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Biomedical subjects

M Bureau

Publications and source records attributed to M Bureau.

At least 55 records · Page 3Linked to original sources
PubMed1991

Hypoxia-induced bronchial responsiveness in awake sheep: role of carotid chemoreceptors.

Hypoxia enhances bronchial responsiveness in sheep and dogs and we recently reported a similar effect in asthmatic subjects. Activation of a reflex arc due to stimulation of peripheral chemoreceptors has been suggested to explain this finding. We evaluated the contribution of carotid body chemoreceptors to hypoxia-induced bronchial responsiveness in conscious sheep. Incremental concentrations of aerosolized methacholine were given to each of seven sheep ventilated successively (in a random order) with a normoxic and a hypoxic gas mixture (15% O2 in N2), both before and after peripheral surgical chemodenervation. Hypoxia alone did not affect lung mechanics in intact or chemodenervated animals. Bronchial responsiveness to methacholine was significantly increased by hypoxia in intact sheep, as compared to chemodenervated sheep. We conclude that hypoxia has a stimulating effect on bronchial responsiveness in awake sheep similar to that seen in human patients with asthma. This increased responsiveness may be mediated by hypoxic stimulation of carotid body chemoreceptors, which in turn may influence the nervous control of airway calibre.

Airway Resistance↗
PubMed1991

[The role of mitochondrial encephalopathies in progressive myoclonus epilepsy].

The authors compare the clinical, neurophysiological and evolutive features of progressive myoclonus epilepsy (PME) associated with mitochondrial encephalomyopathy with ragged-red fibers (MERRF), based on 49 cases from the literature, and the two well-described types of degenerative PME: Baltic myoclonus (BM), of which over 100 cases have been reported from Finland, and Mediterranean myoclonus (MM), based on a personal series of 43 patients. Degenerative PMEs are age-dependent, recessively inherited conditions with homogeneous clinical signs and course; there are no major clinical symptoms beside the cardinal symptoms: generalized epileptic seizures, predominantly action myoclonus and cerebellar dysfunction; mental deterioration when present, is slight and progresses very slowly; associated neurological symptoms are uncommon and limited to mild spino-cerebellar involvement. In MERRF, the transmission is maternal, the age of onset is variable, the evolution is not stereotyped and associated symptoms are many (deafness, muscle weakness, optic atrophy, short stature, sensory disturbances, spasticity, clinical or neurophysiological signs of peripheral neuropathy, absence of motor reflexes); muscle biopsy generally shows ragged-red fibers. The differential diagnosis between these conditions is usually easy, although pathological examination (i.e. muscle biopsy) should be performed.

Biopsy↗
PubMed1990

Protein kinase C and cAMP-dependent protein kinase phosphorylate the beta subunit of the purified gamma-aminobutyric acid A receptor.

A number of recent studies have suggested that phosphorylation of the gamma-aminobutyric acid A (GABAA) receptor could modulate receptor function. Activators of protein kinase C and cAMP-dependent protein kinase have been shown to influence GABAA receptor function. In addition, Sweetnam et al. [Sweetnam, P. M., Lloyd, J., Gallombardo, P., Malison, R. T., Gallager, D. W., Tallman, J. F. & Nestler, E. J. (1988) J. Neurochem. 51, 1274-1284] have reported that a kinase associated with a partially purified preparation of the receptor could phosphorylate the alpha subunit of the receptor. Moreover, Kirkness et al. [Kirkness, E. F., Bovenkerk, C. F., Ueda, T. & Turner, A. J. (1989) Biochem. J. 259, 613-616] have recently shown that cAMP-dependent protein kinase could phosphorylate a muscimol binding polypeptide of the GABAA receptor. To explore the issue further, we have examined the ability of specific kinases to catalyze significant phosphorylation of the GABAA receptor that has been purified to near homogeneity. The GABAA receptor was purified as previously described using benzodiazepine affinity chromatography. The purified receptor possessed no detectable kinase activity. Protein kinase C and cAMP-dependent protein kinase catalyzed the phosphorylation of the beta and alpha subunits of the receptor. However, most of the phosphate incorporation was associated with the beta subunit. Two muscimol binding polypeptides designated beta 58 (Mr 58,000) and beta 56 (Mr 56,000) were present in the preparation. The higher molecular weight polypeptide, beta 58, was phosphorylated specifically by cAMP-dependent protein kinase. beta 56 was phosphorylated specifically by protein kinase C. beta 58 and beta 56 gave distinct patterns in a one-dimensional phosphopeptide analysis. The stoichiometry of phosphorylation (mol of phosphate/mol of muscimol binding) catalyzed by cAMP-dependent protein kinase was 0.52 and that catalyzed by protein kinase C was 0.38. Taken together these data confirm that there are two forms of the beta subunit of the GABAA receptor and suggest that these two forms of the beta subunit are phosphorylated by distinct kinases.

