Performance of a Portable Sleep Monitoring Device in Individuals with High Versus Low Sleep Efficiency.

STUDY OBJECTIVES: Portable and automated sleep monitoring technology is becoming widely available to consumers, and one wireless system (WS) has recently surfaced as a research tool for sleep and sleep staging assessment outside the hospital/laboratory; however, previous research findings indicate low sensitivity for wakefulness detection. Because difficulty discriminating between wake and sleep is likely to affect staging performance, we sought to further evaluate the WS by comparing it to the gold-standard polysomnography (PSG) and actigraphy (ACT) for overall sleep/wakefulness detection and sleep staging, within high and low sleep efficiency sleepers. METHODS: Twenty-nine healthy adults (eight females) underwent concurrent WS, PSG, and ACT assessment in an overnight laboratory study. Epoch-by-epoch agreement was determined by comparing sleep/wakefulness decisions between the WS to both PSG and ACT, and for detection of light, deep, and rapid eye movement (REM) sleep stages between the WS and PSG. RESULTS: Sensitivity for wakefulness was low (40%), and an overestimation of total sleep time and underestimation of wake after sleep onset was observed. Prevalence and bias adjusted kappa statistic indicated moderate-to-high agreement between the WS and PSG for sleep staging. However, upon further inspection, WS performance varied by sleep efficiency, with the best performance during high sleep efficiency. CONCLUSIONS: The benefit of the WS as a sleep monitoring device over ACT is the ability to assess sleep stages, and our findings suggest this benefit is only realized within high sleep efficiency. Care should be taken to collect data under conditions where this is expected.

Improvements in gait speed and weight shift of persons with traumatic brain injury and vestibular dysfunction using a virtual reality computer-assisted rehabilitation environment.

Many people sustaining a traumatic brain injury experience vestibular pathology requiring physical therapy for treatment. This study measured improvements in gait speed and weight shift for subjects receiving vestibular physical therapy using a Computer-Assisted Rehabilitation Environment (CAREN). A 6-session CAREN, 6-session traditional vestibular therapy group was compared with a 12-session CAREN only (0 traditional sessions) therapy group. These two groups were compared to each other and with data from healthy controls performing similar tasks on the CAREN. Those participating in 12 CAREN sessions had greater improvements in gait speed (p=0.014) and weight shift scores (p<0.001) and demonstrated similar values achieved by a healthy control population.

Cortisol stimulates proliferation and apoptosis in the late gestation fetal heart: differential effects of mineralocorticoid and glucocorticoid receptors.

We have previously found that modest chronic increases in maternal cortisol result in an enlarged fetal heart. To explore the mechanisms of this effect, we used intrapericardial infusions of a mineralocorticoid receptor (MR) antagonist (canrenoate) or of a glucocorticoid receptor (GR) antagonist (mifepristone) in the fetus during maternal infusion of cortisol (1 mg·kg⁻¹·day⁻¹). We have shown that the MR antagonist blocked the increase in fetal heart weight and in wall thickness resulting from maternal cortisol infusion. In the current study we extended those studies and found that cortisol increased Ki67 staining in both ventricles, indicating cell proliferation, but also increased active caspase-3 staining in cells of the conduction pathway in the septum and subendocardial layers of the left ventricle, suggesting increased apoptosis in Purkinje fibers. The MR antagonist blocked the increase in cell proliferation, whereas the GR antagonist blocked the increased apoptosis in Purkinje fibers. We also found evidence of activation of caspase-3 in c-kit-positive cells, suggesting apoptosis in stem cell populations in the ventricle. These studies suggest a potentially important role of corticosteroids in the terminal remodeling of the late gestation fetal heart and suggest a mechanism for the cardiac enlargement with excess corticosteroid exposure.

Assessment of cognitive function while on low-dose propranolol: implications for usage by survivors in a disabled submarine.

