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COOKSON W, YOUNG RP, SANDFORD AJ, et al., 1992, MATERNAL INHERITANCE OF ATOPIC IGE RESPONSIVENESS ON CHROMOSOME-11Q, LANCET, Vol: 340, Pages: 381-384, ISSN: 0140-6736
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- Citations: 297
Musk AW, Ryan G, James A, et al., 1992, Factors in job decisions., J Occup Med, Vol: 34, Pages: 593-594, ISSN: 0096-1736
YOUNG RP, SHARP PA, LYNCH JR, et al., 1992, CONFIRMATION OF GENETIC-LINKAGE BETWEEN ATOPIC IGE RESPONSES AND CHROMOSOME-11Q13, JOURNAL OF MEDICAL GENETICS, Vol: 29, Pages: 236-238, ISSN: 0022-2593
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- Citations: 139
DANIELS RJ, THOMAS NH, MACKINNON RN, et al., 1992, LINKAGE ANALYSIS OF SPINAL MUSCULAR-ATROPHY, GENOMICS, Vol: 12, Pages: 335-339, ISSN: 0888-7543
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- Citations: 49
Cookson WOCM, 1992, Erratum: Maternal inheritance of atopic IgE responsiveness on chromosomes (The Lancet (Aug 15) p 381), Lancet, Vol: 340, ISSN: 0140-6736
Cookson WO, De Klerk NH, Ryan GR, et al., 1991, Relative risks of bronchial hyper-responsiveness associated with skin-prick test responses to common antigens in young adults., Pages: 473-479, ISSN: 0954-7894
We studied 143 young subjects by skin-prick testing to common allergens and by the measurement of non-specific bronchial responsiveness (NSBR). A logistic regression model showed a prevalence odds ratio (POR) for bronchial hyper-responsiveness (PD20 less than 10 mumol methacholine) in house dust positive subjects of 4.10 (95% CI 1.77-9.51, P less than 0.001), and in mould positive subjects 5.72 (95% CI 2.06-15.9, P less than 0.001): the PORs for epithelia (2.05, P = 0.12) and grasses (1.78, P = 0.19) were not significant. If bronchial reactivity was assessed as measurable (PD20 less than 102 mumol methacholine) or not, the POR for house-dust-positive subjects was 4.83 (95% CI 2.23-10.5, P less than 0.001), for moulds was 10.5 (95% CI 2.33-47.5, P less than 0.001), for epithelia was 4.79 (95% CI 1.91-12.0, P less than 0.001), and for grasses was 2.21 (95% CI 1.11-4.4, P = 0.022). The results show the risk of bronchial hyper-responsiveness is greater in subjects sensitive to house dust and mould than in those reactive to grasses, and suggests that the presence or absence of increased NSBR in atopic individuals may depend on the antigens to which they become sensitized.
Hopkin JM, Cookson WO, Young RP, 1991, Asthma, atopy, and genetic linkage., Ann N Y Acad Sci, Vol: 629, Pages: 26-30, ISSN: 0077-8923
Gardiner M, Sandford A, Deadman M, et al., 1990, Batten disease (Spielmeyer-Vogt disease, juvenile onset neuronal ceroid-lipofuscinosis) gene (CLN3) maps to human chromosome 16., Genomics, Vol: 8, Pages: 387-390, ISSN: 0888-7543
The ceroid-lipofuscinoses are a group of inherited neurodegenerative disorders characterized by the accumulation of autofluorescent lipopigment in neurons and other cell types. The underlying biochemical defect is unknown. Batten disease (Spielmeyer-Vogt disease, juvenile onset neuronal ceroid-lipofuscinosis) displays autosomal recessive inheritance. Genetic linkage studies were undertaken to determine the chromosomal location of the Batten disease mutation (CLN3). Following identification of linkage to the haptoglobin locus, linkage analysis has been carried out in 42 families by using DNA markers for loci on the long arm of human chromosome 16. The maximal lod score between Batten disease and the locus D16S148 calculated for combined sexes is 6.05 at a recombination fraction theta = 0.00. Multilocus analysis using five loci indicated the most likely order to be HP-D16S151-D16S150-CLN3-D16S148-D16S147. The maximal location score for CLN3 was 48 (equivalent to a lod score of 10.4) in that interval within this fixed marker map.
