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Biomedical subjects

D H Yates

Publications and source records attributed to D H Yates.

At least 19 recordsLinked to original sources
PubMed2006

AMP challenge induces a decrease in FE(NO) in asthmatic subjects modulated by nedocromil.

BACKGROUND: Allergen challenge results in an immediate reduction in exhaled nitric oxide (FE(NO)) followed by a long-term increase. To study mast cell activation in relation to nitric oxide (NO), the study investigated the effect of inhaled adenosine monophosphate (AMP) as a mast cell activator and mast cell stabilizer - nedocromil sodium - on FE(NO). The NO synthase (NOS) iso-enzyme involved was studied by the NOS inhibitor aminoguanidine. MATERIALS AND METHODS: A double-blind, placebo-controlled, cross-over study was performed in two parts. Part I: eight atopic asthmatic subjects inhaled nedocromil or placebo before the AMP challenge. Spirometry and FE(NO) were measured at intervals over a 24-h period. Part II: seven subjects inhaled aminoguanidine before an identical protocol was used, as in Part I. RESULTS: Part I: AMP challenge caused a significant decrease from baseline FE(NO)[placebo, 28.9 (20.3-37.4)%, P < 0.002 and nedocromil, 20.9 (8.2-33.6)%, P < 0.01]. Nedocromil gave partial protection against this decrease in FE(NO). The time-FE(NO) curve (AUC(0-24)) differed significantly between nedocromil and placebo: 2.7% (-3.6 to -9) vs. -6.6% (-12 to -1.3) FE(NO) changes h(-1), P < 0.002, respectively. Nedocromil protected against AMP-induced bronchoconstriction (AMP PC(20)) [nedocromil 182 (72.5-291) mg mL(-1) vs. placebo 21.7 (10.7-33) mg mL(-1), P < 0.002]. Part II: nebulized aminoguanidine resulted in a significant reduction in FE(NO) from baseline and was greater than after AMP alone (P = 0.006). Nedocromil increased AMP PC(20), but no longer protected against the late decrease in FE(NO). CONCLUSIONS: The AMP challenge caused a reduction in FE(NO) as a result of prior treatment with nedocromil. Aminoguanidine abolished the nedocromil-induced protection on the late reduction in FE(NO), but not on AMP PC(20). Inducible NOS was implicated in the late FE(NO) decrease after the AMP challenge.

Adenosine Monophosphate↗
PubMed2004

Laughter-associated asthma.

This study was conducted to assess the prevalence of laughter-induced asthma, and to study any associations with asthma-related triggers and measures of disease activity, using a questionnaire-based survey of asthma subjects in both the community and on presentation to hospital. A total of 105 subjects participated, and 44 (41.9%) reported laughter-associated asthma. Exercise and laughter were strongly associated as triggers (p < 0.006), as well as molds and grass pollen (p = 0.03). It seems to be associated with poor asthma control as well, since hospital admissions are also more frequent in this group (p = 0.043). Laughter-induced asthma is strongly associated with exercise as a trigger; the mechanism remains uncertain, but better understanding of this problem may assist in controlling difficult asthma.

Adult↗
PubMed2004

Cold blast furnace syndrome: a new source of toxic inhalation by nitrogen oxides.

AIM: To describe a new toxic inhalation syndrome in blast furnace workers. METHODS: Fourteen workers developed acute respiratory symptoms shortly after exposure to "air blast" from blast furnace tuyeres. These included chest tightness, dyspnoea, rigors, and diaphoresis. Chest radiographs showed pulmonary infiltrates, and lung function a restrictive abnormality. This report includes a description of clinical features of the affected workers and elucidation of the probable cause of the outbreak. RESULTS: Clinical features and occupational hygiene measurements suggested the most likely cause was inhalation of nitrogen oxides at high pressure and temperature. While the task could not be eliminated, engineering controls were implemented to control the hazard. No further cases have occurred. CONCLUSIONS: "Cold blast furnace syndrome" represents a previously undescribed hazard of blast furnace work, probably due to inhalation of nitrogen oxides. It should be considered in the differential diagnosis of acute toxic inhalational injuries in blast furnace workers.

