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Biomedical subjects

P Badia

Publications and source records attributed to P Badia.

At least 19 recordsLinked to original sources
PubMed2000

Acute effects of bright light and caffeine on nighttime melatonin and temperature levels in women taking and not taking oral contraceptives.

Caffeine and bright light effects on nighttime melatonin and temperature levels in women were tested during the luteal phase of the menstrual cycle (n=30) or the pseudo luteal phase for oral contraceptive users (n=32). Participants were randomly assigned to receive either bright (5000 lux) or dim room light (<88 lux) between 20:00 and 08:00 h under a modified constant routine protocol. Half the subjects in each lighting condition were administered either caffeine (100 mg) or placebo in a double-blind manner at 20:00, 23:00, 02:00 and 05:00 h. Results showed that the combination of bright light and caffeine enhanced nighttime temperature levels to a greater extent than did either caffeine or bright light alone. Both of the latter groups had higher temperature levels relative to the dim light placebo condition and the two groups did not differ. Temperature levels in the bright light caffeine condition were maintained at near peak circadian levels the entire night in the luteal and pseudo luteal phase. Melatonin levels were reduced throughout the duration of bright light exposure for all women. Caffeine reduced the onset of melatonin levels for women in the luteal phase, but it had little effect on melatonin levels for oral contraceptive users. The results for women in the luteal phase of the menstrual cycle are consistent with our previous findings in men. The results also suggest that oral contraceptives may alter the effects of caffeine on nighttime melatonin levels.

Adolescent↗
PubMed1999

Effects of menstrual cycle phase and oral contraceptives on alertness, cognitive performance, and circadian rhythms during sleep deprivation.

The influence of menstrual cycle phase and oral contraceptive use on neurobehavioral function and circadian rhythms were studied in healthy young women (n = 25) using a modified constant routine procedure during 24 h of sleep deprivation. Alertness and performance worsened across sleep deprivation and also varied with circadian phase. Entrained circadian rhythms of melatonin and body temperature were evident in women regardless of menstrual phase or oral contraceptive use. No significant difference in melatonin levels, duration, or phase was observed between women in the luteal and follicular phases, whereas oral contraceptives appeared to increase melatonin levels. Temperature levels were higher in the luteal phase and in oral contraceptive users compared to women in the follicular phase. Alertness on the maintenance of wakefulness test and some tests of cognitive performance were poorest for women in the follicular phase especially near the circadian trough of body temperature. These observations suggest that hormonal changes associated with the menstrual cycle and the use of oral contraceptives contribute to changes in nighttime waking neurobehavioral function and temperature level whereas these factors do not appear to affect circadian phase.

Adolescent↗
PubMed1997

Caffeine and light effects on nighttime melatonin and temperature levels in sleep-deprived humans.

The effects of caffeine ingestion and exposure to bright light, both separately and in combination, on salivary melatonin and tympanic temperature were assessed in humans. Four treatments during a 45.5 h sleep deprivation period were compared: Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright-Light Caffeine. The Dim Light-Caffeine condition (200 mg twice each night) relative to the Dim Light-Placebo condition suppressed nighttime melatonin levels and attenuated the normal decrease in temperature. Combining caffeine ingestion with bright light exposure (> or = 2000 lux) suppressed melatonin and attenuated the normal nighttime drop in temperature to a larger degree than either condition alone; i.e. effects were additive. Circadian effects were also observed in that the amplitude and phase of the temperature rhythm were altered during treatment. These findings establish that the human melatonin system is responsive to caffeine. Other evidence suggests that caffeine may influence melatonin and temperature levels through antagonism of the neuromodulator adenosine.

Adolescent↗
PubMed1997

Combination of bright light and caffeine as a countermeasure for impaired alertness and performance during extended sleep deprivation.

Effects of four conditions (Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright Light-Caffeine) on alertness, and performance were studied during the night-time hours across 45.5 h of sleep deprivation. Caffeine (200 mg) was administered at 20.00 and 02.00 hours and bright-light exposure (> 2000 lux) was from 20.00 to 08.00 hours each night. The three treatment conditions, compared to the Dim Light-Placebo condition, enhanced night-time performance. Further, the combined treatment of caffeine and all-night bright light (Bright Light-Caffeine) enhanced performance to a larger degree than either the Dim Light-Caffeine or the Bright Light-Placebo condition. Beneficial effects of the treatments on performance were largest during the early morning hours (e.g. after 02.00 hours) when performance in the Dim Light-Placebo group was at its worst. Notably, the Bright Light-Caffeine condition was able to overcome the circadian drop in performance for most tasks measured. Both caffeine conditions improved objective alertness on the Maintenance of Wakefulness Test. Taken together, the above results suggest that the combined treatment of bright light and caffeine provides an effective intervention for enhancing alertness and performance during sleep loss.