de Klerk NH, Musk AW, James A, et al., 1990, Comparison of chest radiograph reading methods for assessing progress of pneumoconiosis over 10 years in Wittenoom crocidolite workers., Br J Ind Med, Vol: 47, Pages: 127-131, ISSN: 0007-1072
Thirty three pairs of chest radiographs taken up to 10 years apart were obtained for 33 subjects suffering from asbestosis who had applied for compensation to the Pneumoconiosis Medical Board of Western Australia. Multiple films from the period before the first radiograph in each pair, from the intervening period between the two, and from the period subsequent to the second radiograph were also available and all films were read by two independent readers according to the 1980 ILO classification of pneumoconiosis. Films were read twice as side by side pairs ten years apart, twice as two separate randomly ordered films ten years apart, and once as part of the full series of all available chest radiographs on each subject to assess which method provided the best consistency (between reader variation) and repeatability (within reader variation). Judging by consistency, the full series method performed as well as either of the other methods when assessing radiographic changes and significantly better when assessing the level of profusion of small opacities. There was little to choose between the other two methods either judging by consistency or repeatability, which could not be estimated for the full series method. Use of all available films for a subject is recommended for assessing single films, as in a prevalence study, as well as for documenting change in a longitudinal study.
Durham SR, Keenan J, Cookson WO, et al., 1989, Diurnal variation in serum cortisol concentrations in asthmatic subjects after allergen inhalation., Thorax, Vol: 44, Pages: 582-585, ISSN: 0040-6376
To assess whether differences in the adrenal response to allergen are important in determining the magnitude of the allergen induced late responses in asthmatic subjects, we measured serum cortisol concentrations after inhalation challenge with allergen or control solution (phosphate buffered saline). The two challenges were performed in random order with an interval of 14 days. A normal diurnal decrease in serum cortisol concentrations was observed on both days. Mean blood cortisol concentrations three hours after inhalation of allergen (before the late response), nine hours afterwards (at the time of the late response), and 24 hours afterwards were virtually identical to those observed after inhalation of phosphate buffered saline. Serum cortisol concentrations before challenge and three, nine, and 24 hours after challenge were not related to the diurnal increase in blood eosinophils on the control day, or to the size of the late asthmatic response or accompanying changes in blood eosinophils after allergen challenge. It is concluded that serum cortisol concentrations show normal diurnal variation after allergen challenge and are unrelated to the size of the late response or associated changes in blood eosinophil counts.
de Klerk NH, Cookson WO, Musk AW, et al., 1989, Natural history of pleural thickening after exposure to crocidolite., Br J Ind Med, Vol: 46, Pages: 461-467, ISSN: 0007-1072
Serial plain chest radiographs of 384 men who worked at the Wittenoom crocidolite mine and mill between 1943 and 1966 and who applied for pneumoconiosis compensation between 1948 and 1982 have been examined independently by two trained observers for pleural disease using the 1980 ILO-UICC classification of radiographs to record width and extent of pleural disease. Radiographs covering follow up periods of from two to 38 years were examined (median number of films per subject was nine). The degree of crocidolite exposure was estimated from employment records and a survey of airborne fibre concentrations performed in 1966. Agreement between the observers on the presence and degree of pleural disease in the final film for each subject was moderately close (Kendall's tau B = 0.62) and was least for subjects with thickening less than 5 mm in width. Diffuse pleural thickening extending for greater than 50% of the lateral chest wall was the most common type recorded by both observers. Minor pleural thickening frequently progressed in extent along the lateral chest wall but progression beyond 5 mm in thickness was less common. Pleural plaques were not seen to progress beyond their initial thickness or extent. The rate of onset of thickening in this population increased continually from the time of first exposure and also increased slightly with age. There was evidence that the level of total cumulative exposure to crocidolite increased the rate of onset of pleural thickening in the period between five and 15 years after first exposure. Rate of progression of established thickening was greatest in subjects who first developed thickening early after first exposure. The relative rate of progression decreased slowly with time from first signs of thickening and there was no evidence of any progression more than 15 years after onset.