Animals↗
PubMed1990

Thyroarytenoid muscle activity during hypoxia in awake lambs.

It is generally accepted that hypoxia in early life results in active laryngeal braking of expiratory airflow via the recruitment of glottic adductor muscles. We examined the electromyogram expiratory activity of the thyroarytenoid muscle in seven 11- to 18-day-old awake nonsedated lambs exposed to an inspired O2 fraction of 0.08 for 18 min. The lambs breathed through a face mask and a pneumotachograph. During baseline prehypoxic breathing, the thyroarytenoid muscle was largely inactive in each awake lamb. Unexpectedly, no recruitment of the thyroarytenoid muscle was recorded during hypoxia in any of the seven lambs; simultaneous examination of the flow-volume curves revealed an absence of expiratory airflow braking. Also unexpectedly, marked expiratory activity of the thyroarytenoid muscle was recorded, with each expiration occurring within less than 10 s after the return to room air. The resulting delay of expiration was apparent in the flow-volume loops. Thus, in awake 11- to 18-day-old lambs, 1) active expiratory glottic adduction is absent during hypoxia and 2) a return from hypoxia to room air results in prolonged expiration as well as active glottic adduction that controls end-expiratory lung volume.

Animals↗
PubMed1990

Brainstem auditory evoked potentials in alternating hemiplegia: ictal vs interictal assessment in one case.

The authors report a case of alternating hemiplegia (AH) in a 3yr 6m old boy who had presented, from the age of 4 months on, episodes of alternating hemi- or quadriplegia. Brainstem auditory evoked potentials were recorded both in the interictal state and, for the first time, during an attack. There was no significant difference between the two states. These findings suggest that a massive involvement of the posterior vascular territory is not likely to be associated with attacks in AH.

Brain Stem↗
PubMed1990

Multiple distinct subunits of the gamma-aminobutyric acid-A receptor protein show different ligand-binding affinities.

The purified gamma-aminobutyric acid/benzodiazepine receptor protein from mammalian brain contains at least four discrete polypeptides (Mr 51,000, 53,000, 55,000 and 58,000) by a variety of visualization techniques and in three species (rat, cow, and human). These polypeptide bands vary in their affinity for gamma-aminobutyric acid analogs as shown by inhibition of [3H]muscimol binding, demonstrated by photoaffinity labeling and gel electrophoresis in sodium dodecyl sulfate. One-dimensional peptide maps of proteolytic digests revealed that distinct fragments were produced, indicating that the four polypeptides represent discrete sequences. The four bands were identified by Western blotting with subunit-specific monoclonal antibodies as two species each of previously identified alpha and beta subunits. [3H]Muscimol photolabeled all four bands (beta and alpha) to varying degrees not proportional to the extent of protein staining. The Mr 58,000 beta subunit subtype showed a higher affinity for 4,5,6,7-tetrahydro-isoxazolo-[5,4-c]pyridin-3-ol than the Mr 56,000 beta subtype, whereas the Mr 56,000 beta and Mr 51,000 alpha bands were more enhanced by pentobarbital than the Mr 58,000 band. Furthermore, the alpha subunit pattern revealed by photoaffinity labeling with [3H]flunitrazepam was significantly different for three regions of bovine brain, showing only one major band in cerebellum at Mr 51,000, two major bands in cortex at Mr 53,000 and 51,000, and three bands in hippocampus at Mr 55,000 as well as Mr 53,000 and 51,000. Because the ratio of the amounts of the various polypeptides varies with brain region and the pharmacological properties of the peptides vary, it is likely that a family of oligomeric gamma-aminobutyric acid/benzodiazepine receptors exists in the brain. This is consistent with the reported variable expression of different subunit subtype mRNAs and with brain region-dependent variation in pharmacology and binding behavior.

