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Biomedical subjects

S Breen

Publications and source records attributed to S Breen.

13 recordsLinked to original sources

Autonomic activity during human sleep as a function of time and sleep stage.

While there is a developing understanding of the influence of sleep on cardiovascular autonomic activity in humans, there remain unresolved issues. In particular, the effect of time within the sleep period, independent of sleep stage, has not been investigated. Further, the influence of sleep on central sympathetic nervous system (SNS) activity is uncertain because results using the major method applicable to humans, the low frequency (LF) component of heart rate variability (HRV), have been contradictory, and because the method itself is open to criticism. Sleep and cardiac activity were measured in 14 young healthy subjects on three nights. Data was analysed in 2-min epochs. All epochs meeting specified criteria were identified, beginning 2 h before, until 7 h after, sleep onset. Epoch values were allocated to 30-min bins and during sleep were also classified into stage 2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. The measures of cardiac activity were heart rate (HR), blood pressure (BP), high frequency (HF) and LF components of HRV and pre-ejection period (PEP). During non-rapid eye movement (NREM) sleep autonomic balance shifted from sympathetic to parasympathetic dominance, although this appeared to be more because of a shift in parasympathetic nervous system (PNS) activity. Autonomic balance during REM was in general similar to wakefulness. For BP and the HF and LF components the change occurred abruptly at sleep onset and was then constant over time within each stage of sleep, indicating that any change in autonomic balance over the sleep period is a consequence of the changing distribution of sleep stages. Two variables, HR and PEP, did show time effects reflecting a circadian influence over HR and perhaps time asleep affecting PEP. While both the LF component and PEP showed changes consistent with reduced sympathetic tone during sleep, their pattern of change over time differed.

Adolescent↗

Cardiac and respiratory activity at arousal from sleep under controlled ventilation conditions.

Arousal from sleep is associated with elevated cardiac and respiratory activity. It is unclear whether this occurs because of homeostatic mechanisms or a reflex activation response associated with arousal. Cardiorespiratory activity was measured during spontaneous arousals from sleep in subjects breathing passively on a ventilator. Under such conditions, homeostatic mechanisms are eliminated. Ventilation, end-tidal PCO2, mask pressure, diaphragmatic electromyograph, heart rate, and blood pressure were measured in four normal subjects under two conditions: assisted ventilation and a normal ventilation control condition. In the control condition, there was a normal, sleep-related fall in ventilation and rise in end-tidal PCO2. Subsequently, at an arousal, there was an increase in respiratory and cardiac activity. In the ventilator condition, a vigorous cardiorespiratory response to a spontaneous arousal from sleep remained. These results indicate that sleep-related respiratory stimuli are not necessary for the occurrence of elevated cardiorespiratory activity at an arousal from sleep and are consistent with the hypothesis that such activity is at least in part due to a reflex activation response.

Adult↗

Auditory integration training for children with autism: no behavioral benefits detected.

Auditory integration training and a control treatment were provided for 16 children with autism in a crossover experimental design. Measures, blind to treatment order, included parent and teacher ratings of behavior, direct observational recordings, IQ, language, and social/adaptive tests. Significant differences tended to show that the control condition was superior on parent-rated measures of hyperactivity and on direct observational measures of ear-occlusion. No differences were detected on teacher-rated measures. Children's IQs and language comprehension did not increase, but adaptive/social behavior scores and expressive language quotients decreased. The majority of parents (56%) were unable to report in retrospect when their child had received auditory integration training. No individual child was identified as benefiting clinically or educationally from the treatment.

Acoustic Stimulation↗

Hypoxemia near mid-gestation has long-term effects on fetal brain development.