Cookson WO, Sharp PA, Faux JA, et al., 1989, Linkage between immunoglobulin E responses underlying asthma and rhinitis and chromosome 11q., Lancet, Vol: 1, Pages: 1292-1295, ISSN: 0140-6736
Family studies of IgE responses to common inhaled antigens have suggested dominant inheritance of atopy. Molecular genetic linkage analysis was used to confirm this proposal. In seven families the transmission of atopy was linked, with a maximum lod score of 5.58, to a DNA polymorphism defined by p lambda MS.51, which confirms dominant inheritance and assigns the gene locus to chromosome 11.
Cookson WO, Craddock CF, Benson MK, et al., 1989, Falls in peripheral eosinophil counts parallel the late asthmatic response., Am Rev Respir Dis, Vol: 139, Pages: 458-462, ISSN: 0003-0805
Peripheral eosinophil counts were measured at intervals before and after control and allergen inhalation in 14 asthmatic subjects. A relative fall in eosinophil counts was noted 9 h after allergen challenge, in contrast to the diurnal increase seen on the control day (p = 0.005). This fall in eosinophil count correlated strongly with the magnitude of the late asthmatic response (r = -0.72, p = 0.003) and with the changes in bronchial responsiveness to histamine at 3 and 24 h after allergen was given (r = 0.54, p = 0.044 and r = 0.82, p less than 0.001, respectively). The findings demonstrate eosinophil kinetics are related to the occurrence of late-phase reactions and to the associated worsening of bronchial hyperreactivity.
De Klerk NH, Cookson WOC, Musk AW, et al., 1989, Natural history of pleural thickening after exposure to crocidolite
The effect of exposure to crocidolite asbestos on pleural thickening is investigated.
Durham SR, Craddock CF, Cookson WO, et al., 1988, Increases in airway responsiveness to histamine precede allergen-induced late asthmatic responses., J Allergy Clin Immunol, Vol: 82, Pages: 764-770, ISSN: 0091-6749
Changes in airway responsiveness to histamine after allergen inhalation challenge were studied in 14 nonsmoking atopic adult subjects with asthma. Inhalation challenges with allergen and with phosphate-buffered saline (control challenge) were performed single blind in random order, with an interval of 14 days. The development of a late asthmatic response was accompanied by an increase in airway histamine responsiveness that was significant when it was compared with the airway histamine responsiveness after the control challenge at 3 hours (p less than 0.01), 24 hours (p less than 0.01), and 48 hours (p less than 0.02), with recovery at 2 weeks after allergen inhalation. The 3-hour changes in airway responsiveness occurred independently of changes in airway caliber and correlated with the magnitude of the subsequent late response (r = 0.86; p less than 0.001). These results suggest that the tissue events (possibly airway inflammation) that underlie the late asthmatic response may occur before this response becomes clinically apparent.
Musk AW, de Klerk NH, Cookson WO, et al., 1988, Radiographic abnormalities and duration of employment in Western Australian iron-ore miners., Med J Aust, Vol: 148, Pages: 332-334, ISSN: 0025-729X
Plain chest radiographs of 788 Pilbara iron-ore miners from Western Australia have been examined by two independent observers for evidence of pneumoconiosis. The prevalence of any radiographic abnormality (a profusion grade of 0/1 or greater on the International Labour Office [ILO] scale) was 6.7% for Reader 1 and 9.9% for Reader 2. The prevalence of a definite radiographic abnormality (a profusion grade of 1/0 or greater on the ILO scale) was 1.9% for Reader 1 and 2.8% for Reader 2. The prevalence of any abnormality, as identified by either or by both observers, was significantly related to age. The relationship between a radiographic abnormality and the duration of employment was less clear. The results indicate a need for more detailed and comprehensive studies of the effects of iron-ore dust in this industry.