Environmental Monitoring↗
PubMed2003

Health and stress in Australian interns.

Over a 3-year period, interns completed questionnaires on self-reported health and stress during their orientation week at the beginning of the year, during mid year, and at the end of the first year. Interns experienced increased levels of stress and ill health in the middle of the year as compared with the start and end of the year (chi2=11.9, P=0.003 and chi2=20.4, P<0.001, respectively). Despite workplace reform for junior doctors, this study suggests that interns still feel overburdened with work expectations and this is having a negative effect on their health.

Adult↗
PubMed2002

Particulate masks and non-powdered gloves reduce latex allergen inhaled by healthcare workers.

BACKGROUND: Although allergy to latex is a well-characterized phenomenon, some hospitals continue to provide staff with powdered latex gloves as an option to low- or non-powdered gloves. OBJECTIVE: We aimed to measure the extent to which inhalation of latex particles could be reduced by the use of protective masks or by replacing powdered latex gloves with non-powdered latex gloves. METHODS: Twenty healthcare workers in a hospital setting wore nasal air samplers (NAS) and Institute of Occupational Medicine (IOM) samplers for four 20-min periods. Subjects wore powdered gloves, non-powdered gloves and no gloves during three sampling periods, and in the fourth, subjects applied an aerosol barrier face-mask or a particulate face-mask (N95) while wearing powdered gloves. All samples were stained for particles bearing Hev b 5 allergen by the Halogen assay. RESULTS: All subjects inhaled Hev b 5 bearing particles in all sampling periods. IOM samplers collected particles at 70% of the rate of NAS. The number of particles inhaled while wearing powdered gloves was 23.8-fold higher than when not wearing gloves and 9.7-fold higher than when wearing non-powdered latex gloves (P < 0.0001). Wearing an aerosol barrier mask did not significantly reduce the number of particles inhaled (P = 0.108), while use of particulate masks significantly reduced the number of particles inhaled by 17.4-fold (P = 0.003). CONCLUSIONS: Use of non-powdered gloves is the most effective method of reducing occupational aeroallergen exposure to latex arising from gloves. However, secondary protection using particulate masks is a valid alternative, and may be helpful for preventing respiratory sensitization.

Adult↗
PubMed2002

Caffeine decreases exhaled nitric oxide.

BACKGROUND: Caffeine is known to inhibit phosphodiesterases, to mobilise intracellular calcium, and to act as an antagonist at adenosine receptors, all of which can potentially alter nitric oxide (NO) production. It was therefore hypothesised that caffeine may alter exhaled NO (eNO) levels. METHODS: In a randomised, single blind, crossover manner, 12 normal subjects consumed either (1) coffee and a placebo capsule, (2) decaffeinated coffee and a capsule of 200 mg caffeine, or (3) decaffeinated coffee and a placebo capsule. Serum caffeine levels were measured at baseline and 1 hour later. Exhaled NO levels were also measured at baseline and each hour for 4 hours. RESULTS: A significant percentage fall in mean (SE) eNO from baseline was seen 1 hour after either caffeinated coffee or a caffeine capsule when compared with placebo (13.5 (4.0)%, p=0.009 and 19.0 (3.8)%, p=0.001, respectively). CONCLUSION: Caffeine causes a significant decrease in eNO which will need to be considered when designing trials to measure eNO levels. The mechanism may be via adenosine receptor antagonism or by altering levels of cGMP.

Adult↗
PubMed2001

Passive smoke inhalation decreases exhaled nitric oxide in normal subjects.

