57 research outputs found
Designing optimal sampling configurations with ordinary and indicator kriging
No full textThe objective of this paper is to examine the applicability of two geostatistical approaches, ordinary kriging (OK) and ordinary indicator kriging (IK), to the design of optimal sampling strategies. This paper uses the OK variance and the conditional variance of the conditional cumulative distribution function (ccdf) derived through IK to assess local uncertainty in estimates. The mean OK variance and IK variance for a given grid spacing, using data sampled from a remotely sensed DTM, were used to ascertain the sample spacing required to achieve a particular accuracy. The estimates of optimal sample spacing were assessed with reference to the complete DTM. Judgement on the success of the two approaches was made on the basis of the correlation between the OK variance and the errors of OK estimation and between the IK variance and the errors of IK estimation, and the form of the relationships were discussed. The IK variance was found to represent the estimation errors more accurately than the OK variance, although OK estimates of elevation values were more accurate than those for IK. The IK is significantly more costly to implement than OK in terms of expenditure of time and effort and the implementation of the technique was demonstrated to be problematic in the presence of a low frequency trend. Despite these limitations IK was recommended for the design of optimal sampling strategies where the estimation of accuracy of a specified degree is particularly important and where the analysis relates to an area over which the spatial variability may be considered similar. Comparison and integration with a segmentation approach was suggested for future work, and the results of a related approach presented, to improve the implementation of IK in the context of digital elevation data
Non-rapid eye movement sleep determines resilience to social stress
No full textResilience, the ability to overcome stressful conditions, is found in most mammals and varies significantly among individuals. A lack of resilience can lead to the development of neuropsychiatric and sleep disorders, often within the same individual. Despite extensive research into the brain mechanisms causing maladaptive behavioral-responses to stress, it is not clear why some individuals exhibit resilience. To examine if sleep has a determinative role in maladaptive behavioral-response to social stress, we investigated individual variations in resilience using a social-defeat model for male mice. Our results reveal a direct, causal relationship between sleep amount and resilience—demonstrating that sleep increases after social-defeat stress only occur in resilient mice. Further, we found that within the prefrontal cortex, a regulator of maladaptive responses to stress, pre-existing differences in sleep regulation predict resilience. Overall, these results demonstrate that increased NREM sleep, mediated cortically, is an active response to social-defeat stress that is both necessary and sufficient for promoting resilience. They also show that differences in resilience are strongly correlated with inter-individual variability in sleep regulation.Funding provided by: National Institutes of HealthCrossref Funder Registry ID: http://dx.doi.org/10.13039/100000002Award Number: GM127260Male, C57BL/6J mice (Jackson Laboratory, Bar Harbor, ME, USA; 000664) were seven-weeks old at the start of all studies. CD-1 retired male breeders (Charles Rivers, age 3 to 6 months upon arrival) were used as aggressors. All mice were singly housed on shaved, pine bedding upon arrival, maintained on a 12:12 L:D lighting cycle for the remainder of the study and randomly assigned to treatment groups. Food and water were available ad libitum. All procedures involving animals received prior approval from the Morehouse School of Medicine Institutional Animal Care and Use Committee (approved protocol 21-02).
Surgery: EEG and LFP electrodes.
Electroencephalography (EEG): EEG and Electromyography (EMG) electrodes were implanted in isoflurane (1.5–3%) anesthetized mice. Carprofen was given post operatively for two days. A prefabricated head mount (Pinnacle Technology Inc., Lawrence, KS) was used to position three stainless-steel epidural screw electrodes. The first electrode (frontal—located over the frontal cortex) was placed 1.5 mm anterior to bregma and 1.5 mm lateral to the central suture, whereas the second two electrodes (interparietal—located over the visual cortex and common reference) were placed 2.5 mm posterior to bregma and 1.5 mm on either side of the central suture. The resulting two leads (frontal–interparietal and interparietal–interparietal) were referenced contralaterally. A fourth screw served as a ground. Electrical continuity between the screw electrode and head mount was aided by silver epoxy. EMG activity was monitored using stainless-steel Teflon-coated wires that were inserted bilaterally into the nuchal muscle. The head mount (integrated 2 × 3 pin socket array) was secured to the skull with dental acrylic. Mice were allowed to recover for at least 14 days before sleep recording
Sex chromosomes regulate nighttime sleep propensity during recovery from sleep loss in mice.