Sibbald B, 1988, Dominant inheritance of atopic immunoglobulin-E responsiveness., Lancet, Vol: 1, ISSN: 0140-6736
Cookson WO, Hopkin JM, 1988, Dominant inheritance of atopic immunoglobulin-E responsiveness., Lancet, Vol: 1, Pages: 86-88, ISSN: 0140-6736
The familial occurrence of atopy, defined by skin prick test responses and serum immunoglobulin-E (IgE) titres to common inhaled allergens, was studied in 239 members of 40 nuclear and 3 extended families. 90% of the atopic children in the nuclear families had at least one demonstrably atopic parent. In each extended family, atopy was vertically transmitted, and 31 of 47 (66%) offspring of marriages between atopic and unaffected parents were atopic. Of the designated atopic subjects, 83% admitted to symptoms suggesting atopic disease but only 30% regarded themselves as having any such disorder. It is suggested that atopy, the propensity to produce IgE in response to common, usually inhaled, allergens, is inherited as an autosomal dominant character but that its clinical expression depends on interaction with other factors.
Higgins RM, Cookson WO, Lane DJ, et al., 1987, Cardiac arrhythmias caused by nebulised beta-agonist therapy., Lancet, Vol: 2, Pages: 863-864, ISSN: 0140-6736
Cookson WO, 1987, Bronchodilator action of the anti-histaminic terfenadine., Br J Clin Pharmacol, Vol: 24, Pages: 120-121, ISSN: 0306-5251
Kingsbury AC, Frost F, Cookson WO, 1987, Dysgerminoma, gonadoblastoma, and testicular germ cell neoplasia in phenotypically female and male siblings with 46 XY genotype., Cancer, Vol: 59, Pages: 288-291, ISSN: 0008-543X
46 XY gonadal dysgenesis is a syndrome characterized by a female phenotype with streak gonads and complicated by the frequent occurrence of germ cell tumors. The syndrome and the risk of malignant disease occur in female siblings sharing the XY genotype, and screening of female siblings and prophylactic gonadectomy in those affected is generally recommended. A family of four siblings is described in which two phenotypically female XY children and one male each have developed germ cell tumors, demonstrating that brothers of affected sisters may also be at risk.
Higgins RM, Cookson WOCM, Lane DJ, et al., 1987, Cardiac arrhythmias caused by nebulised beta-agonist therapy, Lancet, Vol: 2, ISSN: 0140-6736
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Higgins RM, Cookson WO, Chadwick GA, 1987, Changes in blood gas levels after nebuhaler and nebulizer administration of terbutaline in severe chronic airway obstruction., Bull Eur Physiopathol Respir, Vol: 23, Pages: 261-264, ISSN: 0395-3890
It has been suggested that patients with severe chronic airway obstruction might suffer dangerous hypoxia after administration of a beta-agonist through an air driven nebulizer. Twenty patients with severe chronic airway obstruction (12 male, mean age 71.1 (SEM 1.5) yr) were monitored with a Biox oximeter and Hewlett-Packard capnometer before and after 4 mg terbutaline was delivered through an air driven nebulizer or Nebuhaler. The eight patients with chronic hypoxia (mean PaO2 6.76 kPa, PaCO2 7.47 kPa. FEV1 0.53 l) experienced a 4.7% increase in oxygen saturation (SaO2) and 2.9% fall in transcutaneous carbon dioxide tension (PtcCO2) (p less than 0.05) during all treatments, followed by a return to initial levels. These changes were attributable to increased ventilation whilst breathing through a mouthpiece. A similar trend was seen in the SaO2 of the twelve normoxic patients (mean PaO2 9.32 kPa, PaCO2 5.34 kPa, FEV1 0.8 l), but there was a sustained fall in PtcCO2 of 3.7% (p less than 0.001) after administration of terbutaline. Inhaled terbutaline in the dosage given did not cause hypoxia in patients with severe chronic airflow obstruction, but nebulizer and Nebuhaler use was associated with a rise in SaO2 related to increased ventilation whilst breathing through a mouthpiece.
