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Biomedical subjects

A Buguet

Publications and source records attributed to A Buguet.

At least 55 records · Page 3Linked to original sources
PubMed1995

Strenuous exercise and immunological changes: a multiple-time-point analysis of leukocyte subsets, CD4/CD8 ratio, immunoglobulin production and NK cell response.

This study was designed to examine the impact of exhaustive endurance exercise on a number of immune parameters of physically fit male subjects (VO2max 66.5 +/- 5.3 ml/min/kg) who performed treadmill exercise at 65% of their VO2max for 120 min. Serial blood samples were taken before, during and after exercise and changes in leukocyte and lymphocyte subset concentrations; immunoglobulin production in vitro; and natural killer (NK) cell response were measured. The exercise regimen was found to induce the well-known phenomenon of leukocytosis which consisted primarily of a granulocytosis and lymphocytosis. Among the lymphocyte subsets, peripheral pan T cells (CD3+) as well as helper (CD4+) and suppressor (CD8+) T cells were found to be elevated. A relatively smaller increase in CD4+ than CD8+ cells resulted in depressed CD4/CD8 ratios throughout the exercise period. After exercise, T cells declined progressively and, 2 h post-exercise, were less than 60% of their pre-exercise level. In contrast, the CD4/CD8 ratio demonstrated a progressive increase, thus representing a reversal in the pattern observed during exercise and a trend towards an elevated ratio during recovery. B cells (CD19+) were relatively unaffected by exercise, although IgM production by pokeweed mitogen-stimulated lymphocytes obtained from blood samples after 120 min of exercise was significantly depressed. NK cells were affected dramatically by exercise. Both CD16+ cell numbers and NK cytotoxicity were increased during exercise, followed by a persistent depression in the post-exercise period. The strenuous exercise induced profound effect on NK cells as evidenced by a 40% depression of the NK cell count for as long as 7 days after the cessation of exercise. Our results provide direct kinetic evidence demonstrating that exhaustive exertion alters both lymphocyte distribution pattern and effector function, suggestive of possible exercise-induced immune compromise, particularly in the post-exercise recovery period.

Adult↗
PubMed1995

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. I. Effects on mood, fatigue, cognitive performance and body temperature.

Modafinil is an alerting substance that is considered safer than amphetamine with fewer side effects. Although modafinil has been used successfully to treat narcolepsy, relatively little is known about its ability to ameliorate fatigue and declines in mental performance due to sleep deprivation (SD) in a normal population. Forty-one military subjects received either 300 mg of modafinil, 20 mg of d-amphetamine, or placebo on 3 separate occasions during 64 hours of continuous cognitive work and sleep loss. Three drug treatments were given: at 23.30 hours and 05.30 hours during the first and second SD nights, respectively, and once at 15.30 hours during the third day of continuous work. Subjective estimates of mood, fatigue and sleepiness, as well as objective measures of reaction time, logical reasoning and short-term memory clearly showed better performance with both modafinil and amphetamine relative to placebo. Both modafinil and amphetamine maintained or increased body temperature compared to the natural circadian cycle observed in the placebo group. Also, from subject debriefs at the end of the study, modafinil elicited fewer side-effects than amphetamine, although more than the placebo group. Modafinil appears to be a good alternative to amphetamine for counteracting the debilitating mood and cognitive effects of sleep loss during sustained operations.

Journal Article↗
PubMed1995

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep.

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.

Journal Article↗
PubMed1995

Twenty-four-hour plasma cortisol and prolactin in human African trypanosomiasis patients and healthy African controls.

We have previously demonstrated that human African trypanosomiasis (sleeping sickness) at the stage of meningoencephalitis results in a major disruption of the circadian rhythmicity of sleep and wakefulness that is proportional to the severity of the disease. This paper examines the corresponding 24-hourly secretion in cortisol and prolactin and compares it with the hourly distribution of sleep composition in infected patients and healthy African subjects. The secretion of cortisol in humans follows a circadian rhythm relatively independent of the sleep-wake cycle, whereas that of prolactin exhibits fluctuations over the 24-hr day that are strongly related to the sleep-wake cycle. After the clinical classification of the patients according to the severity of the disease, hourly blood samples were taken over 24 hr via an indwelling catheter. Plasma cortisol and prolactin were analyzed by radioimmunoassay, and the variations in the hourly concentrations were analyzed for the presence of a potential 24-hr rhythm (circadian). All of the healthy African subjects showed significant circadian rhythms in both cortisol and prolactin secretion, similar to data on humans from temperate regions, and a sleep-related anamnestic afternoon peak of prolactin. Major disruptions in the circadian rhythms of plasma cortisol and prolactin were found in the three patients with the most severe illness, in contrast to the four who were less severely ill and the healthy controls. Thus, it appears that as the disease progresses in severity, major disruptions begin to occur in body circadian rhythms, not only in the sleep-wake cycle as reported elsewhere, but also in cortisol and prolactin secretion, suggesting that sleeping sickness affects the circadian timing system.

