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Since Koebner's first observance of the isomorphic response of psoriasis in a tattoo in 1872, a paucity of written reports has appeared in the literature describing this phenomenon, although it appears to be common knowledge among dermatologists. We report a strep-induced guttate psoriasis isomorphic response in a Winnie the Pooh tattoo in a 19-year-old.

Sleep, especially rapid-eye-movement sleep, causes fundamental modifications of respiratory muscle activity and control mechanisms, modifications that can predispose individuals to sleep-related breathing disorders. One of the most common of these disorders is obstructive sleep apnea (OSA) that affects approximately 4% of adults. OSA is caused by repeated episodes of pharyngeal airway obstruction that can occur hundreds of times per night, leading to recurrent asphyxia, arousals from sleep, daytime sleepiness, and adverse cardiovascular and cerebrovascular consequences. OSA is caused by the effects of sleep on pharyngeal muscle tone in individuals with already narrow upper airways. Moreover, since OSA occurs only in sleep, this disorder by definition is a state-dependent process ultimately caused by the influence of sleep neural mechanisms on the activity of pharyngeal motoneurons. This review synthesizes recent findings relating to control of pharyngeal muscle activity across sleep-wake states, with special emphasis on the influence of neuromodulators acting at the hypoglossal motor nucleus that inervates the genioglossus muscle of the tongue. The results of such basic physiological studies may be relevant to identifying and developing new pharmacological strategies to augment pharyngeal muscle activity in sleep, especially rapid-eye-movement sleep, as potential treatments for OSA.

Three sections, taught by different instructors, of Conceptual Physics were taught energy conservation using three different techniques: traditional — no visualization, energy bar charts, and energy bars. Performance of the groups of students on final exam questions is compared and contrasted.

The concept of a tonic drive activating respiratory muscle in wakefulness but not sleep has been an important and enduring notion in respiratory medicine, not least because it is useful in modeling sleep effects on breathing and understanding the pathogenesis of sleep-related breathing disorders such as obstructive sleep apnea. However, a neurotransmitter substrate mediating respiratory muscle activation across sleep-wake states has not been identified.We determined if alpha1 receptor antagonism at the hypoglossal motor nucleus (HMN) decreases genioglossus (GG) activity consistent with a role for an endogenous noradrenergic drive contributing to GG activation across sleep-wake states. We also determined if alpha1 receptor stimulation could counteract reduced endogenous noradrenergic drive and increase sleeping GG activity.Thirty-five rats were implanted with electroencephalogram and neck electrodes to record sleep-wake states and GG and diaphragm electrodes for respiratory muscle recordings. Microdialysis probes were inserted into the HMN.Microdialysis perfusion of the alpha1 receptor antagonist terazosin into the HMN significantly decreased GG activity in wakefulness and nonrapid eye movement (non-REM) sleep but not REM sleep. The alpha1 receptor agonist phenylephrine increased GG activity in wakefulness and sleep, but periods of motor inactivity persisted in REM sleep; there was no potentiating effect of combined alpha1 and 5-HT2 receptor stimulation.Identification of an endogenous noradrenergic drive contributing to GG activation in wakefulness and non-REM sleep, but not REM sleep, is important given the prevalence and clinical significance of sleep-induced hypoventilation and obstructive sleep apnea in humans and the potential for pharmacologic treatment.

Exogenous serotonin at the hypoglossal motor nucleus (HMN) stimulates genioglossus (GG) muscle activity. However, whether endogenous serotonin contributes to GG activation across natural sleep-wake states has not been determined, but is relevant given that serotonergic neurons have decreased activity in sleep and project to pharyngeal motoneurons.To determine the role of endogenous serotonin at the HMN in modulating GG activity across natural sleep-wake states.Ten rats were implanted with electroencephalogram and neck muscle electrodes to record sleep-wake states, and GG and diaphragm wires for respiratory muscle recordings. Microdialysis probes were implanted into the HMN for perfusion of artificial cerebrospinal fluid and the serotonin receptor antagonist mianserin (100 microM).In room air, there was no effect of mianserin on respiratory-related or tonic GG activities across sleep-wake states (p0.300). In hypercapnia, however, the normal declines in GG activity from non-REM to REM sleep, and wakefulness to REM sleep, were reduced with mianserin (p0.005). These data demonstrate a normally low endogenous serotonergic drive modulating GG activity unless augmented by reflex inputs. We also demonstrated a significant serotonergic drive modulating GG activity in vagotomized rats, but not in vagi-intact rats, under anesthesia, suggesting that previous results in reduced preparations may have been influenced by vagotomy.The results show a minimal endogenous serotonergic drive at the HMN modulating GG activity across sleep-wake states, unless augmented by reflex inputs. This result has implications for pharmacologic strategies aiming to increase GG activity by manipulating endogenous serotonin in patients with obstructive sleep apnea.