Adolescent↗
PubMed1997

Sleep-promoting and hypothermic effects of daytime melatonin administration in humans.

Sleep-promoting and hypothermic effects of orally administered melatonin during the daytime were assessed using a placebo-controlled, double-blind, cross-over design. Following a 7-hour nighttime sleep opportunity, healthy young male subjects (n = 8) were given either a placebo or one of three doses of melatonin (1 mg, 10 mg, and 40 mg) at 1000 hours. Sleep was polygraphically assessed in a 4-hour sleep opportunity from 1200 to 1600 hours. All doses of melatonin significantly shortened the latency to sleep onset. Melatonin also significantly increased total sleep time and decreased wake after sleep onset (WASO). Sleep following melatonin administration contained significantly more stage 2 and less stage 3-4, while stage 1 and rapid eye movement (REM) sleep were unaffected. In addition to the sleep-promoting effects, melatonin completely suppressed the normal diurnal rise of core body temperature. These data suggest that melatonin may be an effective method of promoting sleep for individuals attempting to sleep during their subjective day, such as shiftworkers and individuals rapidly traveling across multiple time zones.

Adolescent↗
PubMed1996

Nonsteroidal anti-inflammatory drugs alter body temperature and suppress melatonin in humans.

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis in humans. Prostaglandins are involved in thermoregulation, melatonin synthesis, and sleep. To determine effects of NSAIDs on body temperature (BT) and melatonin synthesis (MT) in humans, and to elucidate mechanisms by which NSAIDs may alter sleep patterns, a series of experiments using the NSAIDs aspirin and ibuprofen was conducted. Seventy-five subjects were tested under several experimental protocols. BT after NSAID or placebo was assessed in both between- and within-subjects designs at night and during the day. MT levels were assessed after NSAID or placebo at night in a within-subjects design. The normal nocturnal BT decrease was attenuated and MT was suppressed after NSAID relative to after placebo administration. Lower MT levels were associated with a relative flattening of BT. Daytime BT was not affected by NSAIDs. These results are compatible with the hypothesis that some of the behavioral changes associated with NSAIDs, including changes in sleep, are due to changes in BT and MT. We speculate that NSAID effects on sleep and BT are related to prostaglandin synthesis inhibition and/or suppression of MT.

Adult↗
PubMed1996

[Digital necrosis associated with fenoxazoline poisoning. Apropos of a case and review of the literature].

We report the case of a 53 year-old woman with paroxystic hypertension and digital ischemia. The only triggering factor was chronic intoxication by a nasal vasoconstrictor:fenoxazoline. The worsening of the lesions required amputation of the third phalanx of the 3rd and 5th finger and the pulp of the 4th finger of the left hand. The review of literature exhibits association between fenoxazoline intoxication and paroxystic hypertension, myocardial ischemia or stroke, but association between fenoxazoline intoxication and digital ischemia has never been reported. We emphasize the extreme caution necessary with the prescription and the chronic consumption of this kind of drug.

Female↗
PubMed1996

Haemodynamic effects of molsidomine and propranolol in patients with cirrhosis.

Propranolol and molsidomine have both been shown to decrease the hepatic venous pressure gradient in patients with cirrhosis. The present study aimed at assessing the effects of the combination of these two drugs on splanchnic and systemic haemodynamics of cirrhotic patients. Fifteen patients with biopsy proven alcoholic cirrhosis had haemodynamic measurements under basal conditions, 60 min after oral administration of 4 mg molsidomine then 15 min after intravenous administration of 15 mg propranolol. As compared with baseline values, molsidomine was found to decrease mean arterial pressure (-7.9%, (P < 0.01), cardiac output (-7.3%, P < 0.01), pulmonary wedged pressure (-45.8%, (P < 0.05) and hepatic venous pressure gradient (-11.7%, P < 0.01). Propranolol decreased heart rate (-21%, P < 0.01), further decreased cardiac output (-20.6%, (P < 0.01) and hepatic venous pressure gradient (-10.5%, P < 0.01). As a whole, molsidomine plus propranolol decreased mean arterial pressure (-8%, P < 0.01), heart rate (-19%, P < 0.01), cardiac output (-26.5%, P < 0.01) and hepatic venous pressure gradient (-21%, P < 0.01). Pulmonary wedged pressure, liver blood flow and hepatic intrinsic clearance of indocyanine green were not significantly changed by the association of molsidomine and propranolol. We conclude that in patients with cirrhosis, molsidomine and propranolol potentiate their effects on hepatic venous pressure gradient. Such a combination could therefore prove useful in the treatment of portal hypertension.

