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juniperus virginiana/albumin

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AtikEsè klinikPatant
12 rezilta yo
BACKGROUND T cells are known to play a major role in the pathogenesis of atopic allergic asthma, but it is less clear whether they are involved in occupational asthma caused by low molecular weight chemicals such as plicatic acid. OBJECTIVE We sought to determine whether peripheral blood T cells

Cellular and protein changes in bronchial lavage fluid after late asthmatic reaction in patients with red cedar asthma.

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To investigate the sequence of cellular and protein changes after a late asthmatic reaction (LAR), bronchial lavage was carried out in 44 patients with red cedar asthma at different time intervals after bronchial challenge with plicatic acid. The results were compared to five patients with red cedar
In order to investigate the relationship between the pattern of response (immediate, late and dual) to specific bronchial challenge test with plicatic acid or red cedar extract and the clinical features of asthma, 332 patients with asthma induced by western red cedar dust were examined at the time

Plicatic acid-specific IgE and nonspecific bronchial hyperresponsiveness in western red-cedar workers.

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In a cross-sectional survey of 652 workers in a western red-cedar sawmill, we obtained data on symptoms, pulmonary function, immediate skin reactivity to common allergens, nonspecific bronchial responsiveness, total IgE level, and sensitization to plicatic acid conjugated with human serum albumin as

Immunologic studies of the mechanisms of occupational asthma caused by western red cedar.

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BACKGROUND Occupational asthma caused by western red cedar (Thuja plicata) is a common problem in sawmill industries. The objective of this study was to examine the cellular and immunologic mechanisms of western red cedar asthma (WRCA) more closely. METHODS Bronchial biopsy specimens,
Four workers from a cedar sawmill who developed red cedar asthma are described. They had serial measurements of lung function and nonspecific bronchial hyperresponsiveness (NSBH) several years before and after the development of chest symptoms. Measurements of dust concentration and specific IgE
Seventeen patients with occupational asthma due to western red cedar had bronchial lavage during follow-up examination after removal from exposure for at least 1 year. Seven patients were asymptomatic while ten continued to have symptoms of asthma requiring treatment. Symptomatic patients had

Lack of role for mononuclear cell-derived histamine releasing factors in occupational asthma due to western red cedar.

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Occupational asthma due to Western Red Cedar (WRCA) is attributed to sensitization to plicatic acid (PA), but does not appear to be dependent on PA-specific IgE antibodies. Exposure to PA induces histamine release in vivo and in vitro, so if IgE is not important, other mechanisms of histamine

Occupational asthma caused by cedar urea formaldehyde particle board.

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Two carpenters developed asthma and rhinitis related to occupational exposure to a cedar urea formaldehyde (CUF) particle board. One patient developed nasal and chest symptoms and an equivocal early asthmatic response after CUF sawdust exposure, but not after spruce or western red cedar sawdust
A worker developed symptoms of work-related asthma a few weeks after starting to work in a sawmill where eastern white cedar (Thuja occidentalis) was transformed into shingles. The diagnosis of occupational asthma was confirmed by monitoring of peak expiratory flow rates and bronchial responsiveness

Effect of bronchial lavage volume on cellular and protein recovery.

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To investigate the optimal lavage technique to study the airway response in patients with asthma, differential volume lavage was carried out in 22 normal subjects and 18 patients with red cedar asthma. Ten ml of fluid was instilled into a main-stem bronchus followed by 5, 10, 20, 50 and 100 ml into

Bronchial leukocyte proteinase inhibitor levels in bronchial washings in asthma patients.

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To evaluate whether epithelial damage of airways in asthma could be related to diminished levels of the low molecular weight bronchial leukocyte proteinase inhibitor (BLPI) in airways, we determined BLPI in bronchial washings of 13 asthma patients and 13 healthy subjects, using a sensitive
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