This article presents a brief review of the fundamentals of optical information processing. We discuss optical information processing techniques, materials and devices for optical processing, optical pattern recognition, optical security, optical neural computing, and optical memory. Optical image processing algorithms and architectures as well as basic hardware concepts such as the fundamentals of optical spatial light modulators are reviewed. Keywords: optical information processing; optical imaging; optical pattern recognition; optical security; optical spatial light modulators; optical neural computing; optical memory

The genioglossus (GG) muscle of the tongue, innervated by the hypoglossal motor nucleus (HMN), helps maintain an open airway for effective breathing. In vitro studies in neonatal rodents have separately characterized muscarinic and nicotinic receptor influences at the HMN but the net effects of combined nicotinic and muscarinic receptor activation and increased endogenous acetylcholine have not been determined in adult animals in vivo. Urethane-anaesthetized, tracheotomized and vagotomised rats were studied. Microdialysis perfusion of acetylcholine into the HMN significantly decreased respiratory-related GG activity (28.5 +/- 11.0% at a threshold dose of 0.1 mm). Application of the cholinergic agonists carbachol and muscarine have similar suppression effects (GG activity was decreased 11.8 +/- 4.3 and 20.5 +/- 5.8%, respectively, at 0.01 microm). Eserine, an acetylcholinesterase inhibitor, also decreased the amplitude of respiratory-related GG activity (36.4 +/- 11.3% at 1.0 microm) indicating that endogenous acetylcholine modulates GG activity. Although these results showed that suppression of GG activity predominates during cholinergic stimulation at the HMN, application of the nicotinic receptor agonist dimethyl-4-phenylpiperazinium iodide significantly increased tonic and respiratory-related GG activity (156 +/- 33% for respiratory activity at 1.0 mm) showing that excitatory responses are also present. Consistent with this, 100 microm carbachol decreased GG activity by 44.2 +/- 7.5% of control, with atropine (10 microm) reducing this suppression to 13.8 +/- 4.0% (P0.001). However, the nicotinic receptor antagonist dihydro-beta-erythroidine (100 microm) increased the carbachol-mediated suppression to 69.5 +/- 5.9% (P = 0.011), consistent with a role for nicotinic receptors in limiting the overall suppression of GG activity during cholinergic stimulation. Application of eserine to increase endogenous acetylcholine also showed that inhibitory muscarinic and excitatory nicotinic receptors together determine the net level of GG activity during cholinergic stimulation at the HMN. The results suggest that acetylcholine has mixed effects at the HMN with muscarinic-mediated GG suppression masking nicotinic excitation.

Normal spontaneous arousals from sleep are associated with transient increases in blood pressure, heart rate, and ventilation caused by large transient changes in autonomic output. These autonomic changes are out of proportion to obvious physiological need and are in excess of those observed in later periods of quiet wakefulness. This paper discusses some of the mechanisms underlying the cardio-respiratory consequences of arousal from sleep, and discusses why the normal onset of wakefulness may be associated with such large changes in autonomic output.

The hypoglossal motor nucleus innervates the genioglossus (GG) muscle of the tongue, a muscle that helps maintain an open airway for effective breathing. Rapid-eye-movement (REM) sleep, however, recruits powerful neural mechanisms that can abolish GG activity even during strong reflex stimulation such as by hypercapnia, effects that can predispose to sleep-related breathing problems in humans. We have developed an animal model to chronically manipulate neurotransmission at the hypoglossal motor nucleus using in vivo microdialysis in freely behaving rats. This study tests the hypothesis that glycine receptor antagonism at the hypoglossal motor nucleus, either alone or in combination with GABAA receptor antagonism, will prevent suppression of GG activity in natural REM sleep during room air and CO2-stimulated breathing. Rats were implanted with electroencephalogram and neck muscle electrodes to record sleep-wake states, and GG and diaphragm electrodes for respiratory muscle recording. Microdialysis probes were implanted into the hypoglossal motor nucleus for perfusion of artificial cerebrospinal fluid (ACSF) and strychnine (glycine receptor antagonist, 0.1 mM) either alone or combined with bicuculline (GABAA antagonist, 0.1 mM) during room air and CO2-stimulated breathing. Compared to ACSF controls, glycine receptor antagonism at the hypoglossal motor nucleus increased respiratory-related GG activity in room air (P = 0.010) but not hypercapnia (P = 0.221). This stimulating effect of strychnine in room air did not depend on the prevailing sleep-wake state (P = 0.625) indicating removal of a non-specific background inhibitory glycinergic tone. Nevertheless, GG activity remained minimal in those REM sleep periods without phasic twitches in GG muscle, with GG suppression from non-REM (NREM) sleep being > 85 % whether ACSF or strychnine was at the hypoglossal motor nucleus or the inspired gas was room air or 7 % CO2. While GG activity was minimal in these REM sleep periods, there was a small but measurable increase in GG activity after strychnine (P < 0.05). GG activity was also minimal, and effectively abolished, in the REM sleep periods without GG twitches with combined glycine and GABAA receptor antagonism at the hypoglossal motor nucleus. We conclude that these data in freely behaving rats confirm that inhibitory glycine and GABAA receptor mechanisms are present at the hypoglossal motor nucleus and are tonically active, but that such inhibitory mechanisms make only a small contribution to the marked suppression of GG activity and reflex responses observed in periods of natural REM sleep.