Adolescent↗
PubMed1995

Use of a spreadsheet program for circadian analysis of biological/physiological data.

Biological/physiological data sampled over a period of 24 h can be subjected to a mathematical analysis to determine the presence of circadian rhythmicity. Several procedures have been proposed, most being complex. To render such an analysis simpler and easy to use by non-mathematicians, we developed and tested the cosinor technique using a commonly available commercial spreadsheet (Excel). It can be used to analyze equally or unequally time-spaced data over 24 h with missing data, as well as to calculate the significance and the main limit of the resultant circadian rhythm (mesor, amplitude, acrophase and their confidence limits). Examples of its application to hourly samples of plasma cortisol and minute-by-minute rectal temperatures are shown.

Body Temperature↗
PubMed1994

24-hour (nyctohemeral) and sleep-related variations of intraocular pressure in healthy white individuals.

Intraocular pressure was measured hourly during 24 hours in 12 young (20.6 +/- 0.3 years, mean +/- SEM) and 12 older (59.5 +/- 1.6 years) healthy white adults to determine whether intraocular pressure followed a circadian rhythm and whether its nocturnal variations were related to the stages of sleep in the subjects. An electronic tonometer (Tono-Pen), working on the applanation principle, which was shown to give accurate intraocular pressure measurements in any posture, was used to measure intraocular pressure. Nocturnal polysomnography was measured. Wakefulness, light sleep (stages 1 and 2), slow-wave sleep (stages 3 and 4), and rapid eye movement sleep were scored. Intraocular pressure followed a circadian rhythm with a nocturnal peak value (acrophase). The variations in intraocular pressure were related to the stage of sleep, being lowest during rapid eye movement sleep, and highest during slow-wave sleep.

Adult↗
PubMed1994

Time-related changes in the sleep-wake cycle of rats infected with Trypanosoma brucei brucei.

Patients with human African trypanosomiasis, sleeping sickness, show a major disturbance in the circadian distribution of sleeping and waking, with sleep and wake episodes equally distributed throughout the nycthemeron. In order to develop an animal model, polysomnography was taken continuously in 8 male OFA rats in a 12:12 h light-dark cycle, during 1 baseline week and for 2 weeks after infection with Trypanosoma brucei brucei. Considerable sleep fragmentation was observed in the infected rats, with numerous sleep-wake stage changes and an increased number of wakefulness and slow-wave sleep phases. Although the infection produced a progressive disruption of the sleep-wake cycle, the extensive disturbances of the circadian rhythm of the sleep-wake cycle observed in humans with sleeping sickness was not attained in the rats.

Analysis of Variance↗
PubMed1994

Exercise and sleep in four African sportsmen living in the Sahel. A pilot study.

During both the cool and hot periods of the dry season of the Sahelian climate, sleep patterns of four African sportsmen from Niger (23 +/- 0.8 years old) were studied after square-wave cycle ergometer exercise. The sleep patterns were studied in the sedentary (Baseline) condition and under two exercise conditions, with and without rehydration. All conditions were randomly assigned. The exercise programme consisted of 3 sequences of cycling, beginning with 10 min at 30% of maximal aerobic power (MAP), followed by an exhaustive supramaximal effort (130% of MAP), and ending with a 10 min recovery at 30% of MAP. Polysomnography was recorded for 2 consecutive nights in each condition. One adaptation night, to familiarize the subjects to the polysomnography protocol, preceded the first session. Baseline slow-wave sleep (SWS) and REM sleep were high. In the hot season, there was an overall increase in SWS (p < 0.02), due primarily to an increase in Stage 4 (p < 0.01). Stage 2 sleep decreased (p < 0.01). This effect was also observed after exercise with rehydration, but was absent in the non-hydration condition. This distinction between the rehydrated and non-rehydrated condition is thought to be due to the greater stress which may accompany an exercise-induced relative dehydration. REM sleep decreased after exercise in the cool season (p < 0.001), but equalled baseline levels during the hot season. The results suggest a combined action of hyperthermia, water balance and stress, and are further supportive of an underlying hypothalamic control of human sleep.

Adult↗
PubMed1994

[The distribution of sleep and wakefulness in human African trypanosomiasis].