Shale DJ, Wiseman MS, Cookson WO, 1986, Effect of monocrotaline ingestion on the distribution of protein and angiotensin converting enzyme activity in the rat lung., Thorax, Vol: 41, Pages: 914-918, ISSN: 0040-6376
The alveolar accumulation of protein and angiotensin converting enzyme activity was compared with the development of right ventricular hypertrophy in male rats after different periods of monocrotaline exposure. Total doses of monocrotaline were varied by dividing the animals into three groups in which ingestion was limited to three, seven, and 15 days. These groups were studied 21 days after the start of monocrotaline exposure and compared with a group treated continuously for 28 days. The total lung weight increased after three or more days of treatment, while after seven days there was significant alveolar accumulation of protein, which was paralleled by an increase in angiotensin converting enzyme activity in alveolar lavage fluid. Identical changes also occurred after 15 and 28 days of exposure to monocrotaline. Lung angiotensin converting enzyme activity was decreased after three days' ingestion of monocrotaline and did not alter further with longer periods of exposure. None of these effects of monocrotaline in the three and seven day treatment groups was associated with right ventricular hypertrophy, which occurred only in animals treated for 15 or more days. The effects of monocrotaline ingestion on the lung were dose related and had no causal relationship to the development of right ventricular hypertrophy.
Cookson WO, Musk AW, Ryan G, 1986, Associations between asthma history, atopy, and non-specific bronchial responsiveness in young adults., Clin Allergy, Vol: 16, Pages: 425-432, ISSN: 0009-9090
In 105 subjects taken from a student population and aged between 15 and 30 there was a strong positive association between the presence of the atopic state, defined by skin tests, and a high level of non-specific bronchial responsiveness to methacholine (chi 2 = 10.5, d.f. = 2, P = 0.01). Regression analysis showed a history of asthma, and the symptom of wheeze, to be predominantly predicted by the degree of bronchial responsiveness (R2 = 31%), with only a minor independent contribution from the degree of atopy (R2 a further 5%). The genetic or other reasons for the association between bronchial responsiveness and atopy may have importance in understanding the aetiology of allergic asthma.
James AL, Cookson WO, Buters G, et al., 1986, Symptoms and longitudinal changes in lung function in young seasonal grain handlers., Br J Ind Med, Vol: 43, Pages: 587-591, ISSN: 0007-1072
A total of 119 seasonal grain handlers (mean age 23) were assessed before and towards the end (mean work period 18 days) of the 1983 Western Australian grain harvest to determine if respiratory symptoms that occur with exposure to grain dust are associated with changes in ventilatory capacity or non-specific bronchial reactivity to methacholine. Eighteen per cent of subjects had wheeze, breathlessness, or chest tightness and 18% had cough or sputum production at work. Subjects complaining of wheeze, chest tightness, or breathlessness at work had a significantly greater decline in FEV1 than subjects who did not experience these symptoms (p less than 0.05). Symptoms were not associated with changes in bronchial reactivity. In young grain handlers who develop respiratory symptoms on short term exposure to grain dust changes in FEV1 but not in non-specific bronchial reactivity have been demonstrated.
