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26.  ABC of sleep disorders. Function of sleep. 
BMJ : British Medical Journal  1993;306(6874):383-385.
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PMCID: PMC1676416  PMID: 8461688
27.  Is nocturnal asthma caused by changes in airway cholinergic activity? 
Thorax  1988;43(9):720-724.
A randomised, double blind, placebo controlled crossover trial of high dose nebulised ipratropium was carried out in 10 asthmatic patients with documented nocturnal bronchoconstriction. Patients received nebulised saline or ipratropium 1 mg at 10 pm and 2 am on two nights. Absolute peak flow (PEF) rates were higher throughout the night after the patients had received ipratropium (at 2 am, for example, mean (SEM) PEF was 353 after ipratropium and 285 l/min after placebo). The fall in PEF overnight, however, was similar with ipratropium and placebo. Patients were given a further 1 mg nebulised ipratropium at 6 am on both nights. There was a significant overnight fall in PEF on the ipratropium night even when comparisons were made between the times that maximal cholinergic blockade would be expected, PEF falling between 11.30 pm and 7.30 am from 429 to 369 l/min. The percentage increase in PEF, though not the absolute values, was greater after ipratropium at 6 am than at 10 pm. These results confirm that ipratropium raises PEF throughout the night in asthmatic patients, but suggest that nocturnal bronchoconstriction is not due solely to an increase in airway cholinergic activity at night.
PMCID: PMC461462  PMID: 2973665
28.  Twenty four hour heart rate variability: effects of posture, sleep, and time of day in healthy controls and comparison with bedside tests of autonomic function in diabetic patients. 
British Heart Journal  1991;65(5):239-244.
Heart rate variability was measured in 77 healthy controls and 343 diabetic patients by a count of the number of beat-to-beat differences greater than 50 ms in the RR interval during a 24 hour ambulatory electrocardiogram. In the healthy controls the lower 95% tolerance limits for total 24 hour RR interval counts were approximately 2000 at age 25, 1000 at 45, and 500 at 65 years. Six controls confined to bed after injury had normal 24 hour patterns of RR counts, while eight other controls showed loss of diurnal variation in both heart rate and RR counts during a period of sleep deprivation. RR counts in ten controls on and off night duty increased during sleep whenever it occurred. Nearly half (146) the 343 diabetic patients had abnormal 24 hour RR counts. The percentage of abnormal RR counts increased with increasing autonomic abnormality assessed by a standard battery of tests of cardiovascular autonomic function. A quarter of those with normal cardiovascular reflex tests had abnormal 24 hour RR counts. There were close correlations between 24 hour RR count results and the individual heart rate tests (r = 0.6). The assessment of cardiac parasympathetic activity by 24 hour RR counts was reliable. The diurnal variations in RR counts seen in the controls were probably related to sleep rather than either posture or time of day. The method was more sensitive than conventional tests of cardiovascular reflexes.
PMCID: PMC1024623  PMID: 2039667
30.  Breathing patterns during sleep in patients with nocturnal asthma. 
Thorax  1987;42(8):600-603.
Breathing patterns early and late in the night, at the same sleep stage, were compared in six healthy subjects and 15 adults with nocturnal asthma, to try to identify changes of overnight bronchoconstriction, and breathing patterns at different sleep stages, to see whether there were changes related to sleep stages that were indicative of bronchoconstriction. Despite an average 31% fall in FEV1 overnight in the patients with asthma, neither breathing frequency nor expiratory time, which might be expected to change during bronchoconstriction, was different early in the night from late in the night, nor did they differ between sleep stages. There was no evidence of asynchronous movement of the chest and abdomen in any patient. This study did not identify any abnormality of breathing pattern that would indicate the development of nocturnal asthma without the need to awaken the patient.
PMCID: PMC460860  PMID: 3509951
32.  Ketotifen and nocturnal asthma. 
Thorax  1983;38(11):845-848.
Patients with asthma often wheeze at night and they also become hypoxic during sleep. To determine whether ketotifen, a drug with sedative properties, is safe for use at night in patients with asthma, we performed a double blind crossover study comparing the effects of a single 1 mg dose of ketotifen and of placebo on arterial oxygen saturation (SaO2), breathing patterns, electroencephalographic (EEG) sleep stage, and overnight change in FEV1 in 10 patients with stable asthma. After taking ketotifen, the patients slept longer and their sleep was less disturbed than after taking placebo, true sleep occupying 387 (SEM 8) minutes after ketotifen and 336 (19) minutes after placebo (p less than 0.02). On ketotifen nights the patients had less wakefulness and drowsiness (EEG sleep stages 0 and 1) and more non-rapid eye movement (non-REM) sleep than on placebo nights, but the duration of REM sleep was similar on the two occasions. Nocturnal changes in SaO2, the duration of irregular breathing, and overnight change in FEV1 were unaffected by ketotifen.
