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Biomedical subjects

J Arnott

Publications and source records attributed to J Arnott.

10 recordsLinked to original sources
PubMed2000

Parental factors affecting respiratory function during the first year of life.

In a prospective, longitudinal, population-based cohort study of familial and environmental influences on the development of wheezing respiratory illness in early childhood, we identified infant length, weight, gender, and exposure to maternal cigarette smoking as significant determinants of lung function during the first year of life. A cohort of 237 infants (106 females: 131 males) was evaluated, and 496 lung function measurements were made between the ages of 1-12 months. Respiratory function was assessed using the rapid thoracic compression technique to obtain maximum expiratory flow at functional residual capacity (V'maxFRC). Parental history of asthma and smoking habits during pregnancy were obtained by questionnaire. Data were analyzed using a longitudinal random effects model. Infants with a parental history of asthma and/or in utero passive smoke exposure were compared to a reference group of infants who had no parental history of asthma and in whom neither parent smoked pre- or postnatally. Boys were found to have a consistently lower V'maxFRC (-21.05 mL.s(-1)) throughout the first year of life in comparison to girls (P < 0.05). Maternal smoking during pregnancy was associated with a lower V'maxFRC in both genders in comparison to unexposed infants (P < 0.05). V'maxFRC was unaffected by parental history of asthma. Gender-specific normative equations for V'maxFRC throughout the first year of life were derived for the infant cohort as a whole and also for subgroups of infants, based on parental asthma and smoking history. We conclude that lung function during the first year of life differs between genders and is adversely affected by in utero passive tobacco smoke exposure. Gender-specific predictive equations for V'maxFRC should be used during infancy.

Cohort Studies↗
PubMed2000

The association between early life lung function and wheezing during the first 2 yrs of life.

Reports have suggested that certain infants are predisposed to wheezing in the first 2 yrs of life due to abnormal lung function, prior to the first wheezing illness. The authors investigated the association between infant lung function and wheeze during the first 2 yrs of life. A cohort of 253 infants was evaluated. Respiratory function assessment was performed at 1, 6, and 12 months of age. Parental history of asthma, atopy, and maternal antenatal smoking habits were recorded. An infant was identified as having wheezed on the basis of parental report and, where possible, physician diagnosis. One hundred and sixty infants (63%) had complete diary and questionnaire information on wheeze available for analysis. Of these: 79 infants (50%) had never wheezed (NW) during the first 2 yrs of life and 81 had reported wheeze (W) (50%). Of those with a report of wheeze, the distribution through the first 2 yrs of life was; 28 during the first year of life only (Y1), 21 in the second year of life only (Y2), and 32 wheezed in both the first and second years of life (Y1&2). At the age of 1 month, prior to any lower respiratory illness, the W group had impaired lung function in comparison to the NW group. In Y1 infants, the neonatal lung function differences resolved by 12 months of age. In Y2 and Y1&2 infants lung function differences persisted throughout the first year of life. Prevalence of parental asthma and maternal antenatal smoking was increased in the W group p=0.001, p=0.008, respectively), in comparison to the NW infants. Maternal antenatal smoking prevalence was increased in the Y2 and Y1&2 infants in comparison to the NW group (p=0.04), (p=0.01), respectively. Wheezing during the first year of life is often a transient condition which improves with time. It appears to be related to early life reduced small airway calibre. Wheezing that begins or persists into the second year of life is usually associated with a different abnormality of the airways. Commencement or persistence of wheeze into the second year of life may be part of the clinical entity recognized as asthma.

Asthma↗
PubMed1995

The effect of inhaled adrenaline on lung function of recurrently wheezy infants less than 18 months old.

Inhaled bronchodilators have been shown not to improve lung function in infants with wheeze. This observation has led to the suggestion that airway wall edema may be more important than bronchoconstriction in infants with airway narrowing. Inhaled adrenaline is used to relieve upper airway edema in children with croup and has been demonstrated to improve clinical scores and lower pulmonary resistance in some infants with wheeze associated with bronchiolitis. The aim of the present study was to examine the effect of inhaled adrenaline on lung function in a group of infants with recurrent wheeze. Eleven infants aged 10 to 18 months with a history of recurrent wheeze were studied during an asymptomatic interval. Respiratory function was assessed (1) by measuring maximal expiratory flow at functional residual capacity (VmaxFRC) during a forced partial expiratory maneuver and (2) by measuring conductance of the respiratory system (Grs) using a single expiratory occlusion technique. Following baseline measurements, the infants received 0.5 mg/kg adrenaline by nebulizer and serial lung function tests were repeated at 5 min intervals. Ten infants had abnormal baseline lung function (median VmaxFRC 44.2% predicted; median Grs 34% predicted). Using a random effects model, VmaxFRC and Grs declined significantly at 10 and 5 min after adrenaline, respectively. No significant improvements from baseline were observed in either measurement for up to 30 min following adrenaline delivery. It is concluded that inhaled adrenaline did not relieve airways obstruction in this group of asymptomatic infants with recurrent wheeze.

Administration, Inhalation↗
PubMed1995

Lung function, airway responsiveness, and respiratory symptoms before and after bronchiolitis.