No full textSex differences in spontaneous sleep amount are largely dependent on reproductive hormones; however, in mice some sex differences in sleep amount during the active phase are preserved after gonadectomy and may be driven by non-hormonal factors. In this study, we sought to determine whether or not these sex differences are driven by sex chromosome complement. Mice from the four core genotype (FCG) mouse model, whose sex chromosome complement (XY, XX) is independent of phenotype (male or female), were implanted with electroencephalographic (EEG) and electromyographic (EMG) electrodes for the recording of sleep-wake states and underwent a 24-hr baseline recording followed by six hours of forced wakefulness. During baseline conditions in mice whose gonads remained intact, males had more total sleep and non-rapid eye movement sleep than females during the active phase. Gonadectomized FCG mice exhibited no sex differences in rest-phase sleep amount; however, during the mid-active-phase (nighttime), XX males had more spontaneous non-rapid eye movement (NREM) sleep than XX females. The XY mice did not exhibit sex differences in sleep amount. Following forced wakefulness there was a change in the factors regulating sleep. XY females slept more during their mid-active phase siestas than XX females and had higher NREM slow wave activity, a measure of sleep propensity. These findings suggest that the process that regulates sleep propensity is sex-linked, and that sleep amount and sleep propensity are regulated differently in males and females following sleep loss
Reproductive hormones and sex chromosomes drive sex differences in the sleep–wake cycle
No full textThere are well-documented gender differences in the risk and severity of sleep disorders and associated comorbidities. While fundamental sex differences in sleep regulatory mechanisms may contribute to gender disparities, biological responses to sleep loss and stress may underlie many of the risks for sleep disorders in women and men. Some of these sex differences appear to be dependent on sex chromosome complement (XX or XY) and the organizational effects of reproductive hormones. Reproductive development plays a critical role in the ability of sex chromosomes and reproductive hormones to produce sex differences in sleep and wakefulness. Rodent models reveal that reproductive hormones drive many but not all sex differences in sleep–wake architecture. The ability of reproductive hormones to alter sleep are often dependent on responses to sleep loss and stress. However, in the absence of reproductive hormones (in gonadectomized rodents) sex differences in sleep amount and the ability to recover from sleep loss persist. The suprachiasmatic nucleus (SCN) and the ventrolateral preoptic nucleus (VLPO) of the hypothalamus play crucial regulatory roles in mediating the effects of reproductive hormones on the sleep–wake cycle. Taken together, the work reviewed here reveals that the reproductive hormone environment and sex chromosome complement may underlie gender disparities in sleep patterns and the risk for sleep disorders
<i>In Vivo</i>Resetting of the Hamster Circadian Clock by 5-HT<sub>7</sub>Receptors in the Suprachiasmatic Nucleus
No full textSerotonin (5-HT) has been strongly implicated in the regulation of the mammalian circadian clock located in the suprachiasmatic nuclei (SCN); however, its role in behavioral (nonphotic) circadian phase resetting remains elusive. Central to this issue are divergent lines of evidence that the SCN may, or may not, be a target for the phase-resetting effects of 5-HT. We have addressed this question using a novel reverse-microdialysis approach for timed perfusions of serotonergic and other agents to the Syrian hamster SCN with durations equivalent to the increases inin vivo5-HT release during phase-resetting behavioral manipulations. We found that 3 hr perfusions of the SCN with either 5-HT or the 5-HT1A,7receptor agonist 2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydro-naphthalene (8-OH-DPAT) at midday advanced the phase of the free-running circadian rhythm of wheel-running assessed using an Aschoff type II procedure. Phase shifts induced by 8-OH-DPAT were enhanced more than threefold by pretreatment with the 5-HT synthesis inhibitorpara-chlorophenylalanine. Phase advances induced by SCN 8-OH-DPAT perfusion were significantly inhibited by the 5-HT2,7receptor antagonist ritanserin and by the more selective 5-HT7receptor antagonist DR4004, implicating the 5-HT7receptor in mediating this phase resetting. Concurrent exposure to light during the 8-OH-DPAT perfusion abolished the phase advances. Furthermore, coperfusion of the SCN with TTX, which blockedin vivo5-HT release, did not suppress intra-SCN 8-OH-DPAT-induced phase advances. These results indicate that 5-HT7receptor-mediated phase resetting in the SCN is markedly influenced by the degree of postsynaptic responsiveness to 5-HT and by photic stimulation. Finally, 5-HT may act directly on SCN clock cells to inducein vivononphotic phase resetting.</jats:p
Sleep Deprivation alters the influence of biological sex on active phase sleep behavior