PMCID: PMC459674  PMID: 6359563
33.  Effect of sleep deprivation on overnight bronchoconstriction in nocturnal asthma. 
Thorax  1986;41(9):676-680.
Nocturnal cough and wheeze are common in asthma. The cause of nocturnal asthma is unknown and there is conflicting evidence on whether sleep is a factor. Twelve adult asthmatic subjects with nocturnal wheeze were studied on two occasions: on one night subjects were allowed to sleep and on the other they were kept awake all night, wakefulness being confirmed by electroencephalogram. Every patient developed bronchoconstriction overnight both on the asleep night, when peak expiratory flow (PEF) fell from a mean (SE) of 418 (40) 1 min-1 at 10 pm to 270 (46) 1 min-1 in the morning, and on the awake night (PEF 10 pm 465 (43), morning 371 (43) 1 min-1). The morning values of PEF were, however, higher (p less than 0.1) after the awake night and both the absolute and the percentage overnight falls in PEF were greater when the patients slept (asleep night 38% (6%), awake night 20% (4%); p less than 0.01). This study suggests that sleep is an important factor in determining overnight bronchoconstriction in patients with nocturnal asthma.
PMCID: PMC460429  PMID: 3787554
34.  Do asthmatics suffer bronchoconstriction during rapid eye movement sleep? 
Many patients with asthma are troubled by nocturnal wheeze. The cause of this symptom is unknown, but sleep is an important factor. A study was carried out to determine whether nocturnal bronchoconstriction is related to any specific stage of sleep. Eight asthmatics with nocturnal wheeze and eight control subjects performed forced expiratory manoeuvres immediately after being woken from rapid eye movement (REM) or non-REM sleep, wakings being timed to differentiate temporal effects from those related to the stage of sleep. The control subjects showed no significant temporal bronchoconstriction or bronchoconstriction related to the stage of sleep. All patients showed bronchoconstriction overnight, the mean peak expiratory flow rate falling from 410 (SEM 50) 1/min before sleep to 186 (49)1/min after sleep. After the patients had been woken from REM sleep the forced expiratory volume in one second was on average 300 ml lower (p less than 0.02) and peak expiratory flow rate 45 1/min lower (p less than 0.03) than after they had been woken from non-REM sleep. As wakenings from REM sleep were 21(8) minutes later in the night than those from non-REM sleep multivariate analysis was performed to differentiate temporal effects from those related to the stage of sleep. This showed that the overnight decreases in forced expiratory volume in one second and peak expiratory flow rate were significantly related both to time and to REM sleep. This study suggests that asthmatics may suffer bronchoconstriction during REM sleep.
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PMCID: PMC1340176  PMID: 3085766
35.  Sodium cromoglycate in nocturnal asthma. 
Thorax  1986;41(1):39-41.
To investigate whether mast cell degranulation was important in producing nocturnal asthma, the effect of a single high dose of nebulised sodium cromoglycate on overnight bronchoconstriction, oxygen saturation, and breathing patterns in eight patients with nocturnal wheeze was examined. The study took the form of a double blind placebo controlled crossover comparison. Treatment with cromoglycate did not reduce the overnight fall in FEV1 or FVC, although it was associated with improved nocturnal oxygenation. This study suggests that mast cell degranulation may not be important in the pathogenesis of nocturnal asthma.
PMCID: PMC460250  PMID: 3085257
37.  Physiological changes and sleep responses during and following a world record continuous walking record. 
Physiological changes, and subsequent sleep responses, were recorded in a male subject during and following 338 miles of continuous walking and consequent sleep deprivation. One hundred and thirty hours of walking and a seventy-two hours post-walk recovery period were monitored. The subject walked at approximately 55% of maximum oxygen uptake (VO2 max), heart rate ranged between 102-106 b/min, and blood lactate (LA) remained below the 2 mmol/l level. No electrocardiograph abnormalities were observed either during the walk or pre- and post-functional diagnostic graded exercise test (FDGXT). Creatine kinase (CK) and creatine kinase isoenzyme (CK-MB) levels rose throughout the walk but exhibited differing depletion patterns. The ratio of CK-MB to CK (MB/CK%) did not exceed levels which are suggestive of myocardial ischaemia. Haematological variables demonstrated signs of anaemia towards the end of the walk. Catecholamine levels rose throughout the walk, with greater rises being observed in nor-adrenaline and dopamine. During the post-walk recovery phase, adrenaline concentration remained elevated. Following this extreme period of exertion, the subject demonstrated very short sleep latency and rapid entry into slow wave sleep (SWS). These sleep patterns were compared to sleep recordings made over a similar period (72 h) six months post-walk, when the subject was not exercising. Nocturnal growth hormone (GH) levels were significantly raised on the post-walk nights.