Affinity Labels↗
PubMed1989

[Electroencephalographic findings in severe symptomatic partial epilepsies in childhood].

The EEG records of 64 patients affected by a symptomatic severe partial epilepsy have been reviewed retrospectively. The epilepsy started before age 12. The follow-up was at least 5 years after the onset of the disease. In a longitudinal study of interictal EEG, the following parameters were studied: normal or slightly abnormal EEG records at the onset, late appearance of abnormalities of background, multifocal abnormalities and generalized spike and wave discharges. The study of ictal EEG was performed in 32 patients: a good correlation with the interictal and ictal site of the discharges was found. The EEG semeiology of the seizures persisted unchanged throughout the evolution.

Adolescent↗
PubMed1989

[Contribution of ambulatory EEG recording (Medilog 9000) in a population of epileptics].

Thirty-four epileptic patients, aged 9 to 36, were submitted to A/EEG between May 1987 and July 1988. All patients had a thorough clinical and EEG work-up including long-term conventional EEG, afternoon polygraphic sleep recording and, in some cases, full-night EEG and video monitoring. Patients were divided into 2 groups: group I included 19 patients (18 with symptomatic partial epilepsy (SPE) and 1 with idiopathic generalized epilepsy (IGE) in whom no seizure had ever been recorded in spite of EEG recordings averaging a total of 16 hrs 10 min, awake and asleep); group II included 15 subjects (6 with SPE, 5 with IGE, 3 with symptomatic GE and 1 with undetermined epilepsy) in whom one or several seizures had been recorded. A/EEG was performed in order to: 1) obtain better clinical and EEG characterization of seizures, 2) study the circadian distribution of seizures, 3) verify the efficacy of drug treatment and, 4) establish the epileptic or non-epileptic nature of some ictal events. The results of A/EEG were considered positive in 52.63% of group I patients and in 93.33% of group II patients. The authors discuss the specific advantages of A/EEG vs conventional EEG: recording of seizures with random occurrence, of seizures accompanied by falls, checking the remission of seizures.

Adolescent↗
PubMed1988

gamma-Aminobutyric acid/benzodiazepine receptor protein carries binding sites for both ligands on both two major peptide subunits.

Affinity column-purified GABA-benzodiazepine receptor proteins from human, cow, and rat brain were photoaffinity labeled with both [3H]flunitrazepam and [3H]muscimol and examined by gel electrophoresis in sodium dodecyl sulfate. Using high receptor protein concentrations (1 microM), the benzodiazepine ligand [3H]flunitrazepam was incorporated covalently primarily into the expected 52 kiloDalton major subunit but also significantly into a second 57 kiloDalton peptide. Likewise the GABA ligand [3H]muscimol photolabeled primarily the 57 kiloDalton peptide but also to some extent the 52 kiloDalton peptide. This cross-labeling suggests strongly that both major subunits carry binding sites for both GABA and benzodiazepine.

Affinity Labels↗
PubMed1988

Prevention of follicular maturation in endometriosis by subcutaneous infusion of luteinizing hormone-releasing hormone agonist started in the luteal phase.

Six endometriosis patients were treated with continuous subcutaneous (SC) infusion of a luteinizing hormone-releasing hormone (LH-RH) agonist using an external osmotic minipump system. Serum estradiol (E2) was suppressed into the menopausal range within 1 to 2 weeks of treatment started between days 9 and 12 after ovulation. The down-regulation of the pituitary-ovarian axis was maintained for the 24 weeks of treatment. Endometriosis symptoms were relieved during the treatment. At control laparoscopy, implants had regressed markedly and some adhesions had softened, accounting for a significant 58.3% reduction in the mean total American Fertility Society score. Ovulation returned within 14 to 38 days. Four infertile women became pregnant within 2 to 5 months after cessation of treatment. Frequent side effects were hot flushes, and decreased vaginal secretion and libido. There were no significant changes in laboratory blood tests, including cholesterol. The urinary calcium/creatinine ratio increased during the treatment. Thus, starting the treatment in the luteal phase prevented initial follicular stimulation. A better efficacy of treatment would be achieved by the release of an LH-RH agonist at a constant daily rate.

