue in the dermis, which were subepidermal, mid-dermal, perivascular, or involved the whole dermis. These findings indicate that the adipose tissue in the dermis is a result of dermal dysplasia and not hypoplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2230.1992.tb02527.x
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  • 10
    Electronic Resource
    Electronic Resource
    Hereditary angioedema caused by a point mutation of exon 7 in the Cl inhibitor gene (1996)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Hereditary angioedema (HAE) is a genetic disease which may be detected serologically. We present a patient with HAE in whom we examined the gene defect using the polymerase chain reaction. The patient presented with recurrent episodes of abdominal pain, or non-itchy swellings of the hands, feet, and penis. The serum levels of C1 inhibitor (C1-INH and C4 were below normal. We determined that a single base change (C-T) at nucleotide 1482 in the seventh exon was present in the C1-INH gene. This mutation converted the codon for the Gln-339 to a premature translation termination codon TAG. A point mutation in the C1-INH gene can cause type I HAE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2133.1996.tb06980.x
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