Adrenergic beta-Antagonists↗
PubMed1995

Changes in circadian rhythms and sleep quality with aging: mechanisms and interventions.

Literature is reviewed indicating that aging is characterized by changes in circadian rhythms and sleep quality. The most marked change is an attenuation of amplitude. An advance of phase, a shortening of period, and a desynchronization of rhythms are also evident. The mechanisms underlying these changes are unknown. However, age-related changes in the retina, suprachiasmatic nucleus, and pineal gland seem relevant along with behavioral changes such as a reduction in physical activity and exposure to photic stimulation. Changes in circadian rhythms are frequently associated with a reduction in nighttime sleep quality, a decrease in daytime alertness, and an attenuation in cognitive performance; reversing such changes could enhance the quality of life for a large and rapidly increasing percentage of the population. Reversal appears possible by increasing melatonin levels with either appropriately timed exposure to photic stimulation and/or appropriately timed administration of exogenous melatonin. These interventions may increase aspects of genetic expression that have changed with aging. A hypothesis concerning the potential benefits of enhanced circadian amplitude is also offered.

Aging↗
PubMed1995

Mycotic aneurysm of the left subclavian artery presented with hemoptysis in an immunosuppressed man: case report and review of literature.

We report the case of a 32-year-old man with a mycotic aneurysm of the left subclavian artery. This patient had immunosuppression caused by chemotherapy administered for treatment of leukemia. This aneurysm was revealed by two episodes of hemoptysis caused by a lung parenchyma fistulization. The patient was treated successfully by simple ligation and exclusion via a thoracotomy with partial lung resection. Histologic examination confirmed the presence of aspergilloma filaments in the false aneurysm. We suspect that aspergilloma could have been the cause of the mycotic aneurysm in this particular case. The literature on subclavian artery mycotic aneurysms is reviewed.

Adult↗
PubMed1995

Topographical and temporal patterns of brain activity during the transition from wakefulness to sleep.

Changes in electroencephalographic (EEG) spectral power, coherence and frequency were examined for the last minute of wakefulness and the first minute of sleep via topographical mapping. Data were also analyzed across sequential 1-minute samples of wake, stage 1 and stage 2 sleep. Not all brain regions exhibited the same EEG changes during the transition and not all brain regions were found to change at the same time. Brain sites closest to the midline (e.g. F4, C4, P4, O2) showed significant changes in EEG power (increases in theta and decreases in alpha power) during the transition to sleep, whereas brain sites most lateral to the midline (e.g. Fp2, F8, T4) showed little change. Decreases in alpha coherence were observed from wakefulness to sleep for brain site comparisons furthest away from each other (e.g. T3 vs. T4, T5 vs. T6, F7 vs. F8, F3 vs. O1, F4 vs. O2). Spectral analysis of EEG activity revealed that the time of significant change in EEG power varies among brain regions. Decreases in alpha power continued to occur later into the transition period for the posterior regions of the brain (O2, P4).

Adolescent↗
PubMed1994

Nonsteroidal anti-inflammatory drugs affect normal sleep patterns in humans.

Previous studies have demonstrated that some nonsteroidal anti-inflammatory drugs (NSAIDs), specifically aspirin and indomethacin, have acute negative effects on sleep in humans and animals. Whether this finding can be replicated and extended to other NSAIDs, particularly the widely used over-the-counter drugs ibuprofen and acetaminophen, was the focus of the present investigation. Thirty-seven male and female subjects slept in the sleep laboratory on 2 consecutive nights; sleep was polygraphically recorded on the second night. Three doses of a prostaglandin-inhibiting drug (i.e., aspirin, acetaminophen, or ibuprofen) or placebo were administered, one each at 2300 h on the day prior to sleep recording, and at 0815 h and 2300 h on the day sleep was recorded. Subjects slept from 2400-0800 h both nights. Aspirin and ibuprofen disrupted sleep in comparison to placebo by increasing the number of awakenings and percentage of time spent in stage wake, and by decreasing sleep efficiency. Ibuprofen also delayed the onset of the deeper stages of sleep. Acetaminophen did not differ significantly from placebo on any measure of polygraphically recorded sleep. However, every index of objective sleep reflected slight, albeit nonsignificant, sleep disruption for each drug group relative to placebo. The mechanisms of sleep disruption after NSAID administration may relate to direct and indirect consequences of inhibiting prostaglandin synthesis, including decreases in prostaglandin D2, suppression of nighttime melatonin levels, and changes in body temperature.