Adult↗
PubMed1988

Familial encephalopathy with permanent periodic breathing: 4 cases in 2 unrelated families.

In each of 2 unrelated Algerian families, we observed 2 sisters with a severe static encephalopathy which was detected in the first weeks of life. Anoxia at birth occurred in only one case. This previously unreported familial encephalopathy is characterized by severe mental retardation, hypotrophy, abnormal movements with unprovoked startles, major EEG abnormalities with undifferentiated sleep stages and a very particular periodic breathing pattern that persists during waking and sleep. EEG, polygraphic and video recordings were obtained for all patients. The evolution is chronic and stable. There are no major dysmorphic features. No metabolic or anatomic abnormality was found. Gynecotropy is uncertain and the transmission is likely to be recessive.

Brain Diseases↗
PubMed1988

[Multimodal evoked potentials in partial epilepsy in children].

A multimodal evoked potential study was realised in three groups of children or adolescents 5 to 15 years old. The first group included 25 normal non-epileptic subjects; the second group was composed of 27 subjects with partial idiopathic epilepsy (PIE) (benign childhood epilepsy with centro-temporal spike; childhood epilepsy with occipital paroxysms); the third group was formed of 20 subjects with partial symptomatic epilepsy (PSE) without patent anatomical lesion or with anatomical lesion. Recording for each subject included: flash visual evoked potentials, pattern visual evoked potentials, brainstem auditory evoked potentials and somatosensory evoked potentials. Each curve obtained was studied for the response morphology, the measure of the different wave latencies, the inter-peak latencies (conduction time) and the amplitudes. A statistical treatment of the data was performed to evaluate the significance of variation of the different parameter values obtained for the various groups. Among the significantly modified parameters, we found: an increase of the amplitudes in the PIE and a decrease in the PSE, specially when an anatomical lesion exists; an asymmetrical amplitude of the somatosensory responses in the PIE with centro-temporal spike; an increase of the central somatosensory conduction time in the PSE with anatomical lesion.

Adolescent↗
PubMed1988

[Napping sleep EEG in partial childhood epilepsy].

A nap sleep EEG with at least one full sleep cycle has been recorded in 3 groups of children free from diffuse encephalopathy and presenting with partial epilepsy with onset after the age of 3 years: 15 cases with typical benign epilepsy with centrorolandic spikes (BERS), 15 cases with partial symptomatic epilepsy without clinical or radiological evidence of a cerebral lesion, and 12 cases with partial epilepsy symptomatic of a proven cerebral lesion. The time course of paroxysmal abnormalities was quantified according to individual sleep stages; the number of foci was also quantified in the waking vs sleeping state. Paroxysmal abnormalities are significantly enhanced by sleep in all 3 groups: throughout sleep stages in BERS, in slow sleep stages only in the other groups. The enhancement is more striking in BERS, where a clear decrease of abnormalities is also found upon awakening. There is no major difference between the 2 symptomatic groups, with a greater enhancement of paroxysms in the proven lesional group. Contrary to the other groups, only the group including those patients with a documented cerebral lesion showed a significant increase in the number of foci during sleep: numerous foci were found in these patients that were distinct from the primary lesional focus. Under the conditions of our study, the nap EEG seems to provide an accurate evaluation of sleep-induced changes of paroxysmal activity in partial epilepsies of childhood.

Child↗
PubMed1987

Desensitization and antagonism of rat polymorphonuclear leukocytes stimulated with PAF acether.

The activation of rat polymorphonuclear leukocytes (PMN) with PAF-acether (platelet-activating factor) was blocked by two antagonists: 48740 RP and BN 52021. The release of beta glucuronidase was usually better inhibited than that of lysozyme suggesting that the tested antagonists interfere rather with PAF-acether exocytosis of azurophil granules. Inhibition was relatively specific, even though a moderate effect (below 34%) upon PMN activation by the two unrelated agonist n-formyl-Methionyl-Leucyl-Phenylalanine (fMLP) and leukotriene B4 sometimes reached significance. The partial persistence of inhibition to stimulation with PAF-acether after elimination of both inhibitors suggests that they do not act at the PAF-acether receptor only. Furthermore, the observation of cross desensitization between PAF-acether and fMLP may be related to common pathways and/or metabolites, including PAF-acether itself.

Animals↗