Environmental tobacco smoke (ETS) exposure is one of the commonest pollutants in modern society. Despite documented clinical adverse effects of ETS on the lungs, objective methods of assessing airway damage have been lacking. Exhaled nitric oxide (eNO) is a rapid, sensitive method of assessing airway inflammation, and could be useful in this regard. Active smoking decreases eNO in normal subjects and eNO levels are low in habitual smokers, but the effect of ETS exposure on eNO has not previously been examined. In a single-blinded, placebo-controlled cross-over study, we examined the effect of ETS, sham and active smoke inhalation on eNO in non-smoking normal volunteers. Subjects were exposed to smoke over a period of 1 hour in a separately ventilated chamber, and eNO was measured at baseline, 15, 30, 45 and 60 minutes. With sham inhalation (n = 15), eNO levels did not change significantly from baseline, although a small decrease occurred. ETS exposure (n = 15) resulted in a rapid fall in eNO from mean (SE) 134 (29) ppb to 102 (22) ppb, or by 23.6% (p < 0.05), and remained low for 60 minutes. With active smoking (n = 7), levels fell acutely from baseline within the same time interval (71 [16] to 49 [11] ppb, or by 30.3%), and remained low. These changes were significant compared with sham exposure for both ETS (p < 0.05) and active smoke inhalation (p <.01). This suggests that eNO can be used for the investigation of the mechanisms of cigarette-induced lung damage in the experimental setting, and may potentially be useful also for environmental assessment of ETS effects.

Adult↗
PubMed2001

Role of exhaled nitric oxide in asthma.

Nitric oxide (NO), an evanescent atmospheric gas, has recently been discovered to be an important biological mediator in animals and humans. Nitric oxide plays a key role within the lung in the modulation of a wide variety of functions including pulmonary vascular tone, nonadrenergic non-cholinergic (NANC) transmission and modification of the inflammatory response. Asthma is characterized by chronic airway inflammation and increased synthesis of NO and other highly reactive and toxic substances (reactive oxygen species). Pro- inflammatory cytokines such as TNFalpha and IL-1beta are secreted in asthma and result in inflammatory cell recruitment, but also induce calcium- and calmodulin-independent nitric oxide synthases (iNOS) and perpetuate the inflammatory response within the airways. Nitric oxide is released by several pulmonary cells including epithelial cells, eosinophils and macrophages, and NO has been shown to be increased in conditions associated with airway inflammation, such as asthma and viral infections. Nitric oxide can be measured in the expired air of several species, and exhaled NO can now be rapidly and easily measured by the use of chemiluminescence analysers in humans. Exhaled NO is increased in steroid-naive asthmatic subjects and during an asthma exacerbation, although it returns to baseline levels with appropriate anti-inflammatory treatment, and such measurements have been proposed as a simple non-invasive method of measuring airway inflammation in asthma. Here the chemical and biological properties of NO are briefly discussed, followed by a summary of the methodological considerations relevant to the measurement of exhaled NO and its role in lung diseases including asthma. The origin of exhaled NO is considered, and brief mention made of other potential markers of airway inflammation or oxidant stress in exhaled breath.

Animals↗
PubMed2000

Prehospital management of exacerbations of asthma: relation to patient and disease characteristics.

OBJECTIVE: Admission to hospital due to an exacerbation of asthma may represent a failure of prehospital management to prevent an attack or bring about its remission. We aim to describe the steps taken prior to hospital attendance in patients with asthma and to identify patient or disease characteristics that were associated with failure to take appropriate actions. METHODOLOGY: Patients aged over 15 years who were discharged from hospital or the Emergency Department with a primary diagnosis of asthma completed a questionnaire about the impact of asthma and its management prior to the onset of the recent exacerbation. The impact of asthma on quality of life was measured using our Asthma Quality of Life Questionnaire (AQLQ). RESULTS: Seventy-eight subjects completed the questionnaire including 49 who had been inpatients and 29 who had been discharged from the Emergency Department. They included many subjects with severe asthma: 41% had nocturnal symptoms three or more times per week and 41% had been admitted to hospital with asthma in the 12 months prior to this episode. Their AQLQ scores were high (severe) (mean 4.5+/-2.2). Most subjects described their presenting exacerbation as slow in onset and moderate or severe in intensity. During this exacerbation and prior to hospital attendance, only 27% of subjects had measured their peak expiratory flow rate, 19% had commenced or increased the dose of inhaled steroids, and 22% had commenced oral steroids. These actions were not related to the self-perceived speed of onset of the attack. Patients with lower levels of asthma-related concerns for health and more severe mood disturbance associated with asthma were less likely to take these appropriate self-management steps. CONCLUSIONS: This study shows that the failure of prehospital management to prevent the necessity of hospital attendance in most cases stems from a failure to implement currently recommended actions or treatments for exacerbations. Addressing this problem should result in a reduction in rates of hospitalization for asthma.

