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  • Journal article
    Cookson W, 1994,

    The genetics of atopy.

    , J Allergy Clin Immunol, Vol: 94, Pages: 643-644, ISSN: 0091-6749
  • Journal article
    Moffatt MF, Hill MR, Cornélis F, Schou C, Faux JA, Young RP, James AL, Ryan G, le Souef P, Musk AWet al., 1994,

    Genetic linkage of T-cell receptor alpha/delta complex to specific IgE responses.

    , Lancet, Vol: 343, Pages: 1597-1600, ISSN: 0140-6736

    IgE responses to inhaled proteins underlie the clinical syndrome of allergic (atopic) asthma and rhinitis. We have investigated genetic linkage between specific IgE reactions to highly purified major allergens and the T-cell receptor (TCR) alpha and beta gene complexes on chromosome 14 and 7, respectively. Antigens tested included highly purified proteins from the housedust mite Dermatophagoides pteronyssinus, the domestic cat and dog, grass pollen, and the mould Alternaria alternata. Affected sibling-pair methods were used in two independent sets of families, one in the UK and one in Australia. No linkage of IgE serotypes to TCR-beta was detected, but significant linkage to TCR-alpha was seen in both family groups. For several of the IgE phenotypes investigated (positive responses to whole allergen sources or purified antigens or serum IgE above the 70th percentile in the population) the affected sibling-pairs showed significant sharing of TCR-alpha microsatellite alleles from both parents. The results show that a gene (or genes) in the TCR-alpha region modifies specific IgE responses.
  • Journal article
    Shirakawa T, Li A, Dubowitz M, Dekker JW, Shaw AE, Faux JA, Ra C, Cookson WO, Hopkin JMet al., 1994,

    Association between atopy and variants of the beta subunit of the high-affinity immunoglobulin E receptor.

    , Nat Genet, Vol: 7, Pages: 125-129, ISSN: 1061-4036

    The beta-subunit of the high-affinity IgE receptor (Fc epsilon RI-beta) on chromosome 11 is maternally linked to atopy, the state of enhanced IgE responsiveness underlying allergic asthma and rhinitis. We have identified a common variant of Fc epsilon RI-beta, lle181Leu within the 4th transmembrane domain. Leu181 shows significant association with positive IgE responses in a random patient sample. Amongst 60 unrelated nuclear families with allergic asthmatic probands, Leu181 is identified in 10 (17%), is maternally inherited in each, and shows a strong association with atopy. Our data indicate that Fc epsilon RI-beta, subject to maternal modification, may be the atopy-causing locus on chromosome 11q.
  • Journal article
    STAFFORD AN, RIDER SH, HOPKIN JM, COOKSON WO, MONACO APet al., 1994,

    A 2.8 MB YAC CONTIG IN 11Q12-Q13 LOCALIZES CANDIDATE GENES FOR ATOPY - FC-EPSILON-RI-BETA AND CD20

    , HUMAN MOLECULAR GENETICS, Vol: 3, Pages: 779-785, ISSN: 0964-6906
  • Journal article
    Young RP, Dekker JW, Wordsworth BP, Schou C, Pile KD, Matthiesen F, Rosenberg WM, Bell JI, Hopkin JM, Cookson WOet al., 1994,

    HLA-DR and HLA-DP genotypes and immunoglobulin E responses to common major allergens.

    , Clin Exp Allergy, Vol: 24, Pages: 431-439, ISSN: 0954-7894

    In order to test for human histocompatibility leucocyte antigens (HLA) class II restriction of IgE responses, 431 subjects from 83 families were genotyped at the HLA-DR and HLA-DP loci and serotyped for IgE responses to six major allergens from common aero-allergen sources. A possible excess of HLA-DR1 was found in subjects who were responsive to Fel d I compared with those who were not (Odds Ratio (OR) = 2, P = 0.002), and a possible excess of HLA-DR4 was found in subjects responsive to Alt a I (OR = 1.9, P = 0.006). Increased sharing of HLA-DR/DP haplotypes was seen in sibling pairs responding to both allergens. Der p I, Der p II, Phl p V and Can f I were not associated with any definite excess of HLA-DR alleles. No significant correlations were seen with HLA-DP genotype and reactivity to any of the allergens. The results suggest class II HLA restriction is insufficient to account for individual differences in reactivity to common allergens.
  • Journal article
    DESAI SR, WELLS AU, CHEAH FK, COLE PJ, HANSELL DMet al., 1994,

    THE REPRODUCIBILITY OF BRONCHIAL CIRCUMFERENCE MEASUREMENTS USING COMPUTED-TOMOGRAPHY

    , BRITISH JOURNAL OF RADIOLOGY, Vol: 67, Pages: 257-262, ISSN: 0007-1285
  • Journal article
    Fowler PA, Fraser M, Cunningham P, Knight PG, Byrne B, McLaughlin EA, Wardle PG, Hull MG, Templeton Aet al., 1994,

    Higher gonadotrophin surge-attenuating factor bioactivity is found in small follicles from superovulated women