The genioglossus muscle is involved in the maintenance of an open airway for effective breathing. Inhibitory neurotransmitters may be responsible for the major suppression of hypoglossal motor output to genioglossus muscle that occurs in certain behaviours such as rapid-eye-movement sleep. There is evidence for GABA(A) receptor-mediated inhibition of hypoglossal motoneurons in vitro. However, comparable studies have not been performed in vivo and the interactions of such mechanisms with integrative reflex respiratory control have also not been determined. Urethane-anaesthetised, tracheotomized and vagotomized rats were studied whilst diaphragm and genioglossus muscle activities, blood pressure and the electroencephalogram were recorded. Microdialysis probes were implanted into the hypoglossal motor nucleus, with sites verified by histology. Genioglossus responses to microdialysis perfusion of muscimol (GABA(A) agonist: 0, 0.1, 1 and 10 microM in artificial cerebrospinal fluid) were recorded at inspired CO(2)s of 0, 5 and 7.5% in six rats. Responses to bicuculline (GABA(A) antagonist, 0, 1, 10, 100 and 1000 microM) were also studied in six rats with and without CO(2) stimulation. Genioglossus activity decreased with muscimol (P0.0001), with major suppression at 1 and 10 microM during air breathing (decreases=70.2% and 92.8%, P0.005). Genioglossus activity increased with CO(2) (P=0.003), but genioglossus activation with 5 and 7.5% CO(2) were almost abolished with 10-microM muscimol. Responses were specific to genioglossus muscle as there were no changes in diaphragm, respiratory rate or blood pressure with muscimol (P0.144). Antagonism of GABA(A) receptors increased genioglossus activity (P0.001). These results show that GABA(A) receptor stimulation at the hypoglossal motor nucleus suppresses both genioglossus muscle tone and activity in the presence of reflex stimulation produced by hypercapnia. Recruitment of such mechanisms may contribute to the major suppression of genioglossus activity observed with and without CO(2) stimulation in behaviours such as rapid-eye-movement sleep.

Physician can obtain fetal heart rate, electrophysiological information, and uterine contraction activity for determining fetal status from an intrauterine catheters electrocardiogram with the maternal electrocardiogram canceled. In addition, the intrauterine catheter would allow physicians to acquire fetal status with one non-invasive to the fetus biosensor as compared to invasive to the fetus scalp electrode and intrauterine pressure catheter used currently. A real-time maternal electrocardiogram cancellation technique of the intrauterine catheters electrocardiogram will be discussed along with an analysis for the methods effectiveness with synthesized and clinical data. The positive results from an original detailed subjective and objective analysis of synthesized and clinical data clearly indicate that the maternal electrocardiogram cancellation method was found to be effective. The resulting intrauterine catheters electrocardiogram from effectively canceling the maternal electrocardiogram could be used for determining fetal heart rate, fetal electrocardiogram electrophysiological information, and uterine contraction activity.

There is evidence for glycine and GABAA-receptor-mediated inhibition of hypoglossal motoneurons in vitro. However, comparable studies have not been performed in vivo, and the interactions of such mechanisms with integrative reflex respiratory control have also not been determined. This study tests the hypotheses that glycine at the hypoglossal motor nucleus (HMN) will suppress genioglossus (GG) muscle activity, even in the presence of hypercapnic respiratory stimulation, and the effects of glycine will be blocked by strychnine. We also determined whether coapplication of glycine and muscimol (GABAA- receptor agonist) to the HMN is additive in suppressing GG activity. Twenty-four urethane-anesthetized, tracheotomized, and vagotomized rats were studied. Diaphragm and GG activities, the electroencephalogram, and blood pressure were recorded. Microdialysis probes were implanted into the HMN for delivery of artificial cerebrospinal fluid (control), glycine (0.0001–10 mM), or muscimol (0.1 μM). Increasing glycine at the HMN produced graded suppression of GG activity ( P < 0.001), although the GG still responded to stimulation with 7% inspired CO2( P = 0.002). Strychnine (0.1 mM) reversed the glycine-mediated suppression of GG activity, whereas combined glycine and muscimol were additive in GG muscle suppression. It remains to be determined whether the recruitment of such glycine and GABA mechanisms explains the periods of major GG suppression in behaviors such as rapid eye movement sleep.

