A descriptive study was conducted to examine the relationship between social support and adaptation to sleep by Southern Taiwan hospitalized adults. The conceptual framework for this study was based on Roy's adaptation model and social support as a beneficial factor in health and well-being. Sixty-one hospitalized adults, ages 20 to 71 years, participated in this study. Sixteen subjects (26.2%) had a supportive person stay with them. Data analysis showed that only daytime sleep items of the supplementation factor were significantly different between the supported and unsupported groups. However, all the mean values of effectiveness items in the supported group were higher than those in the unsupported group. It is recommended that a larger sample size from diverse hospitals in Taiwan be used to repeat the study.

No description available.

New mothers often complain of impaired cognitive functioning, and it is well documented that women experience a significant increase in sleep disturbance after the birth of a child. Sleep disturbance has been linked to impaired cognitive performance in several populations, including commercial truck drivers, airline pilots, and medical residents, though this relationship has rarely been studied in postpartum women. In the present study 13 pregnant women and a group of 22 non-pregnant controls completed one week of actigraphy followed by a battery of neuropsychological tests and questionnaires in the last month of pregnancy (Time 1) and again at four weeks postpartum (Time 2). Pregnant women experienced significantly more objective and subjective sleep disturbance than the control group at both time points. They also demonstrated more impairment in objective, but not subjective cognitive functioning. Preliminary analyses indicated increased objective sleep fragmentation from Time 1 to Time 2 predicted decreased objective cognitive performance from Time 1 to Time 2, though small sample size limited the power of these findings. Implications for perinatal women and need for future research were discussed.

A common reason why athletes retire from their sport is burnout. Athletic burnout often occurs when athletes are over-trained and do not get enough rest. The present study examines the question: why is it that some athletes are able to perform at a high level for many years while others fizzle out? The purpose of the proposed study is to investigate the effects of perfectionism and anxiety on sleep disturbances and athletic burnout in high school students. The proposed method will be a correlational within-participants design and participants will be high school-age female gymnasts. The gymnasts will complete measures of perfectionism surrounding academics and athletics, anxiety, and burnout. Additionally, the gymnasts’ parents will complete measures of perfectionism and their perceptions of their child’s burnout. Athletes will then be given a sleep tracker to wear each night for a week to measure the athlete’s sleep per night. It is predicted that academic perfectionism and amount of sleep will interact to result in higher burnout levels. Additionally, it is predicted that there will be an interaction between anxiety levels and amount of sleep resulting in higher levels of burnout. The proposed study could give more insight into the mental and physiological processes behind athletic burnout. The relationship between perfectionism, anxiety, sleep, and burnout is one that requires further research but may be useful information for coaches, parents, and athletes to prevent athletic burnout.

STUDY OBJECTIVES: We sought to evaluate the construct validity and factor structure of the Spanish-language version of the Pittsburgh Sleep Quality Index (PSQI) among pregnant Peruvian women. METHODS: A cohort of 642 women were interviewed at ≤ 16 weeks of gestation. During interview, we ascertained information about lifestyles, demographics, sleep characteristics, and mood symptoms. Stress induced sleep disturbance, depressive symptoms, and anxiety symptoms were evaluated using the Ford Insomnia Response to Stress Test (FIRST), Patient Health Questionnaire-9 (PHQ-9), and Generalized Anxiety Disorder-7 (GAD-7) assessment scales, respectively. Consistency indices, exploratory and confirmatory factor analyses, correlations, and logistic regressions were used. RESULTS: Both exploratory and confirmatory factor analyses indicated a three-factor solution: sleep quality, sleep efficiency, and sleep medication. We observed significantly positive correlations of the PSQI with the FIRST (0.42), the PHQ-9 (0.49), and the GAD-7 (0.46). Poor sleepers (PSQI global score > 5) had significantly increased odds of experiencing stress-induced sleep disturbance (odds ratio, OR = 3.57; 95% CI: 2.40, 5.31), depression (OR = 5.48; 95% CI: 3.58, 8.37), and generalized anxiety disorder (OR = 4.57; 95% CI: 3.08, 6.76). CONCLUSION: The Spanish-language version of the PSQI instrument was found to have good construct validity among pregnant Peruvian women. Consistent with some other studies, the PSQI was found to have a three-factor structure. Further assessment and validation studies are needed to determine whether the three, factor-specific scoring of the PSQI is favored over the PSQI global score in diverse populations.

