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  • Journal article
    CADDICK MX, ARST HN, 1986,

    STRUCTURAL GENES FOR PHOSPHATASES IN ASPERGILLUS-NIDULANS

    , GENETICAL RESEARCH, Vol: 47, Pages: 83-91, ISSN: 0016-6723
  • Journal article
    ARST HN, 1986,

    PREVENTING PROTEOLYSIS

    , MICROBIOLOGICAL SCIENCES, Vol: 3, Pages: 12-13, ISSN: 0265-1351
  • Journal article
    DURRENS P, GREEN PM, ARST HN, SCAZZOCCHIO Cet al., 1986,

    HETEROLOGOUS INSERTION OF TRANSFORMING DNA AND GENERATION OF NEW DELETIONS ASSOCIATED WITH TRANSFORMATION IN ASPERGILLUS-NIDULANS

    , MOLECULAR & GENERAL GENETICS, Vol: 203, Pages: 544-549, ISSN: 0026-8925
  • Journal article
    CADDICK MX, BROWNLEE AG, ARST HN, 1986,

    REGULATION OF GENE-EXPRESSION BY PH OF THE GROWTH-MEDIUM IN ASPERGILLUS-NIDULANS

    , MOLECULAR & GENERAL GENETICS, Vol: 203, Pages: 346-353, ISSN: 0026-8925
  • Journal article
    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

  • Journal article
    Cookson WO, De Klerk NH, Musk AW, Glancy JJ, Armstrong BK, Hobbs MSet al., 1985,

    Benign and malignant pleural effusions in former Wittenoom crocidolite millers and miners.

    , Aust N Z J Med, Vol: 15, Pages: 731-737, ISSN: 0004-8291

    Serial plain chest radiographs taken between 1943 and 1982 for 280 claimants for compensation for asbestosis and 32 claimants for malignant pleural mesothelioma from the Wittenoom asbestos industry were reviewed by two observers to identify diffuse pleural thickening and pleural effusion. A pleural effusion which appeared and resolved within two years without radiographic or clinical evidence of underlying malignancy, infection or cardiac failure was seen in 15 cases by reader 1 and 24 cases by reader 2. Eighteen cases of effusion, determined from clinical records to be caused by malignant pleural mesothelioma, were seen by reader 1 and 20 by reader 2. The latent periods between commencing work and the first radiograph showing effusion were much shorter for subjects with benign asbestos pleural effusion than for subjects with effusion due to malignant pleural mesothelioma, although there was considerable overlap in the range. The longest latent period for benign asbestos pleural effusion was 22 years and the shortest period for effusion due to malignant pleural mesothelioma was 12 years. The latent period for benign asbestos pleural effusion was inversely related to total cumulative exposure, whereas that for effusion due to malignant pleural mesothelioma was significantly shorter for subjects who had worked in the mill than for those who had worked in the mine. A long latent period and a history of working in the mill were significant discriminators for a malignant as opposed to a benign basis for an effusion. The appearance of a benign asbestos pleural effusion appeared to be a risk factor for the severity of subsequent diffuse pleural thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Journal article
    Cookson WO, Wiseman MS, Shale DJ, 1985,

    Angiotensin converting enzyme and endotoxin induced lung damage in the mouse.

    , Thorax, Vol: 40, Pages: 774-777, ISSN: 0040-6376

    Acute pulmonary oedema can be induced by intraperitoneal injection of Escherichia coli endotoxin in the mouse. A fall in serum angiotensin converting enzyme activity is found in mice given endotoxin and in patients with septic adult respiratory distress syndrome, and has been proposed as an indicator of lung microvascular injury. Protein concentration and angiotensin converting enzyme activity in serum, lung, and bronchoalveolar lavage fluid were determined in male mice up to eight hours after injection of endotoxin. By six hours the serum protein concentration had increased and the bronchoalveolar lavage fluid protein concentration had fallen, suggesting fluid shift into the lung. Angiotensin converting enzyme activity fell in serum and lung but increased in bronchoalveolar lavage fluid. As these changes in enzyme activity were not paralleled by changes in protein concentration they are unlikely to be a result of fluid shift or protein leak, and may indicate an active role of the enzyme in the response to sepsis.

  • Journal article
    Arst HN, 1985,

    Synthetic deoxyoligonucleotides: increased cloning versatility.

    , Microbiol Sci, Vol: 2, ISSN: 0265-1351
  • Journal article
    Cookson WO, Musk AW, Glancy JJ, de Klerk NH, Yin R, Mele R, Carr NG, Armstrong BK, Hobbs MSet al., 1985,

    Compensation, radiographic changes, and survival in applicants for asbestosis compensation.

    , Br J Ind Med, Vol: 42, Pages: 461-468, ISSN: 0007-1072

    The survival of 354 claimants for compensation for pulmonary asbestosis among former workers of the Wittenoom crocidolite mine and mill in Western Australia has been examined. There were 118 deaths up to December 1982. The median time between start of work and claim for compensation was 17 years. The standardised mortality ratio (SMR) for deaths from all causes was 2.65 (p less than 0.0001). The SMR for pneumoconiosis was 177.2 (p less than 0.0001), bronchitis and emphysema 2.6 (p = 0.04), tuberculosis 44.6 (p less than 0.0001), respiratory cancer (including five deaths from malignant pleural mesothelioma) 6.4 (p less than 0.0001), gastrointestinal cancer 1.6 (p = 0.22), all other cancers 1.6 (p = 0.17), heart disease 1.4 (p = 0.07), and all other causes 2.18 (p = 0.004). Plain chest radiographs taken within two years of claiming compensation were found for 238 subjects and were categorised independently by two observers according to the International Labour Organisation criteria without knowledge of exposure or compensation details. Profusion of radiographic opacities, age at claiming compensation, work in the Wittenoom mill, and degree of disability awarded by the pneumoconiosis medical board were significant predictors of survival, but total estimated exposure to asbestos was not. Radiographic profusion and degree of disability were, however, predictable by total exposure. The median survival from claim for compensation was 17 years in subjects with ILO category 1 pneumoconiosis, 12 years in category 2, and three years in category 3.

  • Journal article
    Cookson WO, Glancy JJ, Frost FA, 1985,

    Asymmetric rapidly progressive lung fibrosis: a cause of pseudotumour in asbestosis.

    , Br J Ind Med, Vol: 42, Pages: 350-353, ISSN: 0007-1072

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