Adult↗
PubMed2000

Teaching asthma management: an evidence-based educational approach.

BACKGROUND: Asthma management plans and asthma education have been incorporated into recent guidelines, and implementation of these reduces asthma morbidity. Junior doctors are frequently involved in asthma management, but teaching about asthma in medical school is seldom assessed. We studied asthma knowledge, confidence in practical asthma management, and the effectiveness of an interactive asthma education workshop in final year medical students. Thirty-five students attended the workshop, with 26 returning questionnaires on both of the two sessions. METHODS: Students attended a two hour asthma workshop comprising interactive teaching sessions on management of acute and stable asthma, and a practical session using asthma devices. Theoretical knowledge was assessed by a 20 item questionnaire, completed immediately prior to the workshop and after two weeks, at a feedback session. Practical knowledge was assessed by confidence scores in use of asthma devices on a five point scale (not at all confident to very confident), before, immediately after the workshop, and after two weeks. RESULTS: Students scored poorly in questions on: predictors of asthma mortality, nebuliser and Turbuhaler use, asthma management plans, and physical signs in acute asthma. Mean (SE) knowledge score increased significantly from 64.4% (6.1) to 74.2% (5.6) (p<0.05; paired t-test) at two weeks. Confidence scores rose significantly for all practical aspects of asthma management (p<0.01; Wilcoxon matched pairs test), and declined at two weeks, but still remained significantly higher than at baseline (p<0.05). CONCLUSIONS: Medical students had poor knowledge about several important features of asthma care. The asthma workshop was effective in increasing knowledge and confidence in management of asthma in the short term, and could be useful in optimising implementation of asthma guidelines in clinical practice and potentially later in training of junior medical officers.

Adult↗
PubMed1999

Influenza vaccination: changes in exhaled nitric oxide levels and sputum cytology.

OBJECTIVE: Influenza vaccination is routinely recommended for patients with chronic lung disease, but has been reported to cause a small increase in airway reactivity. The use of simple, non-invasive methods of assessing changes in airway inflammation could potentially allow improved understanding of the cellular mechanisms underlying such changes. METHODOLOGY: We studied a group of 44 hospital workers before and after routine influenza vaccination, using spirometry, and exhaled nitric oxide (eNO) as a marker of pulmonary inflammation (Group A). In addition, methacholine challenge and sputum induction were also performed in a subgroup (subgroup B, n = 7) at baseline and at 7 days after vaccination. RESULTS: Spirometry did not change in either group. In Group A there was a small but significant rise in mean peak eNO from 47.32 +/- 4.5 (mean NO p.p.b. +/- SEM) to 53.2 +/- 4.9 between days 0 and 7 (P < 0.05). A non-significant rise in eNO was seen in subgroup B. In subgroup B, when the differential cell counts in induced sputum were compared between baseline and sampling 1 week later, there was a significant rise in the percentage of lymphocytes, from 3.9 (1.8-9.8: median %total (range)) to 11.9 (6.0-18.5, P < 0.02) and a non-significant increase in shed respiratory epithelial cells from 3.1 (0.6-5.8) to 13.0 (1-30.3, P=0.06). There was a corresponding significant fall in the percentage of macrophages. Methacholine challenge in subgroup B showed no change in reactivity in these normal subjects. CONCLUSION: Influenza vaccination causes a small increase in exhaled NO, and is accompanied by increased sputum lymphocytosis and respiratory epithelial shedding. An influx of inflammatory cells may help to explain the induction of increased airway reactivity that has been described in other studies.

Adult↗
PubMed1999

Sputum induction as a method of analyzing pulmonary cells: reproducibility and acceptability.

