Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whereas primates restrained in a chair may usually be considered 'normal', the behaviour of baboons in this position was considerably altered: their eyes were closed and they only slightly reacted to the approach of the experimenter (opening of the eyes), in contrast with their active behaviour when left free to move about in their cage. When the ECoG was recorded from certain cortical areas (particularly somatic area I), an unusual pattern developed during the restrained state: 'drowsiness rhythms', which typically appear in this area during transition from wakefulness to sleep, developed in long sustained sequences. Administration of diazepam, an anxiolytic drug, caused both the behaviour and the ECoG of the restrained animal to return to normal (i.e., attentive behaviour and ECoG characteristic of the true waking state). The prolonged drowsy-like ECoG and behaviour may therefore underline a reaction to the 'stress' conditions brought on by restraint.
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PMID:Restraint in primate chair may cause unusual behaviour in baboons; electrocorticographic correlates and corrective effects of diazepam. 7 62

Emotional stress was developed in cats by putting them in one cage with dogs for 24 hours. Then the 24 hours sleep-walking cycles records revealed prolonged REM stage in day time or at night in five animals out of seven, and in six animals a general increase of REM sleep duration over 24 hours. Simultaneously, in six animals the length of drowsiness and of deep slow-wave sleep stages was reduced. Increased overall sleep duration in the 24 hours was recorded in five cats. Sleep changes dynamics analysis reveals three stages: 1) sharp shift of all sleep parameters--27%, 2) deviation in sleep parameters--34% and 3) returning to basic sleep parameters--in 38%. The conclusion is drawn that sleep disorders may be used as an index of higher nervous activity disturbance in waking state.
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PMID:[Effect of emotional stress on sleep dynamics in cats]. 22 15

An obese patient with a ten year history of respiratory failure presented with insomnia and marked daytime somnolence. Respriatory failure had been attributed to obesity, respiratory centre insensitivity to carbon dioxide, and to diffuse airways obstruction. To investigate the possible role of episodic apnoea with frequent nocturnal arousals, continous recordings were obtained during sleep of arterial oxygen saturation, oesophageal pressure and the motions of the rib-cage and abdomen/diaphragm. Repeated episodes of hypoventilation and profound hypoxaemia were found which were due to intermittent obstruction of the upper airway rather than to cessation of breathing efforts. During the episodes of hypoxaemia, values of arterial O2 tension fell to as low as 24 mmHg. Episodic hypoxaemia was relieved but not abolished, by the use of a collar, designed to hold the mandible forward. Previous reports indicated that recognition of intermittent obstruction of the upper airway during sleep and treatment by a permanent tracheostomy, resulted in a significant long-term imporvement of pulmonary and cardiac function and relief of insomnia and day-time somnolence. When tracheostomy is inadvisable, as in the present patient, it is hoped that similar long-term benefits will result from a supportive collar.
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PMID:Intemittent obstruction of the upper airway during sleep causing profound hypoxaemia. A neglected mechanism exacerbating chronic respiratory failure. 107 82

We describe a 40 year-old male with a ball-cage mitral valve prosthesis who suddenly developed bilateral ptosis, bilateral dilated and unreactive pupils, right third nerve palsy, bilateral failure of vertical gaze, somnolence and mild ataxia without major motor deficits. Computed Tomography (CT) revealed bilateral thalamic infarcts in the distribution of the rostral basilar artery. Infarction in this case occurred despite adequate anticoagulation. The recognition of the entity of rostral basilar artery occlusion is important as interruption of anticoagulation may be avoided.
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PMID:Nuclear third nerve palsy and somnolence due to stroke--a case report. 239 42

Locomotion, holeboard exploration and grooming behavior were measured in male rats after injection of LHRH or cerebrospinal fluid (CSF) into the mesencephalic periaqueductal gray substance (PGS). LHRH injection at doses of 75 ng did not alter locomotion and rearing but decreased significantly the scores of head dipping and defecation. Several subcategories of grooming responses were evaluated in a home cage-like environment. Head, body and genital grooming increased significantly after injection of 75 ng LHRH. The frequency of gnawing and head shakes increased as well. Lower doses (50 ng) also raised the scores of head and body grooming and produced a tendency for genital grooming increase. Higher doses (100 ng) did not affect genital grooming responses and produced drowsiness in most of animals. These results demonstrate that some motor activities are selectively modified by the localized administration of LHRH in the PGS.
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PMID:Luteinizing hormone releasing hormone (LHRH) in the periaqueductal gray substance increases some subcategories of grooming behavior in male rats. 267 63

The English bulldog is a natural model of sleep-disordered breathing (SDB). This condition is marked by 1) hypersomnolence and 2) disordered breathing episodes that are most frequent and severe during rapid eye movement (REM) sleep. Modafinil has been found to increase arousal levels in animals and decrease excessive daytime sleepiness in humans. Therefore, in this study we focused mainly on the effects of the drug on total sleep time and sleep latency and secondarily assessed its effect on REM SDB. Five English bulldogs were implanted with subcutaneous electroencephalographic/electrooculographic (EEG/EOG) electrodes and instrumented with respiratory oscillation belts to measure abdominal and rib cage movements and an ear oximeter to measure saturation. The dogs were studied for approximately 8 hours each subsequent day on two consecutive days. On the first day, they received the vehicle dimethyl sulfoxide (DMSO) i.v. as a control. On the following day they received 10 mg/kg body weight of modafinil i.v. dissolved in the DMSO vehicle. Our findings indicate that modafinil significantly alleviates hypersomnolence (p < 0.05) in the bulldog, as evidenced by dramatically decreased mean total sleep time (from a control value of 50.5% to 8.3% with the drug) and increased mean sleep latency (from a control value of 71.0 minutes to a value of 346.6 minutes with the drug). We obtained limited data on the effect of modafinil on SDB because the drug either greatly diminished or entirely eradicated REM sleep in all five dogs.
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PMID:Modafinil decreases hypersomnolence in the English bulldog, a natural animal model of sleep-disordered breathing. 895 32