Last century, patients with human African trypanosomiasis were described as sleepy by day and restless by night, and physicians referred to this condition as sleeping sickness. Such a description could have evoked a disturbance of circadian rhythms. However, it is only in 1989 that the first 24-hour recording was performed by our team in Niamey (Niger) in a patient with sleeping sickness. The patient was a Niger-born farm worker who had contracted the disease near Gagnoa (Côte d'Ivoire). Polysomnographic recordings (electroencephalogram, EEG, electrooculogram, electromyogram, electrocardiogram, buccal and nasal airflow, and chest respiratory movements) showed a disappearance of the circadian distribution of sleep and wakefulness, which tended to occur evenly throughout day and night, with a sleep-wake alternation of approximately 80 minutes. Two investigations were conducted thereafter. The first one was done at Daloa (Côte d'Ivoire) in 8 patients who were recorded during two 24-hour periods, with and without hourly blood samples; the second at Brazzaville (Congo) in 10 patients recorded for 24 hours before and after treatment with melarsoprol. All patients were at the stage of early meningoencephalitis. At Daloa, polysomnographic recordings were taken on two 8-channel EEG machines (Alvar Minihuit, and T3-ECEM), as well as on a portable Oxford Medilog 9000 system from the same electrodes. Sleep and wake structure was altered in the most severely sick patient, the EEG trace being loaded with slow waves. Stages 1 and 2, and stages 3 and 4 could not be distinguished from one another. In the other patients, all sleep stages were easily scored. No difference was seen between recordings, regarding blood collection.(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian Rhythm↗
PubMed1994

[The sleep-wake cycle during Trypanosoma brucei rhodesiense human African trypanosomiasis in 2 French parachutists].

Polysomnography was performed in two military personnel who contracted human African trypanosomiasis (HAT) in Rwanda. They were evacuated to France and gramined during the fourth, sixth and eleventh months of evolution. Patient A presented a meningoencephalitis with Trypanosoma brucei rhodesiense (T. b. r.) in the cerebrospinal fluid. Between the second and third treatments with melarsoprol, the patient presented an acute encephalitic attack with pyramidal and cerebellar symptoms, which were improved by corticotherapy and disappeared progressively in 6 months. Patient B presented a major inflammatory syndrome with T. b. r. in the blood and the medulla. Cerebrospinal fluid and serology remained normal. The patient received only one session of melarsoprol treatment. Polysomnography recordings were continuously taken on an ambulatory Oxford Medilog system during 48 hours. The different stages of vigilance were scored according to the classical Rechtschaffen and Kales criteria. During the fourth month, both subjects presented several long diurnal naps, with the presence of rapid-eye-movement sleep at the end of the sleep episodes. These abnormalities disappeared progressively during the following recordings. Electroencephalographic abnormalities were observed in patient A, particularly during the eleventh month. They consisted in transitory arousal phases concomitant with myoclonic jerks and with the persistence of slow waves during slow-wave sleep. The various anomalies noted in the two patients allow us to recommend the supervision of the evolution of HAT by polysomnographic recording in a sleep laboratory.

Adult↗
PubMed1994

Disruptions in the secretion of cortisol, prolactin, and certain cytokines in human African trypanosomiasis patients.

It has been shown previously that sleeping sickness at the stage of meningoencephalitis manifests itself as a significant disturbance in the circadian rhythm of sleep-wakefulness. The objective of the current study was to examine the extent of circadian disruption in infected patients by measuring 24 hours patterns of plasma cortisol, an example of a classical circadian rhythm relatively independent of sleep, and prolactin, a primarily sleep-related rhythm. Plasma levels of certain cytokines were also measured to examine the immunopathogenesis of human African trypanosomiasis. An attempt was made to relate any circadian disruptions to the severity of the disease. The three most advanced patients demonstrated circadian disruptions in cortisol, prolactin and sleep-wake rhythms. The prime cytokine factor that correlated with the progression of the disease in humans was interferon-gamma, levels being 7- to 12-fold higher in the patients without any circadian rhythms. Our findings support the hypothesis that human African trypanosomiasis induces selective changes in the suprachiasmatic nucleus, important as a pacemaker for biological rhythms, resulting in disruptions of circadian rhythmicity in advanced stages of the disease.

Adolescent↗
PubMed1994

[The nyctohemeral rhythm of melatonin is preserved in human African trypanosomiasis].

We studied plasma melatonin profiles by radioimmunoassay in nine patients suffering from human african trypanosomiasis and six healthy controls matched according to the age and the photoperiodic conditions. The circadian periodicity of the sleep-wake cycle was disturbed proportionally to the degree of severity of the disease. On the contrary, the patients' plasma melatonin profile was similar to the controls' one. These results suggest that, beside the master clock generating the main circadian rhythms (sleep-wake, melatonin and core temperature rhythms), an additional regulating system of the melatonin rhythm could be involved.

Adolescent↗
PubMed1994

[Maintenance of the relation between the pulsed secretion of hormones and the internal sleep structure in human African trypanosomiasis].