We agree with Lalley et al. (2014) that various brainstem sites may contribute to opioid-induced respiratory depression. Our focus here, however, is on respiratory rate depression by systemically administered drugs acting on μ-opioid receptors. Of all the potential neural sites where systemically administered μ-opioids could act, Lalley et al. suggest that the parabrachial/Kolliker–Fuse complex may be critically mediating respiratory rate depression. First, if pontine nuclei were responsible for rate suppression, then depression should not be observed in the absence of the pons. Still, respiratory slowing occurs in preparations where transections are performed caudal to the pons (Takita et al. 1997; Gray et al. 1999). Also, the blocking of μ-opioid receptors alone in pontine regions has a stimulatory effect on respiratory rate that can be misinterpreted as a reversal of opioid-induced respiratory depression (Phillips et al. 2012; Prkic et al. 2012). Using microdialysis tools to locally manipulate cells, we showed that the preBotC is highly sensitive to μ-opioid receptor agonists and mediates respiratory rate depression by systematically administered μ-opioids (Montandon et al. 2011). One caveat raised when using local drug application is that drug concentration in tissue is unknown as diffusion depends on the molecule, concentration and route of perfusion. To circumvent these issues, we designed strategies to assess how effective drug perfusion is. First, we simulated drug diffusion ex situ and found that after 2 h of perfusion less than 18% of the delivered concentration was present beside the probe membrane and 5% was found at a 1 mm distance (Grace et al. 2014), which invalidates the notion that drugs diffuse beyond the preBotC and affect other respiratory nuclei. Secondly, perfusion close to the preBotC was more potent in causing rate depression or its reversal than perfusion further away (Montandon et al. 2011). Also, if the μ-opioid receptor antagonist naloxone was affecting other nuclei, it should also block the impact of systemic μ-opioids on genioglossus muscle activity since the hypoglossal premotor/motor neurons are close to the preBotC. It did not, however, and we previously revealed separate medullary sites for hypoglossal motor suppression (Hajiha et al. 2009; Montandon et al. 2011). In conclusion, we dispute the belief that the preBotC plays an indirect role in opioid-induced respiratory rate depression. Other sites may indeed mediate other components of respiratory depression, such as reduced respiratory drive transmission and upper airway dysfunction, but based on the evidence discussed (Montandon et al. 2011), we restate that the preBotC plays a critical role in mediating opioid-induced respiratory rate depression.

1. We tested two hypotheses: that respiration and metabolism are subject to circadian modulation in wakefulness, non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep; and that the effects of sleep on breathing vary as a function of time of day. 2. Electroencephalogram (EEG), neck electromyogram (EMG) and abdominal body temperature (T(b)) were measured by telemetry in six male Sprague-Dawley rats. The EEG and EMG were used to identify sleep-wake states. Ventilation (V(I)) and metabolic rate (V(CO2)) were measured by plethysmography. Recordings were made over 24 h (12:12 h light:dark) when rats were in established states of wakefulness, NREM sleep and REM sleep. 3. Statistically significant circadian rhythms were observed in V(I) and V(CO2) in each of the wakefulness, NREM sleep and REM sleep states. Amplitudes and phases of the circadian rhythms were similar across sleep-wake states. 4. The circadian rhythm in V(I) was mediated by a circadian rhythm in respiratory frequency (f(R)). Tidal volume (V(T)) was unaffected by time of day in all three sleep-wake states. 5. The 24 h mean V(I) was significantly greater during wakefulness (363.5 +/- 18.5 ml min(-1)) than during NREM sleep (284.8 +/- 11.1 ml min(-1)) and REM sleep (276.1 +/- 13.9 ml min(-1)). V(CO2) and V(T) each significantly decreased from wakefulness to NREM sleep to REM sleep. f(R) was significantly lower in NREM sleep than in wakefulness and REM sleep. 6. These data confirm that ventilation and metabolism exhibit circadian rhythms during wakefulness, and NREM and REM sleep, and refute the hypothesis that state-related effects on breathing vary as a function of time of day. We conclude that the effects of circadian rhythms and sleep-wake state on respiration and metabolic rate are additive in the rat.

Obstructive sleep apnoea is a common and serious breathing problem that is caused by effects of sleep on pharyngeal muscle tone in individuals with narrow upper airways. There has been increasing focus on delineating the brain mechanisms that modulate pharyngeal muscle activity in the awake and asleep states in order to understand the pathogenesis of obstructive apnoeas and to develop novel neurochemical treatments. Although initial clinical studies have met with only limited success, it is proposed that more rational and realistic approaches may be devised for neurochemical modulation of pharyngeal muscle tone as the relevant neurotransmitters and receptors that are involved in sleep-dependent modulation are identified following basic experiments.

Recurrent sleep-related hypoxia occurs in common disorders such as obstructive sleep apnea (OSA). The marked changes in sleep after treatment suggest that stimuli associated with OSA (e.g., intermittent hypoxia) may significantly modulate sleep regulation. However, no studies have investigated the independent effects of intermittent sleep-related hypoxia on sleep regulation and recovery sleep after removal of intermittent hypoxia. Ten rats were implanted with telemetry units to record the electroencephalogram (EEG), neck electromyogram, and body temperature. After >7 days recovery, a computer algorithm detected sleep-wake states and triggered hypoxic stimuli (10% O2) or room air stimuli only during sleep for a 3-h period. Sleep-wake states were also recorded for a 3-h recovery period after the stimuli. Each rat received an average of 69.0 ± 6.9 hypoxic stimuli during sleep. The non-rapid eye movement (non-REM) and rapid-eye-movement (REM) sleep episodes averaged 50.1 ± 3.2 and 58.9 ± 6.6 s, respectively, with the hypoxic stimuli, with 32.3 ± 3.2 and 58.6 ± 4.8 s of these periods being spent in hypoxia. Compared with results for room air controls, hypoxic stimuli led to increased wakefulness ( P < 0.005), nonsignificant changes in non-REM sleep, and reduced REM sleep ( P < 0.001). With hypoxic stimuli, wakefulness episodes were longer and more frequent, non-REM periods were shorter and more frequent, and REM episodes were shorter and less frequent ( P < 0.015). Hypoxic stimuli also increased faster frequencies in the EEG ( P < 0.005). These effects of hypoxic stimuli were reversed on return to room air. There was a rebound increase in REM sleep, increased slower non-REM EEG frequencies, and decreased wakefulness ( P < 0.001). The results show that sleep-specific hypoxia leads to significant modulation of sleep-wake regulation both during and after application of the intermittent hypoxic stimuli. This study is the first to determine the independent effects of sleep-related hypoxia on sleep regulation that approximates OSA before and after treatment.