The purpose of this study was to contribute to the paucity of literature present on educational psychology involvement in supporting primary school-aged children’s sleep. The research was formed using a pragmatic, mixed-methods approach with a two-phase design. Phase one explored the views of 59 participants (teachers, n= 16; parents/carers, n= 21; children, n= 22) about children’s sleep, their academic outcomes and psychosocial functioning. There were some associations between parent, child, and teacher reports of children’s sleep-related difficulties, academic outcomes and aspects of children’s psychosocial functioning. Phase two adopted a time-series pre- and post-intervention design with the aim of evaluating a school-based, six-week Sleep Club intervention for children. Twenty-nine participants (teaching assistants, n= 2; parents/carers, n= 13; and children, n= 14) took part in phase two, with the findings drawing on evaluations, quizzes, field notes, surveys, and parent interviews. Six children were selected to provide greater insight into parent and child views through case study analysis. At the end of the intervention, there was an increase in children’s sleep-related knowledge, and there were improvements in many aspects of children’s sleep-related behaviours. Thematic analysis identified that the Sleep Club facilitated communication about sleep between children and their parents and raised children’s awareness and understanding of their sleep. Children enjoyed being part of a club with other children, from whom they felt they were able to learn. Learning about emotions, sleep and the body was noted by several children, though some children did not enjoy completing the given questionnaires. Overall, participants felt that the individual sessions and the intervention could have lasted longer than the time offered. Twenty-two participants (76%, including parents, children, and school staff) reported that they would recommend the Sleep Club intervention to others. The role of the educational psychologist in supporting children with sleep difficulties is discussed.

No description available.

This thesis describes the use of in vivo and in vitro models to better understand the molecular correlates of sleep and sleep deprivation. Unlike previous studies, we utilise a timecourse based experimental design throughout, which has the advantage of identifying how the abundance of molecules return to baseline following sleep deprivation. Chapter 3 outlines the transcriptome of mouse cortex collected over 54 hours from mice subjected to varied durations of sleep deprivation. The timecourse experimental design aids in the identification of genes that are induced during both spontaneous and enforced wakefulness, and facilitates the dissociation of genes whose expression is tightly linked to the current wake state of the animal from those whose expression is linked to the total amount of wakefulness recently experienced by the animal. Like previous studies, we identify several genes involved in the unfolded protein response and synaptic function that are upregulated by sleep deprivation. We also find that increasing durations of sleep deprivation progressively reduces the total number of rhythmically expressed genes in mouse cortex, with only a handful of transcripts identified as diurnal following 12 hour sleep deprivation. Chapter 4 outlines the proteomic and metabolomic effects of 12 hour sleep deprivation. Proteomic analyses indicate that the abundance of ribosomal and nucleosomal proteins is suppressed for at least 24 hours following sleep deprivation, whilst the abundance of several phosphodiesterases are acutely increased following sleep deprivation. Metabolomic analyses of sleep deprived mouse cortex identified 3 molecular species whose abundance profile implicate them as sleep homeostats. Finally, we also set out to develop an in vitro model of sleep deprivation based on the optogenetic activation of a neuroblastoma cell line, which is outlined in Chapter 5. Following several rounds of optimisation, the stable expression of an opsin was found to induce intracellular calcium spikes and immediate early gene expression during illumination. Transcriptomic profiling of illuminated SH-SY5Y cells induced large scale transcriptomic changes, and modulated the expression of genes involved in synapses, cholesterol synthesis, the molecular clock and the unfolded protein response. Although these functional classes are reminiscent of those modulated by in vivo sleep deprivation, there was only a slight enrichment of individual genes modulated by in vivo sleep deprivation amongst the blue light sensitive genes, indicating further work is required to more closely model in vivo sleep deprivation.

Hypoxia is a common feature of many respiratory disorders including acute severe asthma, chronic obstructive pulmonary disease and pneumonia. Hypoxia also occurs during sleep - disordered breathing in conditions such as sleep hypoventilation syndrome and sleep apnea. In most respiratory diseases hypoxia is coupled with increased respiratory load. Compensatory protective mechanisms are activated to oppose these impediments to respiration. However, hypoxia is associated with impaired neurocognitive function and recent studies have demonstrated that hypoxia suppresses respiratory load perception in healthy individuals and asthma patients. These recent findings raise the possibility that a variety of protective physiological reflex responses to increased respiratory load may be impaired during periods of hypoxia. The effects of hypoxia on several of these protective responses and possible mechanisms of respiratory sensory depression by hypoxia are explored in the experiments outlined in this thesis. In the first study, the respiratory related evoked potential ( RREP ) was used to investigate the mechanisms underlying hypoxia - induced suppression of respiratory load sensation in healthy individuals. As a positive control the effects of hypoxia on respiratory load perception to inspiratory resistive loads were also measured. The amplitude of the first and second positive peaks ( P1 and P2 ) of the RREP were significantly reduced during hypoxia. P1 is thought to reflect the arrival of the ascending respiratory signals to the somatosensory area of the cortex. The perceived magnitude of externally applied inspiratory resistive loads was also reduced during hypoxia. These data provide further support that hypoxia suppresses respiratory load perception and suggest that this is mediated, at least in part, by suppression of respiratory afferent information prior to its arrival at the cortex. In the second study, the effects of acute sustained hypoxia on the cough reflex threshold and cough tachyphylaxis to inhaled capsaicin were explored in healthy individuals. Acute sustained hypoxia suppressed cough reflex sensitivity to inhaled capsaicin. This finding raises the possibility that the cough reflex, important for protecting the lungs from inhalation or aspiration of potentially injurious substances and for clearing excess secretions, may be impaired during acute exacerbations of hypoxic - respiratory disease. In the third study, reflex responses of the genioglossus and scalene muscles to brief pulses of negative airway pressure were compared between hypoxia and normoxia during wake and sleep in healthy males in the supine position. Cortical RREPs to the same stimuli were also examined under these conditions. The genioglossus is the largest upper airway ( UA ) dilator muscle and can be reflexively augmented in response to negative UA pressure. A diminished response of this muscle during sleep has been postulated to be a contributing mechanism to obstructive sleep apnea ( OSA ) in individuals with an anatomically narrow UA. Cortical activation ( i.e. arousal ) to sudden airway narrowing in OSA is an important protective response to help restore ventilation during an obstructive event. In this study, genioglossus reflex responses to negative pressure pulse stimuli were maintained during mild overnight hypoxia. Conversely, reflex inhibition of the scalene muscle to the same stimuli was prolonged during hypoxia. In addition, a previously undescribed morphology of the genioglossus negative pressure reflex consisting of activation followed by suppression was observed with greater suppression during sleep than wake. The amplitude of the P2 component of the RREP was also significantly reduced during hypoxia. In summary, the potential mechanisms underlying hypoxia - induced suppression of respiratory load sensation and the effects of hypoxia on several protective respiratory responses have been investigated in healthy subjects. The potential implications of these findings for patients with hypoxic - respiratory disease are discussed. / Thesis (Ph.D.)--School of Molecular and Biomedical Science, 2006.