Acetaminophen↗
PubMed1994

[Rhabdomyolysis in community-acquired pneumonia].

Several cases of rhabdomyolysis associated with pneumococcal pneumonia have been recently reported. However their significance have been poorly investigated. In this retrospective study, we have compared the patients admitted in ICU for acute community-acquired pneumonia with or without rhabdomyolysis (group A: CPK > or = 1,000 Ul/l and group B: CPK < 1,000 Ul/l). Among the 41 patients of the study, 12 (29%) belonged to the group A (CPK = 1,852 +/- 535 Ul/l) and 29 (71%) to group B (CPK = 190 +/- 35 Ul/l). Neither the initial severity, nor renal impairment were different in the two groups. However the mortality was significantly higher in the group A (4/12) than in group B (2/29) (P < 0.05). In this study, pneumonia is frequently associated with rhabdomyolysis, without etiologic significance. In patients with pneumonia, rhabdomyolysis seems to be a bad prognostic indice unrelated with renal impairment.

Adult↗
PubMed1994

ERP and behavioral changes during the wake/sleep transition.

Event-related potentials (ERPs) following infrequent and frequent stimuli were studied as subjects moved from wakefulness to sleep. Subjects were instructed to respond to the infrequent "target" stimuli (attend condition) or to ignore the stimuli (ignore condition). Parietal P300, prominent following target ERPs in wakefulness under the attend condition, disappeared in association with reduced behavioral responsiveness and emergence of a central negativity (N350). The N350 and preceding and following positivities (P220 and P450) became the dominant feature of both target and nontarget ERPs under both attend and ignore conditions. The P220-N350-P450 complex was larger and peak latencies were shorter under the attend condition. Peak amplitudes tended to be larger following targets, especially under the attend condition. The findings suggest that, although the processes underlying P300 are less likely to be engaged, processing of stimulus deviance and task relevance continues in sleepiness and sleep, and is reflected by variance in N350 and related activity.

Adolescent↗
PubMed1994

A kidney biopsy is clearly mandatory to confirm the indication of plasma exchanges in adult haemolytic uraemic syndrome.

In case of haemolytic uraemic syndrome, it is not always possible to identify on a pure clinical basis the different kidney lesions responsible for the syndrome. We report a series of six cases without thrombotic microangiopathy, which emphasizes the need to perform a kidney biopsy as early as possible, so as to confirm the actual usefulness of plasma exchanges (PE) commonly carried out in emergency in every case of adult haemolytic uraemic syndrome. PATIENTS AND METHODS--Files of patients who were treated for haemolytic uraemic syndrome over the past 14 years were reviewed. Patients in whom thrombotic microangiopathy had been excluded by renal histology data were studied. Every patient was promptly treated with hypotensive drugs, so as to obtain blood pressure levels not exceeding 160-90 mmHg. Dialysis was performed in two patients. Daily PE with fresh frozen plasma were carried out in three patients as early as the first 24 hours after admission, and discontinued immediately after thrombotic microangiopathy could be excluded. RESULTS--All the patients met the usual criteria for diagnosis of haemolytic uraemic syndrome. Elevated liver enzymes were also found in the four cases of preeclampsia, consisting with diagnosis of severe HELLP syndrome. One case was associated with oestrogen therapy. Glomerular lesions were seen in four patients: slight endotheliosis in three cases of preeclampsia; marked lesions of IgA mesangial deposits in the patient who had been treated by contraceptive pill. Three patients had acute tubular necrosis and three had intense lesions of nephrosclerosis. Complete remission was obtained in every case of preeclampsia. Renal failure persisted in two cases (IgA glomerulopathy and one case of nephrosclerosis). DISCUSSION--The histological heterogeneity of haemolytic uraemic syndrome has been already well demonstrated. Typical lesions of thrombotic microangiopathy are usually classified into predominant glomerular lesions, pure arteriolar and mixed lesions. In other cases, thrombotic microangiopathy is not found: kidney lesions may be glomerular (endotheliosis, various subtypes of glomerulonephritis), tubular (acute tubular necrosis) or vascular (nephroangiosclerosis). In every aetiological circumstance, several different lesions may be found together. The usefulness of PE has been proved in thrombotic thrombocytopenic purpura, has been suggested in haemolytic uraemic syndrome and to a lesser extent in persistently severe HELLP syndrome. Unfortunately, none of these reports gave any information about kidney lesions responsible of acute renal failure. CONCLUSION--The haemolytic uraemic syndrome is a syndrome: thrombotic microangiopathy has to be proven when treatment by PE is planned, except in some severe clinical circumstances.

Adult↗