1. Serotonin (5-hydroxytryptamine, 5-HT) excites hypoglossal (XII) motoneurons in reduced preparations, and it has been suggested that withdrawal of 5-HT may underlie reduced genioglossus (GG) muscle activity in sleep. However, systemic administration of 5-HT agents in humans has limited effects on GG activity. Whether 5-HT applied directly to the XII motor nucleus increases GG activity in an intact preparation either awake or asleep has not been tested. 2. The aim of this study was to develop a novel freely behaving animal model for in vivo microdialysis of the XII motor nucleus across sleep-wake states, and test the hypothesis that 5-HT application will increase GG activity. 3. Eighteen rats were implanted with electroencephalogram and neck muscle electrodes to record sleep-wake states, and GG and diaphragm electrodes for respiratory muscle recording. Microdialysis probes were implanted into the XII motor nucleus and perfused with artificial cerebrospinal fluid (ACSF) or 10 mM 5-HT. 4. Normal decreases in GG activity occurred from wakefulness to non-rapid eye movement (non-REM) and REM sleep with ACSF (P < 0.01). Compared to ACSF, 5-HT caused marked GG activation across all sleep-wake states (increases of 91-251 %, P < 0.015). Importantly, 5-HT increased sleeping GG activity to normal waking levels for as long as 5-HT was applied (3-5 h). Despite tonic stimulation by 5-HT, periods of phasic GG suppression and excitation occurred in REM sleep compared with non-REM. 5. The results show that sleep-wake states differentially modulate GG responses to 5-HT at the XII motor nucleus. This animal model using in vivo microdialysis of the caudal medulla will enable the determination of neural mechanisms underlying pharyngeal motor control in natural sleep.

Suppression of respiratory muscle activity in sleep, particularly evident in the pharyngeal muscles, is pivotal to the pathogenesis of common sleep-related breathing disorders such as obstructive sleep apnea. Obstructive apneas are caused by sleep-related decrements in pharyngeal muscle activity that leads to snoring and airway obstruction in individuals with underlying structural narrowing of the upper airway. Since obstructive apneas occur exclusively during sleep, this disorder by definition is state-dependent and ultimately caused by the influences of brainstem sleep mechanisms on pharyngeal motoneurons in individuals with compromised upper airway anatomy. This paper reviews the central neuronal mechanisms by which sleep reduces the output to the pharyngeal muscles and the neurotransmitters implicated in this alteration. The experimental approaches used to address this problem are also mentioned and their relative advantages and disadvantages discussed. In particular, the information derived from reduced animal preparations is reviewed and the need for studies in natural sleep is emphasised. Identifying the central neuronal mechanisms and neurotransmitters involved in sleep-related suppression of pharyngeal muscle activity not only has important basic relevance to understanding state-dependent respiratory control, it also has immediate clinical relevance to understanding common sleep-related breathing disorders at the central neuronal level. Determining these basic mechanisms also has immediate clinical relevance to understanding the pathogenesis of airway occlusions, and guiding neuro-pharmacological approaches aimed at preventing the sleep-related decrements in pharyngeal muscle tone that are ultimately the root cause of obstructive sleep apnea.

I read with interest the recent article by Dr. Michael Levitzky on using the pathophysiology of obstructive sleep apnea (OSA) to teach cardiopulmonary integration ([2][1]). With 10 years of experience of teaching courses in both respiratory physiology and sleep at the University of Toronto, I also

From the Publisher: This book presents important recent advances in optical information processing, pattern recognition, neural computing, and materials for devices in optical computing.

We used a canine model of chronic obstructive sleep apnea (OSA) to examine the effects of intermittent airway occlusion during sleep on left ventricular (LV) performance. Studies were performed in four dogs. The effects of acute airway occlusion on LV pressure and volume (on a background of chronic OSA) were determined with an impedance catheter and a high fidelity manometer. In conscious animals (n = 3), experiencing spontaneous episodes of sleep, acute airway occlusion caused significant increases in LV transmural systolic pressure that were associated with increased end-systolic volume and reduced stroke volume. To determine the effects of chronic OSA on baseline LV function, two-dimensional echocardiograms were performed in conscious animals (n = 4) during unobstructed breathing before and after a 1- to 3-mo period of OSA. During chronic OSA, there was a significant decrease in LV ejection fraction as a result of increases in end-systolic volume. We conclude that in chronic OSA acute airway occlusion during sleep is associated with increases in LV afterload and decreases in fractional shortening. Chronic OSA also leads to sustained decreases in LV systolic performance that could be caused by the development of systemic hypertension and/or transient increases in LV afterload during episodes of airway obstruction.

Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. We recorded cortical and hippocampal electroencephalograms and genioglossus and inspiratory intercostal muscle activities in 13 urethane-anaesthetized, spontaneously breathing, tracheotomized and vagotomized rats. In steady-state periods with high-voltage/low-frequency electroencephalogram activity, carbachol microinjections (15-40 nl, 10 mM) were placed in the medial pontine reticular formation. In 12 rats, carbachol elicited episodes of stereotyped hypotonia of genioglossus but not intercostal muscle activity, typical of rapid eye movement sleep, with a latency and duration of 2.2+/-0.3min (mean+/-S.E.M.) and 11.0+/-2.9 min, respectively. In four of these rats, also similar to rapid eye movement sleep, the major suppression of genioglossus activity (-74+/-9%) was accompanied by electroencephalogram desynchronization, appearance of hippocampal theta rhythm, and a respiratory rate increase (+ 14+/-3%). In the remaining eight rats, the stereotyped suppression of genioglossus activity (-48+/-3%) occurred without electroencephalogram desynchronization and hippocampal theta, and was accompanied by a respiratory rate decrease (-6+/-2%); a pattern of response typical of decerebrate animals. Within a rat, similar patterns of response to repeated carbachol injections at the same anatomical site were obtained. Pontine atropine prevented responses to subsequent carbachol injections. Thus, in urethane-anaesthetized rats, pontine carbachol consistently produced a differential suppression of pharyngeal versus respiratory pump muscle activity, and in a subset of animals, this was also accompanied by cortical and hippocampal electrographic changes typical of rapid eye movement sleep. This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.

Obstructive sleep apnea (OSA) causes recurrent sleep disruption that is thought to contribute to excessive daytime sleepiness in patients with this disorder. The purpose of this study was to determine the specific effects of OSA on overall sleep architecture in a canine model of OSA. The advantage of this model is that sleep during long-term OSA can be compared to both normal sleep before OSA and recovery sleep after OSA. Studies were performed in four dogs in which sleep-wake state was monitored continuously by a computer that received telemetered EEG and EMG signals. Whenever sleep was detected, the computer sent a signal to close a valve through which the dog breathed; when the dog awoke the occlusion was released. In each dog, data were analyzed from 4 consecutive nights in three phases: a control phase before induction of OSA, a phase during long-term OSA (mean = 85 days, apnea index = 59/hour), and a recovery phase after cessation of OSA. During recovery there was a significant increase in the amount of rapid-eye-movement (REM) sleep compared to the OSA phase (p0.01), as well as significant increases in sleep efficiency and decreases in wakefulness (p0.01), similar to that reported in OSA patients. The REM rebound during recovery, however, could not be attributed to overall REM deprivation since the amount of REM sleep during the OSA phase was not different from the control phase (p = 0.708). This finding suggests that REM rebound during recovery from OSA is not the result of an overall REM sleep deficit per se. Rather, repeated sleep disruption due to the effects of repetitive apneas and hypoxia may lead to an increased REM sleep drive that manifests itself as a REM sleep rebound during recovery sleep after OSA.

Obstructive sleep apnea (OSA) causes recurrent sleep disruption that is thought to contribute to excessive daytime sleepiness in patients with this disorder. The purpose of this study was to determine the specific effects of OSA on overall sleep architecture in a canine model of OSA. The advantage of this model is that sleep during long-term OSA can be compared to both normal sleep before OSA and recovery sleep after OSA. Studies were performed in four dogs in which sleep-wake state was monitored continuously by a computer that received telemetered EEG and EMG signals. Whenever sleep was detected, the computer sent a signal to close a valve through which the dog breathed; when the dog awoke the occlusion was released. In each dog, data were analyzed from 4 consecutive nights in three phases: a control phase before induction of OSA, a phase during long-term OSA (mean = 85 days, apnea index = 59/hour), and a recovery phase after cessation of OSA. During recovery there was a significant increase in the amount of rapid-eye-movement (REM) sleep compared to the OSA phase (p < 0.01), as well as significant increases in sleep efficiency and decreases in wakefulness (p < 0.01), similar to that reported in OSA patients. The REM rebound during recovery, however, could not be attributed to overall REM deprivation since the amount of REM sleep during the OSA phase was not different from the control phase (p = 0.708). This finding suggests that REM rebound during recovery from OSA is not the result of an overall REM sleep deficit per se. Rather, repeated sleep disruption due to the effects of repetitive apneas and hypoxia may lead to an increased REM sleep drive that manifests itself as a REM sleep rebound during recovery sleep after OSA.

Publisher Summary This chapter discusses the Fourier-plane nonlinear techniques used for pattern recognition. The chapter describes that nonlinear transformation of the joint power spectrum results in good correlation performance in terms of correlation peak size, peak to output noise ratio, and sensitivity against similar objects. The binary joint transform correlators (JTC) works well than the sliding-window local-median threshold method and can provide input-image illumination invariance. Computer simulations and experimental results show that for varying illumination, the variable threshold function and the sliding-window local-median thresholding perform well by providing large correlation peak intensity, and large peak to noise ratio. The chapter illustrates the use of nonlinear techniques in the design of composite filters that enable these filter designs to be used in a nonlinear joint transform correlator. The chirp-encoded technique reduces the redundant and self-correlation terms of the JTC. The other technique uses random phase encoding. The chapter also discusses security validation and security verification.

