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Biomedical subjects

J Perret

Publications and source records attributed to J Perret.

At least 109 records · Page 6Linked to original sources
PubMed1982

[Bromazepam in anxiety. Clinical evaluation (author's transl)].

In an open study, 30 patients with anxiety were treated with bromazepam 6 to 9 mg/day and followed-up for 15 days either as out-patients or in hospital. The results, assessed by anxiety scores, showed a 71,4% improvement, which was often perceptible as early as the third day of treatment. The best responses were obtained in patients who had not previously received anxiolytic drugs and in those who had less anxiety at the beginning of treatment. In two cases the drug was discontinued on account of daytime drowsiness.

Adolescent↗
PubMed1982

[Modification of extrapyramidal signs by apomorphine associated with various dopaminergic antagonists].

An acute administration of various doses of apomorphine, a dopaminergic agonist, and of dopaminergic receptor blockers (domperidone, sulpiride, haloperidol), was double-blindly achieved in a parkinsonian patient also suffering from dyskinesia. Apomorphine improved tremor and dyskinesia proportionnally to the dose. Domperidone did not prevent from this beneficial effect whereas sulpiride or haloperidol revealed a competitive antagonism versus apomorphine.

Aged↗
PubMed1980

[Shy-Drager syndrome and megaesophagus (author's transl)].

Authors report the case of a Shy-Drager syndrome (idiopathic postural hypotension due to a central degenerative lesion) syndrome which evolution uncovered a megaesophagus. The knowledge of degenerative lesions of the vagus nerve in megaesophagus, the effectiveness of motory lesions of the esophagus in Parkinson's disease where lesions of the vagoglosso pharyngeal dorsal nucleus frequently occurs, allow to discuss the central nervous origin of the megaesophagus appeared in the reported case.

Adult↗
PubMed1979

Kinetic study of a phosphoryl exchange reaction between fructose and fructose 1-phosphate catalyzed by the membrane-bound enzyme II of the phosphoenolpyruvate-fructose 1-phosphotransferase system of Bacillus subtilis.

A phosphoryl exchange reaction between fructose 1-phosphate and fructose was found to be catalyzed by a membrane preparation isolated from Bacillus subtilis. The regulation of the biosynthesis of the activity in the wild type as well as in the regulation mutants fruB closely correlates with that of the membrane-bound enzyme II of the phosphoenolpyruvate fructose 1-phosphotransferase system which is known to mediate the transmembrane vectorial phosphorylation of fructose. The computed analysis of the kinetic data shows that the mechanism of the enzyme II is ping-pong, i.e. that a phosphoryl-enzyme intermediate occurs in the reaction. The apparent dissociation constants of the enzyme II/fructose 1-phosphate complex and of the phosphoryl enzyme II/fructose complex are estimated. The value of the standard free energy of the hydrolysis of the bond between the phosphoryl moiety and the enzyme suggests a covalent bonding. This intermediate is assumed to occur in the physiological functioning of the enzyme which utilizes the phosphocarrier protein HPr as phosphoryl donor. The exchange reaction is competitively inhibited by high fructose concentrations: this indicates that the same site of the enzyme binds fructose and fructose 1-phosphate, this site being accessible to fructose on the external side of the membrane when the enzyme is phosphorylated.

Bacillus subtilis↗
PubMed1977

Does O-methyl-dopa play a role in levodopa-induced dyskinesias?

Clinically scored levodopa-induced dyskinesias were correlated with plasma dopa and O-methyl-dopa levels determined every hour during one day in 30 Parkinsonian-treated patients. In patients treated with a combination of L-dopa and a peripheral decarboxylase inhibitor (PDI), those with dyskinesias have very high plasma O-methyl-dopa levels compared with those who have no dyskinesias. In contrast, no significantly different plasma dopa levels are found in these two subgroups of patients, leaving open the question of the possible involvement of such elevated plasma O-methyl-dopa levels in favouring dyskinesias.