Obstructive sleep apnoea (OSA) is characterised by repetitive reductions or pauses in breathing during sleep due to upper airway narrowing or closure. Due to disruption to normal sleep patterns, many patients with OSA suffer from increased daytime sleepiness. Epidemiological studies have established a link between OSA and driver fatigue and accidents, generally showing a two to seven times increased risk of road traffic accidents in non-commercial drivers with OSA. There is emerging evidence that commercial drivers have a higher prevalence of OSA than the general population, being predominately male, middle-aged and overweight, three important risk factors for OSA. However, little is known about the relationship between OSA and driver sleepiness in commercial drivers, whether road accidents are increased in commercial drivers with OSA, and whether OSA interacts with other fatigue promoting factors, such as sleep deprivation, to further escalate road accident risk. One thousand randomly selected commercial drivers were surveyed in the field. In addition, 61 randomly selected NSW commercial drivers had in hospital sleep studies and daytime performance testing, including a PC based driving simulator task. The prevalence of OSA, defined as Respiratory Disturbance Index (RDI) < 10, was approximately 50% in NSW commercial drivers. Approximately one quarter of the drivers reported pathological daytime sleepiness, and 12-14% had both OSA and pathological daytime sleepiness. A diagnosis of OSA was the most important factor predicting excessive daytime sleepiness in these drivers: OSA was more important than 15 other work-related, lifestyle and medical factors that could be expected to promote, or be associated with, daytime sleepiness. Drivers with sleep apnoea syndrome (both OSA and pathological daytime sleepiness) had an increased driving accident risk, using driving simulator and daytime performance testing as proxy measures for accident risk. These results demonstrate the importance of OSA as a cause of driver fatigue in commercial drivers and suggest that all commercial drivers should be screened for the presence of sleep apnoea syndrome in order to potentially reduce road accident risk through treatment. A separate, but related body of work examined the combined effects of mild OSA and other fatigue promoting factors (sleep deprivation and circadian influences) on driving performance. Twenty nine subjects, consisting of a group with mild OSA and a group of non-OSA controls, were tested on several occasions throughout the night and day using an intensive performance battery, under both baseline conditions and after a period of 36 hours of total sleep deprivation. The results suggest that drivers with mild OSA are not different to the control group in their response to sleep deprivation or time of day influences. However, the subjects with mild OSA were less aware of their impairment due to sleep deprivation, which is of concern if drivers with OSA are relying on their subjective awareness of fatigue to make decisions about when to stop driving. A final perspective on OSA and driver fatigue is provided through a clinical case series of seven fall-asleep fatality associated MVA�s associated with unrecognised or under-treated sleep disorders. As well as demonstrating the day to day potential for devastating road accidents due, at least in part, to un-recognised or untreated sleep disorders, these cases also serve to highlight some of the current medico-legal controversies and difficulties in this area of driver fatigue. In conclusion, this body of work has provided novel information about the epidemiology and implications of OSA in commercial drivers, and about how OSA interacts with other fatigue promoting factors. Finally, it has explored some of the medico-legal issues that relate to sleep disorders and driver fatigue. As well as providing much needed information in the area of driver fatigue, at the same time this work raises many more questions and suggests areas of future research. For instance, such research should examine the relationship between objective accident rates and OSA/sleep apnoea syndrome in commercial drivers, the interaction between mild sleep apnoea syndrome and other fatigue risk factors, and driver perception of sleepiness prior to sleep onset in drivers with sleep disorders.