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PMCID: PMC1859379  PMID: 6487943
38.  Arterial oxygenation during sleep in patients with right-to-left cardiac or intrapulmonary shunts. 
Thorax  1983;38(5):344-348.
We have studied arterial oxygen saturation (SaO2), breathing patterns, and electroencephalographic (EEG) sleep stage during nocturnal sleep in six patients with right-to-left cardiac or intrapulmonary shunts and six patients with chronic bronchitis and emphysema, chosen because they were equally hypoxaemic when awake (SaO2 during wakefulness: bronchitis 74-90%, mean 83%; shunt 77-89%, mean 83%). The patients with bronchitis had far greater falls in SaO2 when asleep than those with shunts (maximum fall in SaO2 during sleep: bronchitis 14-47%, mean 29%; shunt 5-10%, mean 8%; p less than 0.01). Significant episodes of hypoxaemia (defined as SaO2 falls greater than 10%) occurred in all six bronchitic patients, from once to seven times per night, but in none of the patients with shunts (p less than 0.05). Twenty-four of the 27 episodes of hypoxaemia occurred in rapid-eye-movement (REM) sleep and 24 were associated with hypopnoea. The two groups of patients had similar EEG sleep patterns and the same amount of hypopnoea during sleep. Thus the level of arterial oxygenation when the patient is awake is not the sole determinant of the degree of nocturnal hypoxaemia; the pathological process is also important.
PMCID: PMC459555  PMID: 6879482
40.  The aromatic amino acid pathway branches at L-arogenate in Euglena gracilis. 
Molecular and Cellular Biology  1981;1(5):426-438.
The recently characterized amino acid L-arogenate (Zamir et al., J. Am. Chem. Soc. 102:4499-4504, 1980) may be a precursor of either L-phenylalanine or L-tyrosine in nature. Euglena gracilis is the first example of an organism that uses L-arogenate as the sole precursor of both L-tyrosine and L-phenylalanine, thereby creating a pathway in which L-arogenate rather than prephenate becomes the metabolic branch point. E. gracilis ATCC 12796 was cultured in the light under myxotrophic conditions and harvested in late exponential phase before extract preparation for enzymological assays. Arogenate dehydrogenase was dependent upon nicotinamide adenine dinucleotide phosphate for activity. L-Tyrosine inhibited activity effectively with kinetics that were competitive with respect to L-arogenate and noncompetitive with respect to nicotinamide adenine dinucleotide phosphate. The possible inhibition of arogenate dehydratase by L-phenylalanine has not yet been determined. Beyond the latter uncertainty, the overall regulation of aromatic biosynthesis was studied through the characterization of 3-deoxy-D-arabino-heptulosonate 7-phosphate synthase and chorismate mutase. 3-Deoxy-D-arabino-heptulosonate 7-phosphate synthase was subject to noncompetitive inhibition by L-tyrosine with respect to either of the two substrates. Chorismate mutase was feedback inhibited with equal effectiveness by either L-tyrosine or L-phenylalanine. L-Tryptophan activated activity of chorismate mutase, a pH-dependent effect in which increased activation was dramatic above pH 7.8 L-Arogenate did not affect activity of 3-deoxy-D-arabino-heptulosonate 7-phosphate synthase or of chorismate mutase. Four species of prephenate aminotransferase activity were separated after ion-exchange chromatography. One aminotransferase exhibited a narrow range of substrate specificity, recognizing only the combination of L-glutamate with prephenate, phenylpyruvate, or 4-hydroxyphenylpyruvate. Possible natural relationships between Euglena spp. and fungi previously considered in the literature are discussed in terms of data currently available to define enzymological variation in the shikimate pathway.
PMCID: PMC369338  PMID: 6152855
41.  Sleep and the athlete. 
Sleep is generally considered to be restorative and the notion of exercise being associated with the changes in subsequent sleep is popular but has only recently been demonstrated. There are several facets of exercise performed that have an influence on sleep. These include the intensity and duration of the exercise, and the interval between the cessation of exercise and sleep onset. Other factors that may alter sleep after exercise are the age and fitness of the subject, and his lean body mass. Most studies on the effect of exercise on sleep can be interpreted as being partially or totally supportive of the restorative theory of sleep function.
PMCID: PMC1859073  PMID: 7248684

Results 26-41 (41)