Acute viral respiratory illness during infancy has been implicated as a precursor for subsequent lower respiratory morbidity in childhood. A prospective, longitudinal study of respiratory function, airway responsiveness, and lower respiratory illness during early childhood was performed in a cohort of 253 healthy infants to characterise those who experienced bronchiolitis. Seventeen infants (7% of the cohort), were given a diagnosis of bronchiolitis during the first two years of life with two (1%) requiring hospital admission. Seventy one per cent of those infants with bronchiolitis had a family history of atopy, 53% of asthma, and 29% had a mother who smoked cigarettes. These family history characteristics in this group with bronchiolitis were not different from the rest of the cohort. There were also no differences in the number of older siblings, the number breast fed, the duration of breast feeding, or socioeconomic status of the families between those that did and did not get bronchiolitis. Respiratory function was assessed at 1, 6, and 12 months of age. Maximum flow at functional residual capacity (VmaxFRC) was measured using the rapid thoracic compression technique. Resistance (Rrs) and size corrected compliance (Crs/kg) were obtained from a single brief occlusion at end inspiration. Airway responsiveness was assessed by histamine inhalation challenge and the provocation concentration of histamine resulting in a 40% fall on VmaxFRC from baseline (PC40) was determined. Respiratory measurements were ranked into terciles to assess the distribution of infants who developed bronchiolitis through the cohort. Cough and wheeze were noted to be frequent before the episode of bronchiolitis. This study has demonstrated that infants who develop bronchiolitis have evidence of pre-existing reduced respiratory function and lower respiratory symptoms. It is proposed that bronchiolitis, although potentially contributory, is not usually causative of subsequent lower respiratory morbidity.

Asthma↗
PubMed1994

Flow limitation during tidal expiration in symptom-free infants and the subsequent development of asthma.

During a longitudinal study of lung function and airway responsiveness in a cohort of healthy infants, we identified a subgroup of symptom-free infants at the age of 1 month with flow limitation during tidal expiration. We report a 2-year follow-up of 252 infants who were first studied at 1 month of age. Maximal flow at functional residual capacity (VmaxFRC) was measured from a forced expiratory flow-volume curve by the rapid thoracic compression technique. The pattern of tidal breathing was assessed with the ratio of the time to reach maximal expiratory flow during expiration to the total expiratory time (Tme/Te ratio). Histamine inhalation challenge was used to determine the level of airway responsiveness. Compliance and resistance of the total respiratory system were measured from a passive expiration after occlusion at end inspiration. Data regarding the family history of asthma, atopy, and parental smoking were obtained by questionnaire. Flow limitation was considered present when the forced expiratory flow did not exceed tidal flow at functional residual capacity. Nineteen infants were identified with flow limitation at 5 weeks of age; all had a family history of asthma, atopy, and/or parental smoking. These 19 infants were compared with 35 infants with no family history of asthma or parental smoking and 38 gender-, history-, and age-matched control infants without flow limitation during tidal expiration. At the age of 1 month, the flow-limited group had reduced VmaxFRC, Tme/Te, and respiratory compliance and increased respiratory resistance. At 6 and 12 months of age, although no longer flow limited, these infants still had significantly reduced lung function and increased airway responsiveness. Flow limitation in early life was also significantly associated with the development of physician-diagnosed asthma by the age of 2 years (odds ratio, 7.4; 95% confidence interval, 1.4 to 35.2). Infants with abnormal lung function soon after birth may have a genetic predisposition to asthma or other airway abnormalities that predict the risk of subsequent lower respiratory tract illness.

Asthma↗
PubMed1992

Syntax PAL: a system to improve the written syntax of language-impaired users.

In our work with children who have difficulty with spelling or with the physical action of writing, we have found a number of children who also have difficulty with written grammar. As an extension of PAL, an existing predictive spelling and typing aid, we have developed a writing aid to help these children with sentence construction. The enhanced system uses the syntax of the initial part of a sentence to enhance the position in the prediction list of syntactically correct words. It was postulated that this would discourage the use of incorrect syntax and encourage the use of correct syntax. In two case studies, the use of Syntax PAL significantly improved the quality and quantity of one child's written output, but had little effect on the other child's work.

Adolescent↗
PubMed1991

Bronchial responsiveness and lung function in recurrently wheezy infants.

Although most wheezy infants are considered asthmatic, they generally respond poorly to antiasthma treatment, and there is inadequate knowledge about the pathologic mechanisms that cause wheezing at this age. The aim of this study was to determine whether the strong association between wheezing and bronchial responsiveness (BR) seen in older subjects was also present in infants. We compared BR with inhaled histamine in 19 recurrently wheezy infants with a group of age-, height-, weight-, and sex-matched control infants. Maximal flow at FRC (VmaxFRC) was determined from partial expiratory flow-volume curves generated using the "squeeze" technique. Histamine was delivered during 1 min of tidal breathing in doubling concentrations from 0.125 g/L to a maximum of 8 g/L or until VmaxFRC fell by 40% (PC40). The median baseline VmaxFRC for the wheezy infants was 100.0 ml/s compared with 182.0 ml/s for the control infants (p less than 0.01). However, there was no significant difference in the PC40 between the two groups (2.1 versus 2.3 g/L).

Asthma↗
PubMed1987

Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia.

Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Nonimmune aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In-labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.

Animals↗