Sputum induction has been proposed as a noninvasive method of sampling airway cells for assessing airway inflammation in asthma. Although useful in the research setting, the applicability of this technique to a respiratory clinic, where it might prove useful for clinical management of anti-inflammatory therapy, has not been assessed. We therefore studied the effect of sputum induction in terms of patient acceptability, effect upon airway caliber, and reproducibility of the total cell and differential cell count at 2 weeks in 20 asthmatic subjects first attending an asthma clinic. We compared such patients with normal controls. Thirty-seven subjects underwent sputum induction on two occasions (20 asthmatics and 17 normal subjects) separated by a 2-week interval, using a standardized protocol. Acceptability was assessed by questionnaire. Airway caliber was measured by serial spirometry, using albuterol premedication for asthmatic subjects. Sputum was induced by inhalation of 3.5% saline over 12 min. Total cell and differential counts on induced sputum were assessed and correlated with bronchial hyperresponsiveness, as well as reproducibility of the technique in the clinical setting. All subjects found the process acceptable, although mild side effects occurred in more than 90% of subjects. No differences in acceptability were found between asthmatic and normal subjects. Sputum induction was associated with a significant decrease in forced expiratory volume in 1 sec (FEV1) in normal subjects (from 4.1 +/- 0.17 to 4.02 +/- 0.19 L [p < 0.01] on visit 1 and on visit 2 from 4.01 +/- 0.15 to 3.90 +/- 0.16 L [p < 0.01]), but not in asthmatic subjects after albuterol premedication. Total pulmonary cell yield on the first and second sputum induction days was 1.97 +/- 0.06 x 10(6) cells/mL of sputum and 2.01 +/- 0.05 x 10(6) cells/mL of sputum, respectively, giving a reliability coefficient of 0.77. Less agreement was seen between individual cell differential counts within subjects, but most fell within the expected range on Bland-Altman plots. Sputum induction appears to be safe and acceptable in both normal and asthmatic subjects. A small decrease in FEV1 occurs in normal subjects, which is prevented by albuterol premedication in asthmatics. Reproducibility at 2 weeks yielded similar total numbers of pulmonary cells, but in a clinic population some variability was seen in the number of inflammatory cells, probably because of the small numbers of these cells. This technique may be less valuable in a clinical than a research setting.

Administration, Inhalation↗
PubMed1998

Exhaled and nasal nitric oxide is increased in laboratory animal allergy.

BACKGROUND: Allergens from rats, mice, guinea pigs or rabbits cause up to 30% of exposed persons to develop specific immunoglobulin E (IgE) responses. Laboratory animal allergy (LAA) is among the highest occupational risks for asthma in the UK. Elevated levels of nitric oxide (NO) are found in exhaled breath in asthma. In LAA symptoms may progress from conjunctivitis, rhinitis to asthma. Health surveillance aims to detect early sensitization. OBJECTIVE: To assess whether an association exists between LAA and exhaled NO. METHODS: A cross-sectional study was performed in 39 laboratory workers undergoing LAA health surveillance. Volunteers completed two health questionnaires, had skin-prick tests, spirometry, total IgE and RAST tests. Exhaled and nasal NO was measured by chemiluminescence analyser (LR2000, Logan Research, Rochester, UK). RESULTS: There were 23 asymptomatic subjects (mean age 29.53 years) and 16 symptomatic subjects (29.63 years, P=0.95); 9 early LAA, seven LAA asthma. Exhaled NO was raised in those with LAA symptoms 17.97 ppb+/-1.24 (mean+/-SEM) compared with asymptomatics 6.08 ppb+/-1.15, P < 0.05. A trend of increased NO by allergic status was observed; asymptomatic, to early LAA, to asthma. One-way analysis of variance compared differences between groups (F ratio 13.93, P < 0.001). Symptomatic subjects also had raised nasal NO, vs asymptomatic subjects (mean difference 378 ppb, P < 0.05). A trend was again observed by allergic status (F ratio 5.28, P=0.01). CONCLUSION: Raised NO levels in LAA increasing with symptom severity suggest NO may prove a useful additional tool in monitoring for LAA, and possibly the response to exposure reduction or allergy due to other respiratory sensitizers.