In order to determine whether sleep disturbances would affect the hormonal patterns and the normal relationships between hormone pulses and sleep stages, the 24-hour profiles of cortisol, prolactin and plasma renin activity (PRA) were analysed in 6 sleeping sickness patients studied at Brazzaville and in 5 healthy African controls studied in Abidjan. Polysomnographic recordings were done continuously and blood was taken every 10 minutes throughout the 24-hour period. Plasma was analyzed for cortisol, prolactin and PRA. The circadian rhythm of cortisol, considered as an example of an endogenous rhythm was attenuated in all the patients but one, but as in normal subjects, slow wave sleep (SWS) remained associated with the declining phases of the secretory episodes. Prolactin and PRA profiles, which are strongly influenced by the sleep-wake cycle did not show the increase normally associated with long sleep periods and reflected the spreading of sleep and wakefulness throughout the 24-hour period. However, rapid-eye movement (REM) sleep began in sleeping sickness patients, as in normal subjects, during the descending phases of prolactin pulses. In both groups, PRA reflected the sleep stage distribution with non rapid-eye movement (NREM) sleep occurring during the ascending phases and REM sleep during the descending phases of the oscillations. However, in sleeping sickness patients, the marked sleep fragmentation often did not allow sufficient time for PRA to increase significantly, as observed with regular NREM-REM sleep cycles. These results demonstrate that, together with the disruption of the sleep-wake cycle, there are profound differences in the temporal organization of the 24 hour hormone profiles in human African trypanosomiasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗
PubMed1994

[Sickle cell disease and depression: preliminary study using the Hamilton rating scale for depression].

Prolonged latency in the appearance of REM sleep as a marker of depression has been demonstrated in patients with the sickle-cell disease. To detect the possible existence of depressive disturbances in patients with sickle-cell disease, the Hamilton rating scale for depression (17 items) was used in 30 patients with homozygote sickle-cell disease and 31 carriers of the sickle-cell trait, treated or not with vasodilator drugs. None of the 61 subjects studied presented a score of 18 or more on the Hamilton rating scale, this being the threshold value for confirming the existence of moderate depression. However, analysis of variance showed an increase in mental dullness, agitation and somatization disorder. Dullness was related to the extent of anemia and the number of sickle-cell crises per year. Treatment had an effect on agitation in patients, with pentoxyfylline having a soothing effect unlike cinepazide maleate. Women complained of insomnia in the middle of the night and somatic anxiety and presented higher total scores than men. Men exhibited a higher degree of mental dullness. The findings of this preliminary study indicate that while not associated with frank depression, the sickle-cell gene has psychological repercussions on various depressive parameters and that these patients can benefit from treatment with pentoxyfylline.

Adolescent↗
PubMed1993

Sleep-wake cycle in human African trypanosomiasis.

Sleeping sickness patients are classically described as sleepy by day and restless by night. Prior to this study, we had objectively confirmed this description by recording 24-h sleep patterns in a patient with human African trypanosomiasis. We report 24-h polysomnographic recordings (EEG, electrooculogram, electromyogram, electrocardiogram, and nasal, buccal, and thoracic respiratory traces) performed on two eight-channel electroencephalographs in eight patients with untreated sleeping sickness at an early stage of meningoencephalitis. As in our previously reported patient, there was no hypersomnia. The patients presented mainly a disorganization of the circadian alternation of sleeping and waking, with no or little alteration in the states of vigilance at this early stage of the disease. The disorganization was proportional to the degree of severity of the clinical symptoms. It may be due to an alteration in biological clock mechanisms.

Adolescent↗
PubMed1992

Sleep patterns of European expatriates in a dry tropical climate.

Night sleep in sedentary African subjects living in the sahelian zone lasts from 7 h to 8 h, with high amounts of slow-wave sleep (SWS) and paradoxical sleep (PS), SWS being present in each sleep cycle. We report here on sleep patterns in 6 healthy male European expatriates (aged 32-39 years) living in the same tropical climate. Polysomnography was taken for 3 consecutive nights in February (mean ambient temperature, Ta: 29.5 degrees C), March (Ta: 31.6 degrees C) and May (Ta: 33.3 degrees C). Comparisons between seasons were made with an analysis of variance, with P >/= 0.05. Because of a first night effect, the first nocturnal recording was discarded. Total sleep time (TST) increased in May vs February and March (P < 0.05). Stage 2 was shorter in March than in February (P < 0.001) and its proportion decreased from February to March (P < 0.02) and from March to May (P < 0.05). Conversely, SWS increased from February to March and March to May (duration, P < 0.001; proportion, P < 0.05), due to an augmentation in stage 4 with more numerous and longer stage 4 phases. Stage 3 was also increased in May vs March. The latency to SWS was shorter in March. SWS was present in each sleep cycle. PS was high, but did not vary. The sleep pattern changes were directly correlated with Ta. In conclusion, Caucasians living in the tropics slept similarly to Africans. The seasonal sleep variations favour the hypothesis that SWS is increased when thermoregulatory processes are triggered, either through passive climatic heating or exercise-induced hyperthermia.

Journal Article↗