Currently, the invasive scalp electrode has proved to be a reliable technique for monitoring fetal status via heart rate (HR) during delivery. However, the scalp electrode has various limitations. These limitations include an inability to obtain fetal electrophysiological information and little flexibility for placing a biosensor on the scalp electrode to monitor maternal contractions from the electromyogram (EMG). A fetal electrocardiogram (FECG) obtained via an intrauterine catheter electrode during delivery has potential to convey fetal HR and electrophysiological information. Furthermore, the intrauterine catheter can be modified to contain a pressure sensor to monitor maternal contractions. The modified catheter would enable fetal HR and electrophysiological information along with contractions to be monitored with one biosensor. Finally, this paper presents clinical data from the intrauterine catheter to determine the feasibility of obtaining a FECG from this approach. The clinical data obtained from the five patients studied indicates that after maternal electrocardiogram (EGG) cancellation, a FECG with a good signal-to-noise ratio can be obtained in an ECG diagnostic bandwidth of 0.05 to 100 Hz. From the diagnostic bandwidth, fetal HR and electrophysiological information can be determined.

Objective: To examine the therapeutic effect of a treatment package on the motor function of persons with Parkinson’s disease (PD). Design: Randomized crossover study. Setting: Urban medical center. Participants: 50 persons with PD. Interventions: Reciprocal mechanical ranging and therapeutic exercise during weekly visits for 6 weeks (group 1), or 6 weeks of daily reciprocal mechanical ranging supplemented by therapeutic exercise once weekly (group 2). The groups were crossed over after 6 weeks. Main Outcome Measures: United Parkinson’s Disease Rating Scale (UPDRS), Functional Ambulation Profile, balance, and motor planning. Results: Weekly ranging proved as effective as daily ranging. Compared with baseline performance, both groups improved on all 8 computerized motor tests. Center of pressure tracking tests (performed while standing) yielded lower error scores (better performance) than head tracking (performed while seated). Poorest tracking performance occurred when stimulus-response relations were incompatible. When head tracking was performed under compatible conditions, difficulty was encountered only when continuous video feedback was withheld. These results reflect difficulties with motor planning that some of the sitting tasks require. Both groups yeilded statistically significant improvement relative to baseline performance. Steadiness, whether head or standing, statistically improved over baseline. There was a 4° increase in the active range of knee extension. Of a possible 100, functional ambulation performance increased from a mean of 79.5 at baseline to 85.5, 85.7, and 86.3 at the first, final, and follow-up evaluations, respectively. Statistically significant improvements from baseline were yielded by section III items (motor evaluation subscale) of the UPDRS, indicating test sensitivity and selectivity. Conclusions: The study confirmed that persons with PD recover functionality from mechanical ranging and exercise. Whether mechanical ranging was done daily or weekly, subjects showed statistically significant improvement compared with baseline performance on all computerized motor tests.

In this paper several systematic and random filter plane errors are related through a single parameter that describes the amount of phase mismatch. A model of peak-to-noise ratio (PNR) is also presented that describes the combined effects of random and systematic errors. This expression contains the products of two functions, one that depends only on systematic, the other on random, phase mismatch. PNR is also a function of the number of pixels in the filter plane modulator and a normalized moment the amplitude of the image spectrum. The model is useful for developing phase error budgets for correlation systems.

This report describes a canine model of obstructive sleep apnea (OSA) developed in our laboratory and the results of its preliminary short-term application. Healthy adult dogs were prepared with a tracheostomy and with implanted electroencephalographic and nuchal electromyographic recording electrodes. A silent occlusion valve was attached to the outer end of the endotracheal tube. The electroencephalogram and electromyogram were monitored continuously by a computer that determined sleep-wake state using software developed in our laboratory. At a predetermined time (e.g., 12 s) after each sleep onset, a signal was transmitted from the computer to the valve controller, resulting in airway occlusion. When the dog aroused from sleep, the occlusion was released. These events therefore mimic those that occur in human OSA. Successful operation of the model was confirmed during 5-day continuous trials in two dogs. During the trials, the dogs became increasingly somnolent both by behavioral observation and objective measurement. The frequency of occlusions increased, and measures of apnea severity, including apnea duration and end-apneic arterial oxygen saturation, worsened. We conclude that this experimental model of repeated airway occlusion during sleep provides a potentially powerful tool for investigating the sequelae of OSA.