No full textPoor sleep is a hazard of daily life that oftentimes cannot be avoided. Gender differences in daily sleep and wake patterns are widely reported; however, it remains unclear how biological sex, which is comprised of genetic and endocrine components, directly influences sleep regulatory processes. In the majority of model systems studied thus far, sex differences in daily sleep amount are predominant during the active (wake) phase of the sleep-wake cycle. The pervasiveness of sex differences in sleep amount throughout phylogeny suggests a strong underlying genetic component. The goal of the current study is to determine if sex differences in active-phase sleep amount are dependent on sex chromosomes in mice. Sleep was examined in the four-core genotype (FCG) mouse model, whose sex chromosome complement (XY, XX) is independent of sex phenotype (male or female). In this line, sex phenotype is determined by the presence or absence of the Sry gene, which is dissociated from the Y chromosome. Polysomnographic sleep recordings were obtained from gonadectomized (GDX) FCG mice to examine spontaneous sleep states and the ability to recover from sleep loss. We report that during the active-phase, the presence of the Sry gene accounts for most sex differences during spontaneous sleep; however, during recovery from sleep loss, sex differences in sleep amount are partially driven by sex chromosome complement. These results suggest that genetic factors on the sex chromosomes encode the homeostatic response to sleep loss
Author response: Bmal1 function in skeletal muscle regulates sleep
No full textSleep loss can severely impair the ability to perform, yet the ability to recover from sleep loss is not well understood. Sleep regulatory processes are assumed to lie exclusively within the brain mainly due to the strong behavioral manifestations of sleep. Whole-body knockout of the circadian clock gene Bmal1 in mice affects several aspects of sleep, however, the cells/tissues responsible are unknown. We found that restoring Bmal1 expression in the brains of Bmal1-knockout mice did not rescue Bmal1-dependent sleep phenotypes. Surprisingly, most sleep-amount, but not sleep-timing, phenotypes could be reproduced or rescued by knocking out or restoring BMAL1 exclusively in skeletal muscle, respectively. We also found that overexpression of skeletal-muscle Bmal1 reduced the recovery response to sleep loss. Together, these findings demonstrate that Bmal1 expression in skeletal muscle is both necessary and sufficient to regulate total sleep amount and reveal that critical components of normal sleep regulation occur in muscle
Sleep Is Critical for Remote Preconditioning-Induced Neuroprotection.
No full textStudy objectivesEpisodes of brief limb ischemia (remote preconditioning) in mice induce tolerance to modeled ischemic stroke (focal brain ischemia). Since stroke outcomes are in part dependent on sleep-wake history, we sought to determine if sleep is critical for the neuroprotective effect of limb ischemia.MethodsEEG/EMG recording electrodes were implanted in mice. After a 24 h baseline recording, limb ischemia was induced by tightening an elastic band around the left quadriceps for 10 minutes followed by 10 minutes of release for two cycles. Two days following remote preconditioning, a second 24 h EEG/EMG recording was completed and was immediately followed by a 60-minute suture occlusion of the middle cerebral artery (modeled ischemic stroke). This experiment was then repeated in a model of circadian and sleep abnormalities (Bmal1 knockout [KO] mice sleep 2 h more than wild-type littermates). Brain infarction was determined by vital dye staining, and sleep was assessed by trained identification of EEG/EMG recordings.ResultsTwo days after limb ischemia, wild-type mice slept an additional 2.4 h. This additional sleep was primarily comprised of non-rapid eye movement (NREM) sleep during the middle of the light-phase (i.e., naps). Repeating the experiment but preventing increases in sleep after limb ischemia abolished tolerance to ischemic stroke. In Bmal1 knockout mice, remote preconditioning did not increase daily sleep nor provide tolerance to subsequent focal ischemia.ConclusionsThese results suggest that sleep induced by remote preconditioning is both sufficient and necessary for its neuroprotective effects on stroke outcome
Analysis and Measurement of the Sympathetic and Sensory Innervation of White and Brown Adipose Tissue
No full textEffects of speed and grade on the biomechanics and energetics of walking in obese adults
No full textDepartment Head: Richard Gay Israel.2010 Summer.Includes bibliographical references (pages 56-61).Brisk walking is a recommended form of exercise for obese individuals. However, lower extremity joint loads and the associated risk of musculoskeletal injury or pathology increase with walking speed. Walking uphill at a slower speed may offer an alternative form of moderate intensity exercise that reduces joint loading. The purpose of this study was to quantify the biomechanics and energetics of level and uphill walking in obese adults. We hypothesized that compared to brisk level walking, walking slower up a moderate incline would reduce lower extremity joint loading while providing appropriate physiologic stimulus. Twelve obese adult volunteers, age = 27 (5.5) years, mass = 100.5 (15.7) kg, BMI = 33.4 (2.6) kg/m2, (mean (S.D.)), participated in this study. We measured ground reaction forces, three-dimensional lower extremity kinematics and oxygen consumption while subjects walked on a dual-belt force measuring treadmill at several speed (0.50-1.75m/s)/grade (0-9°) combinations. We calculated net muscle moments at the hip, knee and ankle and metabolic rate for each condition. Walking slower uphill significantly reduced net muscle moments at the knee compared to faster level walking (p<0.05). Peak knee extension and adduction moments were reduced by ~19% and 26%, respectively, when subjects walked at 0.75m/s, 6° vs. 1.50m/s, 0°. The greater knee moments during level walking suggests subjects had greater medial compartment knee joint loads. All walking trials were moderate intensity (48.5-59.8% of VO2max). A slower walking speed combined with a moderate incline appears to be an effective strategy for reducing knee joint loads while providing appropriate cardiovascular stimulus in obese adults
- …