While awaiting rescue from a disabled submarine (DISSUB), survivors will likely endure an atmosphere of rising CO2 which will eventually be lethal. Previously, it was determined that low-dose propranolol reduces resting metabolic carbon dioxide production and therefore may increase survival time in this scenario. The actions and decisions survivors would carry out in a DISSUB situation would require an unaltered cognition state. Therefore, we wanted to determine if low-dose propranolol impairs cognitive function. Eight healthy males completed a counterbalanced, randomized, placebo-controlled, double-blinded crossover study in which each subject received propranolol (40 mg twice daily) or placebo (lactose pill twice daily) over a 72-hour period. The alternate condition was separated by a minimum 96-hour washout period. Subjects performed a series of 6 tasks from the Automated Neuropsychological Assessment Metrics (ANAM) battery and answered a self-report sleepiness scale each morning and afternoon. Subjects exhibited increased accuracy in one of the ANAM tasks while on propranolol compared to placebo, but showed no difference between treatments on the other 5 tasks and sleepiness scale. These results suggest that 40 mg of propranolol taken twice daily does not significantly impair cognitive function and may be a viable option for use in a DISSUB scenario.

Propranolol's potential to increase survival time in a disabled submarine.

BACKGROUND: While awaiting rescue from a disabled submarine, survivors will likely endure an atmosphere of rising CO2 that will result in CO2 toxicity once the available emergency CO2 scrubbing materials are exhausted. Propranolol is a beta-blocker that may increase survival time by reducing metabolic CO2 production (VCO2). The purpose of this study was to determine if propranolol reduces resting VCO2 in healthy men. METHODS: Eight healthy men completed a counterbalanced, randomized, placebo-controlled, double-blinded crossover study in which each subject received propranolol (40 mg twice daily) or placebo (lactose pill twice daily) over 72 h. The alternate condition was separated by a minimum 96-h washout period. Resting VCO2, oxygen consumption (VO2), ventilation (VE), respiration rate (RR), respiratory exchange ratio (RER), mean arterial pressure (MAP), heart rate (HR), and cardiac output (Q) were measured each morning and afternoon. RESULTS: When compared to placebo, propranolol significantly reduced VCO2 (-6.5%), MAP (-3.6%), HR (-10.4%), and Q (-8.2%); however, there were no significant differences in VO2, RR, VE, or RER. DISCUSSION: These results show that 40 mg of propranolol taken twice daily reduces resting VCO2 in healthy men and suggests that this treatment strategy may increase survival time in a disabled submarine scenario.

Hypercortisolism as a potential concern for submariners.

Cortisol is a stress-response hormone that is important for survivability in fight or flight situations. Hypercortisolism is a state of chronically elevated cortisol levels due to a failure to return to, or maintain baseline levels. It is a condition that is often undiagnosed and can aid in the development of many physiological and psychological health problems. Some of the health ailments associated with hypercortisolism include metabolic syndrome, decreases in bone mineral density, and depression. Chronic stress and sleep deprivation are two common causes of hypercortisolism, both areas of concern within the submarine community. This review discusses the etiology of hypercortisolism and the likelihood of submariner vulnerability to the condition along with health problems associated with it. Lastly, strategies to prevent chronic elevation of cortisol and mitigate the potential health risks associated with the condition are covered.

The ontogeny of genes related to ovine fetal cardiac growth.

The objective of this study was to determine the ontogenetic profiles in left and right ventricle of genes implicated in cardiac growth, including mineralocorticoid (MR) and glucocorticoid (GR) receptor, 11 beta-hydroxysteroid dehydrogenase (11beta-HSD) 1 and 2 and genes of the angiotensin system and insulin-like growth factor (IGF) family. Samples from left and right ventricles (LV, RV) were collected from hearts of sheep fetuses at 80, 100, 120, 130, and 145 days of gestation and from newborn lambs. Quantitative real-time PCR was performed to determine the MR, GR, 11beta-HSD 1 and 2, angiotensin converting enzyme (ACE) 1 and 2, IGF1, IGF2, IGF receptors IGF-1R and IGF-2R, and IGF-binding proteins (IGFBP) 2 and 3. In the LV, MR and GR both decreased toward term. In the RV, MR and GR expression did not decrease, but both 11beta-HSD 1 and 2 mRNA levels increased after birth. ACE1 expression in LV and RV sharply increases just before parturition, whereas ACE2 decreased in the LV and RV in late gestation. IGF2, IGF2R, and IGFBP2 expression levels substantially decreased in late gestation in LV and RV; IGF2R also decreased with age in LV. These patterns suggest that reduced expression of genes related to IGF and angiotensin II action occur as proliferative activity declines and terminal differentiation occurs in the late gestation fetal heart.

