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Introduction: In extending work on early life antecedents of parenting, we investigate associations between childhood family history of disadvantage, adolescent socioemotional wellbeing, and age at first parenthood and subsequent parenting behaviour., Methods: Parent-child interactions were recorded when participants in the longitudinal Dunedin Multidisciplinary Health and Development Study (New Zealand) had a three-year-old child. Data were available for 358 mothers and 321 fathers, aged between 17.7 and 41.5 at the time of their child's birth. Associations between parenting and antecedent data on socioeconomic disadvantage, adolescent wellbeing and mental health, as well as current adult mental health and age at parenting, were tested for using structural equation modelling., Results: Family disadvantage in childhood and lower adolescent wellbeing was associated with less positive future parenting, but only adult (not adolescent) anxiety/depression symptoms were directly associated with parenting behaviour. Childhood family disadvantage was associated with further disadvantage across the life course that included less positive parenting of the next generation. In contrast, socioemotional wellbeing during adolescence and later age of onset of parenting were associated with more positive parenting., Conclusions: Reducing childhood disadvantage and improving socioemotional wellbeing during childhood and adolescence is likely to have intergenerational benefits through better parenting of the next generation., (Copyright © 2020 The Foundation for Professionals in Services for Adolescents. Published by Elsevier Ltd. All rights reserved.)

There is uncertainty about the development of airway tolerance to beta-agonists and the phenomenon of rebound bronchoconstriction on beta-agonist withdrawal. We have recently completed a study of the regular terbutaline and budesonide treatment in asthma. We report our observations on the effect of starting and stopping terbutaline treatment on morning and evening peak flows. The study was a randomized four-way, double-dummy, cross-over comparison of regular inhaled terbutaline (500-1000 microg four times daily), budesonide, combined treatment and matching placebo. Each treatment was given for 6 weeks following a 4 week single-blind placebo washout. Ipratropium was used for symptom relief. No other asthma medication was permitted during either the treatment or wash-out periods. Evaluable data were obtained from 52 subjects for both placebo and terbutaline treatment. Changes in mean morning and evening peak flows during terbutaline treatment were compared to the baseline peak flows during the last 2 weeks of the preceding washout. The peak flow changes on stopping terbutaline were also analysed. Mean morning peak flow was not significantly different during terbutaline treatment when compared to either baseline or placebo treatment. Evening peak flows were significantly higher during terbutaline treatment [mean increase 23.1 l min(-1) (95% CI = 18.8, 27.4)]. Analysis of the peak flow changes on a day-by-day basis revealed an initial increase in morning peak flows for the first 2 days of treatment of 19.2 and 13.41 min(-1) [increases of 25.0 and 17.31 min(-1) in comparison with the corresponding values during placebo (P<0.01)] followed by a return to baseline. The increase in evening peak flows was also greater for the first 2 days of treatment than for the remainder of the treatment period (P<0.01). On ceasing terbutaline treatment there was a fall in mean morning peak flow below the baseline on the following morning of 21.6 l min(-1) (P<0.05 compared to placebo). The temporary increase in morning peak flows and greater than expected rise in evening peak flows for the first 2 days of treatment suggest the development of tolerance to the bronchodilator effect of terbutaline. Similarly, the fall in morning peak flows on treatment withdrawal suggests rebound bronchoconstriction. These effects are likely to be mediated by downregulation of the beta-receptor during treatment. The clinical significance of these changes is uncertain in view of the stability of overall asthma control during terbutaline treatment, but sudden withdrawal of beta-agonist treatment could conceivably lead to a deterioration in asthma control.

A mathematical model is presented which describes the relationship between intrauterine pressure and uterine wall tension. Wall tension is evaluated in terms of muscular contraction in an active myometrium and the modulating effect of a passive, compliant cervix. Using a computer programme which simulates the recruitment of contractile elements in the uterine wall, it is possible to generate theoretical pressure waveforms. The effects on these waveforms produced by changing cervical properties are demonstrated and compared with observed phenomena. The physiological and clinical implications are evaluated.

Thirteen-channel visual evoked potentials (VEPs) to pattern-onset were recorded with stimuli restricted to individual octants of the peripheral field, to halves and to quadrants of the fovea. The voltage of the CI component was measured in each channel to define its topography for each stimulated sector. The potential fields so obtained were then analysed to find the orientation and location of a dipole that would produce a corresponding pattern of voltages at the scalp. The locations of the computed dipoles are consistent with the hypothesis that CI is generated in striate cortex. The computed locations and orientations are not compatible with alternative arrangements of sources in extrastriate cortex. A significant problem remains. If CI is indeed generated by the striate cortex then the orientation of the dipoles excited by stimulation of the peripheral field indicates that the cortex is surface negative. This leads to the prediction that foveal stimuli will elicit a CI which is negative at posterior electrodes. The experiments reported here confirm that CI is positive with such stimuli, and its source is calculated as a horizontal dipole with its positive pole oriented posterolaterally. Two possible explanations are considered for the reversed polarity of foveal CI: (a) that macropotentials associated with stimulation of the fovea are opposite in polarity from those associated with stimulation of the peripheral field; (b) that the foveal area of the retinotopic map extends into the lateral calcarine fissure with the effect that much of it faces in the reverse direction from the cortex at the pole.