Adult↗
PubMed1977

Plasma O-methyldopa in levodopa-induced dyskinesias. A bioclinical investigation.

The peripheral metabolism of Dopa has been studied in correlation with the clinical occurrence of Leyodopa-induced dyskinesias in Parkinson patients. Within the group of patients treated with a peripheral decarboxylase inhibitor (PDI), the combination of all the plasma levels of O-Methyldopa from patients with dyskinesias shows significantly higher values than those from patients without dyskinesias. For Dopa itself, no significant differnece can be detected. Such high O-Methyldopa levels seem to be due to a progressive accumulation of this compound and not to a higher degree of formation. In contrast, no significantly different Dopa or O-Methyldopa levels are found within the group of patients treated with L-Dopa alone. These results are discussed in relation to some of the suspected mechanisms involved in Levodopa-induced dyskinesias.

Aged↗
PubMed1977

[Results of determination of plasma methoxydopa in parkinsonian patients with or without dyskinesia induced by L-Dopa].

Horary plasmatic dosages of Dopa and metabolites in 30 treated parkinsonian patients have shown that, within the group of patients treated with L-Dopa combined with an extracerebral decarboxylase inhibitor, highly significant by increased plasmatic O-methyl-dopa levels can be found in patients with dyskinesias compared with those without dyskinesias. On the contrary, in these two subgroups of patients, plasmatic Dopa levels are not significantly different. By comparing some favoured Dopa and O-methyl-dopa levels between these two subgroups of patients, it seems more likely, that the elevated plasmatic O-methyl-dopa levels are due to an progressive accumulation on of its compound than to an excessive formation from Dopa.

Aged↗
PubMed1976

[Anatomoclinical and angiographic study of a case of disseminated thromboangiosis with predominant cerebral manifestations].

The authors describe the case of a patient of 22 with hypertension and livedo reticularis who, after presenting with a left brachial monoparesis became progressively demented over a period of five years and died at the age of 27 from a cerebro-meningeal haemorrhage. Angiographically, diffuse distal obliteration of the cerebral arteries was seen with deep networks of the moyamoya type involving the lenticulostriate arteries; similar changes were present in the upper left limb. Histopathological investigations showed obliterative thromboangiitis affecting not only the cerebrum, the brain stem and the cerebellum, but also the viscera. Analysis of this case and consideration of the theoretical possibilities leads the authors to urge that thromboangiosis together with its cerebral manifestations should be considered a nosological entity.

Adult↗
PubMed1975

[Familial form of cutaneous epitheliomatosis with complex neurological characteristics similar to hereditary spinocerebellar degeneration. Apropos of 4 cases including one case with anatomo-clinical description].

The authors report an observation in which four siblings were affected by both multiple cutaneous epitheliomatosis and complex but relatively stereotyped neurological disorders. Clinically, the main syndrome was cerebello-spinal ataxia with involvement of the anterior horns of the spinal cord with less marked pyramidal and extra-pyramidal features. Neuropathological examination of one of the cases revealed lesions of essentially cerebello-spinal degeneration suggestive of Menzel's disease. The possible connection between the neural and cutaneous lesions is discussed. All the various etiological categories possible have been ruled out; not one being entirely satisfactory, except for the very broad category of genetic neuro-dermatoses.

Adult↗
PubMed1975

[Sylvian stenosis with networks of the Moya-Moya type. Anatomo-clinical observation].

The authors report an angiographic observation, where a stenosis of the left middle cerebral artery, with Moya-Moya networks, is described. The anatomical study has shown an atresy of the middle cerebral artery, and has confirmed the hypothesis of a supplying role played by the Moya networks. Most of their anatomical findings are in agreement with a malformative aspect, which is speculated by the authors to be related to the failure, at the embryon level, of a good development of the middle cerebral artery; in this way, Moya might represent the remaining features of primitive plexiform networks. From this particular anatomical observation, the authors discuss some nosological problems and propose the hypothesis of several groups, which may be related to the moment when the stenosis is suspected to occur.

Arterial Occlusive Diseases↗