Respiratory muscle weakness may be the sole cause of dyspnea or may aggravate dyspnea due to another respiratory disease, and is often difficult to recognise clinically. The assessment of respiratory muscles should follow a graded approach using tests of increasing complexity. Clinical examination should look for dyspnea, orthopnea, morning headache, daytime somnolence, fatigability, tachypnea, abdominal, or rib cage paradox, and amyotrophy. Imaging is useful in diagnosing diaphragmatic paralysis using chest radiograph, fluoroscopy or ultrasound. In cases of moderate to severe respiratory muscle weakness, lung volumes show reduced vital capacity and total lung capacity. Measuring the change in vital capacity from sitting to supine position is useful since it shows a 25-50% fall in cases of diaphragmatic paralysis. The specific and classical tests of respiratory muscle strength are maximum inspiratory and expiratory pressures (MIP and MEP) sustained during one second against near complete occlusion. Sniff nasal inspiratory pressure (SNIP) is a new and easier test of inspiratory muscle strength. Normal values obtained with these simple tests rule out clinically significant respiratory muscle weakness. In case of doubt, more complex and invasive tests can be used such as transdiaphragmatic pressure and magnetic stimulation of the phrenic nerves.
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PMID:[Evaluation of respiratory muscles]. 975 85

To compare a novel controlled-release formulation of metoclopramide with placebo in patients with cancer-associated dyspepsia syndrome, 26 adult patients with a >/=1 month history of cancer-associated dyspepsia syndrome were randomized to receive either controlled-release metoclopramide 40 mg every 12 hours or matching placebo for a period of 4 days. On day 5, patients crossed over to the alternate treatment for a further period of 4 days. Dose adjustments and rescue antiemetics were permitted during both phases. Nausea, anorexia, bloating, vomiting/retching, and drowsiness were assessed on a 100-mm VAS scale in a daily diary. On the last day of treatment of each phase, nausea was significantly lower in the controlled-release metoclopramide group compared to placebo (17 +/- 12 mm versus 12 +/- 10 mm). Nausea scores tended to increase across days during the placebo phase and to decrease during the controlled-release metoclopramide phase. There was a trend for improvement in the intensity of all symptoms on controlled-release metoclopramide with the exception of appetite, but this trend only reached statistical significance for nausea. The frequency and severity of elicited adverse events did not differ significantly between treatments, although drowsiness, dizziness, and poor sleep were somewhat higher in the placebo group. In no case was it necessary to discontinue controlled-release metoclopramide because of toxicity. These results indicate that controlled-release metoclopramide reduces gastrointestinal symptoms in this population of advanced cancer patients.
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PMID:A double-blind, crossover study of controlled-release metoclopramide and placebo for the chronic nausea and dyspepsia of advanced cancer. 1090 23

Narcolepsy is caused by a lack of orexin (hypocretin), but the physiologic process that underlies the sleepiness of narcolepsy is unknown. Using orexin knock-out (KO) mice as a model of narcolepsy, we critically tested the three leading hypotheses: poor circadian control of sleep and wakefulness, inadequate activation of arousal regions, or abnormal sleep homeostasis. Compared with wild-type (WT) littermates, orexin KO mice had essentially normal amounts of sleep and wake, but wake and non-rapid eye movement (NREM) bouts were very brief, with many more transitions between all behavioral states. In constant darkness, orexin KO mice had normal amplitude and timing of sleep-wake rhythms, providing no evidence for disordered circadian control. When placed in a new, clean cage, both groups of mice remained awake for approximately 45 min, demonstrating that, even in the absence of orexin, fundamental arousal regions can be engaged to produce sustained wakefulness. After depriving mice of sleep for 2-8 hr, orexin KO mice recovered their NREM and rapid eye movement sleep deficits at comparable rates and to the same extent as WT mice, with similar increases in EEG delta power, suggesting that their homeostatic control of sleep is normal. These experiments demonstrate that the fragmented wakefulness of orexin deficiency is not a consequence of abnormal sleep homeostasis, poor circadian control, or defective fundamental arousal systems. Instead, the fragmented behavior of orexin KO mice may be best described as behavioral state instability, with apparently low thresholds to transition between states.
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PMID:Behavioral state instability in orexin knock-out mice. 1525 84

Many of the neuromuscular and thoracic cage disorders are associated with disorders of breathing during sleep. The abnormal mechanics of the chest wall impairs respiratory muscle function and this is compounded if there is underlying muscle weakness. Respiratory abnormalities appear during REM sleep before NREM or wakefulness. Central sleep apnoeas are characteristic, but obstructive apnoeas are also occur because of loss of tone in the upper airway dilator muscles. Arousals from sleep return the blood gases towards normal, but cause fragmentation of sleep, leading to daytime sleepiness. Ventilatory failure occurs particularly if the vital capacity is less than 1.0-1.5 litres or if the maximal inspiratory mouth pressure is less than 20-25cmH2O. Non invasive ventilation effectively prevents both central and obstructive apnoeas and improves the sleep architecture and daytime blood gases.
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PMID:Respiration during sleep in neuromuscular and thoracic cage disorders. 1536 36


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