We tested the hypotheses that an episode of hypoxemia near mid-gestation in fetal sheep has long-term effects on brain development and that the extent and type of damage is related to the stage of development within a particular brain structure at the time of the hypoxemia. Fetal sheep (n = 8) were made hypoxemic at 90 +/- 2 days (term approximately 147 days) by restricting the maternal blood supply to the placenta for 12 hours (h) using a vascular clamp so as to reduce fetal arterial O2 saturation by 50%-60%. Fetuses were killed 35 days later and the brains analysed histologically and immunohistochemically. Age-matched fetuses (n = 8) were used as controls. Gross brain damage was observed in only 1 fetus, the most acidemic during the period of hypoxemia. There was a reduction of 12% (p < 0.05) in the cross-sectional area of the cerebral cortex in hypoxemic fetuses compared with controls. In lobule 6 of the cerebella of hypoxemic fetuses, significant reductions were seen in (a) the volume density of Purkinje cells (33%), (b) the width of the molecular layer (13%), (c) the area of the inner granule cell layer (13%), (d) the area of the white matter (18%), and (e) the total cross-sectional area (15%). There were also significant reductions in the area of arborization of Purkinje cell dendritic trees (50%), in the branching density (25%), and in the number of dendritic spines (31%). In the ventral hippocampi of hypoxemic fetuses, there was a 36% reduction (p < 0.05) in the volume density of CA1 pyramidal cells and a 50% increase (p < 0.05%) in the number of astrocytes. We conclude that an episode of hypoxemia near mid-gestation reduces neuronal numbers in the hippocampus and cerebellum and probably also in the cerebral cortex. The growth of neural processes in a particular region will be significantly retarded if the hypoxemia occurs at an early stage of the growth of neural processes (e.g. cerebellum) but not if development is well advanced at the time of the insult (e.g. hippocampus). Damage is sustained in the white matter of the cerebral hemispheres if the insult is particularly severe. Together, these deficits could affect neural connectivity and impair postnatal brain function.

Animals↗

Fetal brain injury following prolonged hypoxemia and placental insufficiency: a review.

It is well-established that severe, acute episodes of hypoxemia can damage the brain before birth, but the effects of more sustained hypoxemia are less well understood. We have used fetal fetal sheep in a series of studies aimed at determining the effects of prolonged hypoxemia, induced by placental insufficiency of differing severity and duration, on fetal brain structure. Restriction of placental, and hence fetal, growth by carunclectomy caused impaired development of neural processes and connections in the hippocampus, cerebellum, and visual cortex; neuronal migration and neuronal numbers did not appear to be affected. Twenty days of placental insufficiency during late gestation induced by umbilicoplacental embolisation also caused abnormalities in brain structure; the cerebellum, which develops late in gestation, was particularly affected. In the cortex, there was evidence of white matter lesions, an increase in the size of capillaries and a proliferation of astroglia. We also examined the effects of shorter periods of hypoxemia (6-12 hr) near mid-gestation on brain structure; fetuses were allowed to recover for 7 or 35 days after the hypoxemic challenge. The major changes were mild focal damage in the cortical white matter, a reduction in the number of Purkinje cells, a delay in the growth of neural processes in the cerebellum and proliferation of blood vessels. The hippocampus was also affected, in particular the areal density of pyramidal cells was reduced. The use of several classes of pharmacological agents with the potential to protect neurons from hypoxemic injury is discussed in relation to the developing brain.

Animals↗

Identification of brainstem neurons responding to hypoxia in fetal and newborn sheep.

Hypoxia causes a reversible decrease in the level of respiratory, oculomotor and postural muscle activity in fetal sheep, an effect not seen in newborn lambs. We have used Fos immunohistochemistry to identify neurons which are activated by hypoxia and which may mediate this motor inhibition in the fetus. Pregnant sheep of either 117 or 138 days gestation were made hypoxic by allowing them to breathe 8-9% O2 for 2 h. Compared to age-matched control fetuses, hypoxia caused a significant increase in Fos-immunoreactivity in several medullary nuclei including the nucleus tractus solitarius, lateral reticular nucleus and the rostral ventrolateral medulla and also in the lateral parabrachial nucleus, locus coeruleus and subcoeruleus region in the pons. Hypoxia in newborn lambs, 7-18 days old, resulted in Fos staining in the same medullary and pontine nuclei with the exception of the subcoeruleus region which was devoid of Fos-immunoreactivity. In newborn lambs in which the carotid sinus nerves had been sectioned bilaterally, Fos-immunoreactivity was increased in the nucleus tractus solitarius in the medulla and in the locus coeruleus, lateral parabrachial and Kölliker-Fuse nuclei in the pons when compared to intact control newborn lambs. When carotid sinus nerve denervated-lambs were subjected to hypoxia the pattern of Fos-ir was similar to the pattern seen in the denervated control lambs but in addition staining was present in the subcoeruleus. These results suggest that a specific set of pontine neurons are activated by low oxygen levels in the fetus but not in the newborn lamb in the presence of an intact innervation from the carotid sinus. We hypothesise that: (a) in the fetus hypoxia activates neurons in the region of the subcoeruleus and this causes cessation of breathing movements and muscle atonia; and (b) that after birth stimulation of the carotid chemoreceptors by hypoxia normally inhibits activation of these subcoeruleus neurons.

