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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 8 (1981), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Fifty-seven members from ten families in which one parent and at least one child have asthma were studies with dilutional skin tests and RAST to grass pollens after determination of HLA haplotypes. We found no direct evidence for linkage of a hypothetical asthma locus with HLA or for a significant association of asthma with HLA haplotypes. Linkage between the HLA loci and a gene or genes which allow for the expression of clinical asthma could neither be proven nor disproven due to the small sample size. All of the asthmatic children had positive dilutional skin tests and RAST, suggesting that atopic asthma may be genetically controlled by the HLA chromosome (chromosome 6). Nonetheless, determination of the histocompatibility antigens can increase the value of predictive risk analysis for asthma. Such a determination may be important in the early identification of a child born to a family with atopic asthma.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 3 (1976), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Two children in a family were found to be homozygous for C2 deficiency; both parents and a third child were heterozygous. C2 deficiency was associated with the HLA haplotypes carrying the antigens B18 and DW2. Antigen A10 was absent in this family. Mixed lymphocyte culture studies among the family members confirmed the association of C2 deficiency with the HLA-D locus.
    Type of Medium: Electronic Resource
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  • 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: Backgound Birch pollen allergens have been implicated as asthma triggers; however, pollen grains are too large to reach the lower airways where asthmatic reactions occur. Respirable-sized particles containing birch pollen allergens have been detected in air filters, especially after rainfall but the source of these particles has remained speculative.Objective To determine the processes by which birch pollen allergens become airborne particles of respirable size with the potential to contribute to airways inflammation.Methods Branches with attached male catkins were harvested and placed in a controlled emission chamber. Filtered dry air was passed through the chamber until the anthers opened, then they were humidified for 5 h and air-dried again. Flowers were disturbed by wind generated from a small electric fan. Released particles were counted, measured and collected for immuno-labelling and high-resolution microscopy.Results Birch pollen remains on the dehisced anther and can rupture in high humidity and moisture. Fresh pollen takes as long as 3 h to rupture in water. Drying winds released an aerosol of particles from catkins. These were fragments of pollen cytoplasm that ranged in size from 30 nm to 4 μm and contained Bet v 1 allergens.Conclusion When highly allergenic birch trees are flowering and exposed to moisture followed by drying winds they can produce particulate aerosols containing pollen allergens. These particles are small enough to deposit in the peripheral airways and have the potential to induce an inflammatory response.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Complement activation is known to enhance neutrophil binding to human umbilical vein endothelial cells (HUVECs). Recently, we have shown that recombinant human C5a upregulates P-selectin in HUVECs. Unstimulated human neutrophil binding is also increased on C5a stimulated HUVECs. We demonstrate in this report that C5a upregulates CD11b/CD18 in human neutrophils. Also shown is that synthetic C3a57–77 and an analog 15 amino acid C3a peptide (C3a15) neither upregulate CD11b/CD18 nor do the C3a peptides increase P-selectin, ICAM-1 or E-selectin in HUVECs. Thus C5a and not C3a is responsible for early (∼30 minutes) neutrophil adhesion to endothelial cells after complement activation.
    Type of Medium: Electronic Resource
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