We propose an idea for security verification of credit cards, passports, and other ID so that they cannot easily be reproduced. A new scheme of complex phase/amplitude patterns that cannot be seen and cannot be copied by an intensity sensitive detector such as a CCD camera is used. The basic idea is to permanently and irretrievably bond a phase mask to a primary identification amplitude pattern such as a fingerprint, a picture of a face, or a signature. Computer simulation results and tests of the proposed system will be provided to verify that both the phase mask and the primary pattern are separately readable and identifiable in an optical processor or correlator.© (1994) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

Phase-modulating devices, especially spatial light modulators, are often incapable of producing a full 360 degrees of phase modulation. Other limitations due to calibration errors, signal distortion, and quantization can cause the actual phase modulation to differ from the desired modulation. Such limitations on the filter plane modulator can reduce the performance of phase-only correlators. We quantify these performance losses for various phase limitations, both through simulation and through the development of an approximate model of performance. In one case we quantitatively compare the performance of phase-only filters that are optimized for limited-range phase modulation (as prescribed by Juday's `minimum Euclidean distance' principle) with the performance of nonoptimal filters. In another case we analyze the effect of not compensating a quadratic dependence of phase on signal voltage which is anticipated for some spatial modulators, e.g. deformable mirror devices.© (1994) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

1. The present study was designed to determine the effect of sleep on the tonic output to respiratory muscle and on the level of chemical respiratory stimulation required to produce rhythmic respiratory output. 2. Chronically implanted electrodes recorded expiratory (triangularis sterni) and inspiratory (diaphragm and parasternal intercostal) electromyographic (EMG) activities in three trained dogs during wakefulness and sleep. The dogs were mechanically hyperventilated via an endotracheal tube inserted into a permanent tracheostomy. During the studies, a cold block of the cervical vagus nerves was maintained to avoid the complicating effects of vagal inputs on respiratory drive and rhythm. 3. During wakefulness, steady-state hypocapnia (partial pressure of CO2, PCO2 = 30 mmHg) abolished inspiratory EMG activity, resulting in apnoea, but the expiratory muscle became tonically active. Compared to wakefulness, the level of the tonic expiratory EMG activity was decreased in non-REM (non-rapid eye movement) sleep (median decrease = 34%, P = 0.005) and was further decreased in REM sleep (median decrease = 78%, P < 0.0001). During REM sleep, the tonic expiratory EMG activity was highly variable (mean coefficient of variation = 39% compared to 7% awake, P < 0.0001) and in some periods of REM, bursts of inspiratory EMG activity and active breathing movements were observed despite the presence of hypocapnia. 4. During constant mechanical hyperventilation, progressive increases in arterial PCO2 (in hyperoxia) were produced by rebreathing. Measurement of the CO2 threshold for the onset of spontaneous breathing showed that this threshold was not different between wakefulness and non-REM sleep (mean difference = 0.1 mmHg from paired observations, 95% confidence interval for the difference = -1.0 to +1.1 mmHg, P = 0.898). 5. The results show that sleep reduces the tonic output to respiratory muscles but does not increase the CO2 threshold for the generation of rhythmic respiratory output. These observations suggest that changes in the tonic drives to the respiratory motoneurones may be a principal mechanism by which changes in sleep-wake states produce changes in respiratory output.

The correlation performance of binary joint transform correlators with unknown input light illumination is investigated for different thresholding methods. It is shown that a binary joint transform correlator that uses a spatial frequency dependent threshold function for binarization of the joint power spectrum is illumination invariant. The performance of the binary joint transform correlator with unknown input light illumination using a variety of thresholding methods is investigated.© (1993) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

A 4-f lens system is positioned over one half of the joint input image presentation SLM device of a conventional joint transform correlator (JTC). An image displacement lens is positioned in the Fourier transform plane of the 4-f correlator and can shift the virtual displacement of the reference image plane relative to the input image plane. By the appropriate choice of this lens, any virtual displacement can be achieved to provide for substantial design flexibility of the JTC.

In the output plane of the optical joint transform correlator, the correlation peaks are often difficult to detect and to accurately distinguish from noise spikes.

We present an optoelectronic pattern recognition system that can perform image detection in the presence of unknown input scene illumination. The binary joint transform correlator with unknown light illumination is investigated for different thresholding methods. >

We describe an optical fingerprint identification system that optically reads a latent fingerprint for correlation using a binary joint transform correlator. The fingerprint is read using the total internal reflection property of a prism. The system was built and tested, and the experimental results are presented.

The chapter links National and State agricultural policy models with a regional agricultural production and ground-water hydrology model to track the effects of environmental and commodity policies. Results indicate that a policy which would eliminate subsurface drainage disposal would not significantly effect the amount of agricultural production within the 10-year time horizon assumed in the analysis. A 20-percent decrease in the demand for cotton is projected to decrease total irrigated acreage by 20 percent but subsurface drainage water is projected to double. This phenomenon is explained by decreased unconfined ground-water pumping which serves to reduce perched ground-water tables. The two policy scenarios illustrate the importance of unconfined ground-water pumping and the spatial allocation of surface water supplies in reducing the production of subsurface drainage, if disposal is restricted.

A 1 lens focal length binary joint transform correlator is described. This correlator uses a iuagneto-optic spatial light inodu lator, lens, and standard 8bit resolution CCD camera. Computer simulations and experimental results of the effects of changes in scale, in-plane rotation, and multiple targets are discussed.

The inactive areas of certain pixellated SLMs are transmissive rather than opaque, while their active areas modulate the optical phase or amplitude. Computer simulations of optical correlators are made for a continuous-input SLM and a filter SLM implementing either a classical matched, phase-only, or binary phase-only filter. The correlation peak and signal-to-noise ratio are studied as a function of dead-zone area in both the input and filter SLMs. These results are compared with those obtained from correlators whose SLMs have only opaque dead zones.