Adult↗
PubMed1998

Effect of an inhaled glucocorticosteroid on mast cell and smooth muscle beta 2 adrenergic tolerance in mild asthma.

BACKGROUND: Regular inhaled beta 2 agonist therapy is associated with loss of bronchoprotection to indirect bronchial provocation challenges such as allergen or adenosine monophosphate (AMP), while directly acting challenge is less affected, implying preferential mast cell tolerance. Glucocorticosteroids may reverse such beta 2 adrenoreceptor tolerance and upregulate mast cell beta 2 adrenoceptor function. METHODS: The effect of single high dose glucocorticosteroids on terbutaline induced loss of bronchoprotection was studied in a placebo controlled, double blind, cross-over study. Fifteen asthmatic subjects who were not taking inhaled glucocorticosteroids underwent two 10-day treatment periods with terbutaline (500 micrograms four times daily via Turbohaler), each followed by a single dose of inhaled budesonide (800 micrograms via Turbohaler) or identical placebo. RESULTS: Regular treatment with terbutaline resulted in significant loss of bronchoprotection to AMP (mean difference (95% CI) -1.7 (-3.0 to 0.4) doubling dilutions) but not to methacholine (mean difference -0.1 (-1.0 to 0.8) doubling dilutions). Single high dose budesonide increased the protective effect of terbutaline more to AMP than to methacholine challenge (+0.76 (0.3) doubling dilutions compared with +0.13 (0.4) doubling dilutions, respectively). The mean (SE) difference between budesonide and placebo for methacholine challenge was 0.08 (0.14) whereas that for AMP was 0.075 (0.15); p = NS. The difference in PC20 was not statistically significant when compared with placebo for either challenge agent. CONCLUSIONS: Inhaled glucocorticosteroids in a single dose had no significant effect in restoring terbutaline induced loss of bronchoprotection, implying that mast cell beta 2 adrenoceptor sensitivity is not restored by a single dose of an inhaled glucocorticosteroid in asthma.

Adenosine Monophosphate↗
PubMed1997

Malignant mesothelioma in south east England: clinicopathological experience of 272 cases.

BACKGROUND: Malignant mesothelioma is a rare pleural tumour associated with asbestos exposure. The proportion of malignant mesothelioma unrelated to asbestos exposure, and any differentiating features between exposed and unexposed cases, are not well described. This study describes occupational, clinical, and pathological features in a large cohort of cases of malignant mesothelioma from south east England. METHODS: All 272 cases from this region were studied, either in life or after death when necropsy examination suggested malignant mesothelioma. Detailed information was gathered regarding the occupational history, clinical course, and mode of death. Necropsies were performed in 98% of cases. Lung tissue was examined histologically to confirm the diagnosis, subtype of tumour, presence or absence of asbestosis and asbestos bodies. RESULTS: Exposure to asbestos was documented in 87% of cases, while in the remainder, no asbestos exposure was found nor were asbestos bodies seen; 94.5% were pleural, 5.1% peritoneal, and 0.4% pericardial. Right sided tumours were more common than left sided tumours (ratio 1.6:1). Patients usually presented with breathlessness and chest pain, but 33% presented with pleural effusion in the absence of chest pain. The mean (SD) time from first exposure to asbestos to symptoms was 40 (12) years with a median (interquartile range (IQR) survival of 14 (12.5) months. The median (IQR) survival time in sarcomatous, epithelial, and mixed cell type malignant mesothelioma was 9.4 (10) months, 12.5 (18) months, and 11 (14) months, respectively, and was significantly greater in cases detected by chance. Clinical features were similar in asbestos related and non-asbestos related malignant mesothelioma. CONCLUSIONS: In south east England most cases of malignant mesothelioma are associated with asbestos exposure. Clinical features do not differentiate between asbestos related and non-asbestos related disease.

Adult↗