Cookson WO, De Klerk NH, Musk AW, et al., 1986, Prevalence of radiographic asbestosis in crocidolite miners and millers at Wittenoom, Western Australia., Br J Ind Med, Vol: 43, Pages: 450-457, ISSN: 0007-1072
An estimate has been made of the prevalence of unrecognised pneumoconiosis in former crocidolite workers from Wittenoom, Western Australia. All plain chest radiographs relating to a one in six random sample (1025 men) of all former Wittenoom workers who had never entered a compensation claim to the Pneumoconiosis Medical Board of Western Australia were sought from Perth teaching hospitals and from the Perth Chest Clinic where compulsory examination of all workers in the mining industry takes place. Radiographs were recovered for 83% of the men and read independently by two observers. By means of logistic regression analysis a current prevalence of parenchymal abnormality (defined as a radiographic profusion of small opacities of category 1/0 or greater on the ILO classification) of nearly 20% was calculated after adjustment for age, time since first exposure, and cumulative exposure level. One hundred men randomly selected from those known to be alive in the sample were invited to attend for a new radiographic examination. Seventy four men attended and the predicted prevalence was confirmed. It is estimated from these data that there were between 450 and 900 former Wittenoom workers in Australia at the end of 1980 who had radiographic abnormality consistent with pneumoconiosis but had not claimed compensation or had asbestosis diagnosed. The data are consistent with there being no threshold dose of crocidolite exposure for the development of radiographic abnormality in this group.
Cookson WO, Ryan G, MacDonald S, et al., 1986, Atopy, non-allergic bronchial reactivity, and past history as determinants of work related symptoms in seasonal grain handlers., Br J Ind Med, Vol: 43, Pages: 396-400, ISSN: 0007-1072
One hundred and five young subjects with little or no previous exposure to grain dust were studied before and after a seven week period of grain handling work to determine if there was an association between symptoms experienced at work and pre-employment respiratory symptoms, allergy skin test responses, and non-allergic bronchial reactivity. The incidence of work related symptoms was cough 18%, wheeze 13%, and dyspnoea 14%. The results showed that pre-employment history of respiratory symptoms, positive allergy skin test responses, and a high level of non-allergic bronchial reactivity were significantly associated with these symptoms. These measurements may be useful to predict symptoms associated with exposure to grain dust in new employees and the results suggest that these work related symptoms may be due to allergen induced asthma.
Cookson W, De Klerk N, Musk AW, et al., 1986, The natural history of asbestosis in former crocidolite workers of Wittenoom Gorge., Am Rev Respir Dis, Vol: 133, Pages: 994-998, ISSN: 0003-0805
The course of pulmonary asbestosis and its determinants have been examined in 280 applicants for compensation among former workers of the crocidolite mine and mill at Wittenoom Gorge, Western Australia. Serial chest radiographs accrued over more than 3 decades were graded for parenchymal disease separately by two observers according to the 1980 ILO Classification of Radiographs for Pneumoconioses and without knowledge of exposure histories or compensation details. In 136 subjects whose median duration of exposure was 37 months, radiographic asbestosis appeared between 1 and 34 yr after initial exposure and then progressed continuously. Total exposure to asbestos and time from first exposure to the appearance of definite radiographic asbestosis were significant determinants of the rate of progression of profusion of radiographic abnormality. Asbestosis should be considered to be an active disease even 3 decades after exposure has ended.
COOKSON WOCM, MUSK AW, RYAN G, 1986, Associations between asthma history, atopy, and non‐specific bronchial responsiveness in young adults, Clinical & Experimental Allergy, Vol: 16, Pages: 425-432, ISSN: 0954-7894
In 105 subjects taken from a student population and aged between 15 and 30 there was a strong positive association between the presence of the atopic state, defined by skin tests, and a high level of non‐specific bronchial responsiveness to methacholine (χ2= 10·5, d.f. = 2, P= 0·01). Regression analysis showed a history of asthma, and the symptom of wheeze, to be predominantly predicted by the degree of bronchial responsiveness (R2= 31%), with only a minor independent contribution from the degree of atopy (R2 a furthur 5%). The genetic or other reasons for the association between bronchial responsiveness and atopy may have importance in understanding the aetiology of allergic asthma. Copyright © 1986, Wiley Blackwell. All rights reserved
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