Cardiac corticosteroid receptors mediate the enlargement of the ovine fetal heart induced by chronic increases in maternal cortisol.

Previous studies have demonstrated that modest, physiologically relevant increases in maternal cortisol in late gestation result in enlargement of the fetal heart. In this study, we investigated the role of mineralocorticoid receptor (MR) or glucocorticoid receptor (GR) in this enlargement. Ewes with single fetuses were randomly assigned at approximately 120 days of gestation to one of four groups: maternal cortisol infusion (1 mg/kg per day, cortisol); maternal cortisol infusion with fetal intrapericardial infusion of the MR antagonist (MRa) potassium canrenoate (600 microg/day; cortisol+MRa); maternal cortisol infusion with fetal intrapericardial infusion of the GR antagonist (GRa) mifepristone (50 microg/day, cortisol+GRa); and maternal saline infusion (control). At approximately 130 days of gestation, fetal heart to body weight ratio and right ventricular (RV) and left ventricular (LV) free wall thicknesses were increased in the cortisol group when compared with control group. Fetal hearts from the cortisol+MRa group weighed significantly less, with thinner LV, RV, and interventricular septum walls, when compared with the cortisol group. Fetal hearts from the cortisol+GRa group had significantly thinner RV walls than the cortisol group. Fetal arterial pressure and heart rate were not different among groups at 130 days. Picrosirius red staining of fetal hearts indicated that the increased size was not accompanied by cardiac fibrosis. These results suggest that physiologic increases in maternal cortisol in late gestation induce fetal cardiac enlargement via MR and, to a lesser extent, by GR, and indicate that the enlargement is not secondary to an increase in fetal blood pressure or an increase in fibrosis within the fetal heart.

Increased maternal cortisol in late-gestation ewes decreases fetal cardiac expression of 11beta-HSD2 mRNA and the ratio of AT1 to AT2 receptor mRNA.

Moderately elevated maternal cortisol levels late in gestation cause enlargement of the fetal sheep heart. We have used quantitative real-time PCR to examine expression of candidate genes in fetal hearts from mothers in whom cortisol levels were increased (by infusion of 1 mg cortisol.kg(-1).day(-1)) or decreased (by adrenalectomy and replacement to 0.5 mg cortisol.kg(-1).day(-1)) from 115 to 130 days gestation. Control ewes were not treated with steroid. Expression of mineralocorticoid receptor (MR), glucocorticoid receptor (GR), 11beta-hydroxysteroid dehydrogenases 1 and 2 (11beta-HSD1 and -2), IGF I and II, IGF receptors 1 and 2 (IGF-1R and IGF-2R), endothelial nitric oxide synthase, VEGF, myotrophin, angiotensinogen, the angiotensin receptors 1 and 2 (AT1R and AT2R), and the angiotensin converting enzymes 1 and 2 were measured. MR mRNA abundance in fetal hearts was found to be similar to that in adult kidney and hippocampus. Although there were no significant changes in most genes, 11beta-HSD2 and IGF-1R expression were significantly decreased in the high cortisol group and 11beta-HSD2 expression negatively correlated to left ventricular wall thickness. There was also a significant change in the ratio of AT receptor expression, with increased AT2R and decreased AT1R in the high cortisol group. MR, GR, and 11beta-HSD1 immunoreactivity was found in cardiomyocytes and cardiac blood vessels in 126-128 day fetal sheep; in contrast 11beta-HSD2 staining was predominantly in blood vessels. These results indicate that cortisol could indeed act in the fetal heart to induce enlargement and suggest that the renin-angiotensin system may play a role.