    , Journal of Endocrinology, Vol: 143, Pages: 33-44

    Ovine and rat pituitary bioassays for gonadotrophin surge-attenuating factor (GnSAF) were utilized to determine whether the level of GnSAF bioactivity in pooled human follicular fluid (hFF) from superovulated women varied according to follicle diameter (< or = 11 mm, 12-15 mm and 16-21 mm follicles examined using the ovine bioassay, or < or = 10 mm, 11-13 mm, 14-17 mm, 18-20 mm, 21-24 mm and > or = 25 mm follicles examined using the rat bioassay). When tested using dispersed ovine pituitary cells, GnSAF bioactivity, expressed in terms of the reduction in gonadotrophin-releasing hormone (GnRH)-induced LH secretion, was inversely related to follicle diameter (P < 0.01). In response to 5 microliters hFF/well from follicles of < or = 11, 12-15 and 16-21 mm diameter, GnRH-induced LH secretion was reduced to 40.5 +/- 6.9%, 65.2 +/- 6.6% and 83.7 +/- 7.9% of control respectively. A similar inverse relationship was observed when a second batch of hFF samples from different sized follicles was tested using rat pituitary cell monolayers. Expressing GnSAF bioactivity in terms of the dose required to suppress GnRH-induced LH secretion by rat pituitary cells to 50% of the maximal suppression observed (ED50), the three smallest follicle size pools contained the most GnSAF (ED50 values of 0.13, 2.79 and 5.36 microliters hFF/well from follicles of < or = 10, 11-13 and 14-17 mm respectively). The ED50 values for follicles of 18-20, 21-24 and > or = 25 mm were 8.81, 27.1 and 60.0 microliters hFF/well respectively. Thus hFF from follicles < or = 11 mm was over 450 times more potent than hFF from follicles > or = 25 mm in suppressing GnRH-induced LH release. The ED50 values for inhibin bioactivity (measured as the suppression of basal FSH secretion from rat pituitary monolayers) were much less variable than those for GnSAF bioactivity (between 0.85 and 0.13 microliters hFF/well). Inhibin immunoreactivity, measured by a two-site immunoradiometric assay, follow
  • Journal article
    DIALLINAS G, GORFINKIEL L, ARST HN, CECCHETTO G, SCAZZOCCHIO Cet al., 1994,

    GENETIC AND MOLECULAR CHARACTERIZATION OF PURINE PERMEASE GENES OF ASPERGILLUS-NIDULANS REVEALS A NOVEL FAMILY OF TRANSPORTERS CONSERVED IN PROKARYOTES AND EUKARYOTES

    , FOLIA MICROBIOLOGICA, Vol: 39, Pages: 513-514, ISSN: 0015-5632
  • Journal article
    Arst HN, 1994,

    Regulation of gene expression by oxygen, phosphorus and pH.

    , Prog Ind Microbiol, Vol: 29, Pages: 369-380, ISSN: 0079-6352
  • Journal article
    Fowler PA, Cunningham P, Fraser M, MacGregor F, Byrne B, Pappas A, Messinis IE, Templeton Aet al., 1994,

    Ciruclating gonadotrphin surge attenuating factor from superovulated women suppresses in vitro gonadotrophin-releasing hormone self-priming

    , Journal of Endocrinology, Vol: 143, Pages: 45-54

    A perifusion system based on ovine pituitary tissue explants was used to investigate the effects of follicular fluid (hFF) and serum from superovulated women on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH). The specific aims of the study were to determine both if gonadotrophin surge-attenuating factor (GnSAF) bioactivity is present in the peripheral circulation as well as in the follicles of superovulated women and if GnSAF suppresses GnRH self-priming in vitro. Two pulses of GnRH, 1 h apart, produced marked peaks in LH secreted from control chambers, with GnRH self-priming evident in the significant difference between the first (134.4 +/- 1.7 - 232.1 +/- 24.0% of basal secretion) and second (183.9 +/- 15.8 - 313.9 +/- 14.0% of basal secretion) LH peaks. Both follicular fluid and serum pooled from two different groups of women produced marked suppression of the first (unprimed) and second (primed) LH peaks. The hFF reduced the first LH peak to 69.6 +/- 7.8 and 60.2 +/- 9.7% and the second LH peak to 57.4 +/- 6.7 and 42.6 +/- 6.5% of control LH secretion. Overall, the serum reduced the first and second LH peaks to 76.8 +/- 4.2 and 62.9 +/- 3.6% of control respectively. These results demonstrated that GnSAF bioactivity suppresses GnRH self-priming, and is present in both the peripheral circulation and hFF. The same material administered to dispersed ovine pituitary monolayers produced similar marked suppression of GnRH-induced LH secretion, with approximately 50-fold less GnSAF bioactivity in serum compared with hFF. Combined doses of oestradiol and progesterone, or hFF from large follicles containing little GnSAF, produced stimulation of GnRH-induced LH secretion and GnRH self-priming (second peaks 78.1 +/- 38.9 and 27.4 +/- 15.7% respectively higher than first peaks). Thus, in conclusion, GnSAF in hFF and serum markedly attenuated both unprimed and primed pituitary response to GnRH, virtually abolishing the GnRH self-priming effect.

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