Aging↗

The development of diurnal rhythmicity in fetal suprachiasmatic neurons as demonstrated by fos immunohistochemistry.

Using Fos immunohistochemistry as a marker of cellular activity, we have shown that neurons in the suprachiasmatic nucleus of fetal sheep are active by 75 days gestation. From at least 90 days gestation (term is 146 days), these neurons are more active during the day (12.00) than at night (03.00) when pregnant ewes are exposed to a 12-h light-dark cycle with lights on at 07.00. The day-night difference in Fos immunoreactivity persisted when the lighting schedule was extended by 8 h to 03.00, although neurons were now more active at 03.00 than they were in fetuses maintained on the normal light-dark cycle. When ewes were maintained in constant light from 133 to 138 days, the day-night difference in Fos immunoreactivity in the fetal suprachiasmatic nucleus was abolished, suggesting that diurnal activity of the fetal suprachiasmatic nucleus is maintained by a signal related to the external lighting regime. In a twin pregnancy where one fetus was optically enucleated at 100 days gestation, the density of Fos-immunoreactive neurons in the suprachiasmatic nucleus during the day at 138 days was similar to the unoperated twin. This suggests that the effects of dim light in the uterus on the fetal retina do not account for the high level of Fos immunoreactivity in the suprachiasmatic nucleus in the daytime. We propose that a chemical messenger of maternal origin, possibly melatonin, suppresses the activity of fetal suprachiasmatic neurons during the night, and that fetal suprachiasmatic neurons have endogenous activity which is expressed fully during the daytime.

Animals↗

Sexual health care in British Columbia: a model of service delivery.

The Sexual Health Program at British Columbia Rehabilitation Society has been providing comprehensive sexual health care to people with spinal cord injuries for the past 20 years. The focus of this paper is to describe this model of service delivery to nurses who may be interested in implementing similar models of service delivery to other health care settings. Sexual health care occurs within the context of the readiness, values and beliefs of the client. The Sexual Health Clinician provides a continuum of consumer-driven services to assist individuals, couples and family members to understand and manage the sexual outcomes of spinal cord injury. As part of the client team, the Sexual Health Clinician provides comprehensive assessment, education, and management for clients and staff. Assessment involves clarifying sexual concerns, establishing present sexual function status using the Sexual Assessment Framework, and exploring past functioning and partnership issues. Concerns are normalized, validated, and support is provided to the client and/or family. This paper will assist nurses to identify the benefits of having a Sexual Health Program as part of spinal cord injury nursing care and be able to identify principles of sexual health care practice that may be able to be incorporated into their present clinical setting.

British Columbia↗

Radial mosaicism and tangential cell dispersion both contribute to mouse neocortical development.

The mammalian neocortex is generated by waves of migrating cells originating from the ventricular zone. Radial migration along radial glia has been proposed as the dominant mechanism for this process. The radial unit hypothesis is poorly supported by retroviral lineage studies, however, and although some clones show limited radial organization, the emphasis appears to be on widespread tangential dispersion. Here we investigate the pattern of cortical cell dispersion using transgenic mice in which roughly half of the brain cells are coloured by a transgene. We find that the neocortex is randomly divided into diffused bands, the majority of cells within each band have the same colour, and their radial orientation suggests radial dispersion. Superimposed upon this was a significant contribution by tangentially dispersed cells that did not respect clonal borders. These observations indicate that cortical specification is not dependent upon a single mechanism of cell allocation, but that both radial mosaicism and tangential cell migration are involved.

Animals↗

After the birth.

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Female↗