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Biomedical subjects

A Bonardet

Publications and source records attributed to A Bonardet.

At least 19 recordsLinked to original sources

Spontaneous in vitro anti-human immunodeficiency virus type 1 antibody secretion by peripheral blood mononuclear cells is related to disease progression in zidovudine-treated adults.

As part of a continuous search for surrogate markers of therapeutic efficacy in AIDS, spontaneous in vitro production by peripheral blood mononuclear cells of antibody to human immunodeficiency virus type 1 (HIV-1) was investigated in 50 HIV-1-infected adults. It was independent of CD4+ cell counts, p24 antigenemia, serum beta 2-microglobulin concentration, and clinical status of the patients. The effect of zidovudine on this antibody secretion and the appearance of signs or symptoms of HIV-1 disease progression were evaluated in 20 patients over 24 weeks. Anti-HIV-1 antibody secretion decreased significantly (P = .002) as of the first month of zidovudine treatment only in the 13 HIV-1-infected patients without disease progression. This is earlier than the occurrence of variations in CD4+ cell count and serum beta 2-microglobulin concentration. These results suggest that in vitro antibody production could be a surrogate marker for evaluation of the in vivo antiretroviral efficacy of zidovudine, even in p24 antigen-negative patients.

Adult

Metabolism of cyclosporine after orthotopic liver transplantation.

The aim of this work was to determine whether the extensive metabolism of cyclosporine, acquired in a donor by treatment with an inducer of cytochrome P450 3A (P450 3A) (cyclosporine oxidase), was transmissible to the recipient by orthotopic liver transplantation. For this purpose, male Wistar rats were divided into five groups including: control animals (group C), animals treated with dexamethasone (an inducer of P450 3A, 50 or 300 mg/kg/day, for 4 days, group D), animals transplanted with the livers of control rats (group G) or with the livers of dexamethasone-induced rats (group GD), and animals treated with beta-naphthoflavone (an inducer of P450 1A, group B). All animals received a single i.v. dose of 10 mg/kg cyclosporine 24 hr after either the last dose of inducer or the transplantation. For each group of animals, the area under the curve (AUC) of cyclosporine was calculated from the curves of blood cyclosporine levels (by radioimmunoassay) against time; liver microsomes were assayed for cyclosporine oxidase activity by HPLC, erythromycin demethylase and P450 3A level by western blot with specific anti-P450 3A antibodies. The decrease in the AUC in groups D and GD with respect to C and G was correlated with increased level of P450 3A (4-5-fold with respect to control) as well as of microsomal cyclosporine oxidase. In addition, cyclosporine oxidase activity of liver microsomes was specifically inhibited by anti-P450 3A antibodies and troleandomycin. The animals in group B did not exhibit increased metabolism of cyclosporine either in vivo or in vitro. We conclude that: (1) cyclosporine is predominantly oxidized in the rat liver by a form of P450 from the 3A subfamily; (2) the extensive metabolism of cyclosporine acquired by donor rats after treatment with dexamethasone is transmissible to the recipients through orthotopic liver transplantation.

Animals

[Evaluation of the size of thrombolysed myocardial infarction by serum myosin determination].

The prognosis of myocardial infarction is very dependent on the size of the infarct. The measurement of the infarct size after thrombolysis remains difficult despite the large number of methods available, all of which have drawbacks. This parameter is however essential to assess prognosis and the efficacy of thrombolytic therapy. Serum beta heavy chain myosin determination is a recently introduced method of evaluating infarct size; there are relatively few published studies, especially concerning post-thrombolytic patients. A prospective study was undertaken in 40 patients (37 men and 3 women: average age 55.6 years) with a primary myocardial infarction treated by thrombolysis. Myosin levels (peak and area under curve of 5 samples in 10 days) were compared with other methods of assessing infarct size: electrocardiogram (number of leads with Q waves, ST segment analysis), cardiac enzymes (peak and release integrals of CK abd LDH), contrast ventriculography (segmental asynergy score, ejection fraction), coronary angiography and resting MIBI myocardial scintigraphy. The peak and integral of myosin release correlated well with the other methods (p < 0.01): a correlation was particularly apparent between the integral of myosin release and MIBI scintigraphy scores (r = 0.77, p < 0.001). Complex myosin release kinetics were observed significantly more often in patients with large infarcts (p < 0.01) or in those with occlusion of the artery responsible for infarction at coronary angiography on the 6th day (p = 0.001). In conclusion, with 5 blood samples over a 10 day period, it is possible to estimate the infarct size after thrombolysis in everyday cardiological practice: this method could help identify high risk subjects (complex kinetics of myosin release and high peak myosin levels) and also could be used to assess efficacy of thrombolytic therapy in large scale trials.

Adult

[Cyclosporin A metabolism and induction of cytochrome P-450 in orthoptic hepatic transplantation in rats].

The aim of our study were 1) to establish that cyclosporin (CsA) metabolism was correlated with the rate of cytochrome P4503A (cyt.) in Wistar rats induced with dexamethasone (Dex.), 2) to demonstrate that the induction of cyt. with Dex. in liver "rat donor" was transmissible to "recipient rat" after liver transplantation. Sixty rats were divided in 5 groups. In group T, a single dose of CsA (10 mg/kg) was administered intravenously in 10 rats; in group D, 10 rats were treated with Dex (300 mg/kg daily for 4 days) and then received CsA as above; in group BN 5 rats were treated with beta-naphthoflavone. Thirty five rats underwent a liver transplantation either from "non induced donors" (group G, n = 11) or from "induced donors with Dex." (group GD, n = 24) followed by CsA injection the next day. For each rat, CsA plasma levels were determined by radioimmunoassay in 6 samples. Liver microsomes cyt. from samples of the liver of donor rats (group G and GD) or after sacrifice (group T, D, BN) were quantitated by immunoblot analysis and estimated from densitometric analysis of the blot. Mean maximal plasma concentration (Cmax) were 2,822 +/- 997 ng/ml in group T, 1,447 +/- -458 ng/ml in group D, 2,685 +/- 1,383 ng/ml in group G, 1,337 +/- 713 ng/ml in group GD and 3,094 +/- 685 ng/ml in group BN. Considering the Cmax and the ASC (area under curve), there was a significant difference between all groups and separately between groups T and D, G and GD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Testosterone secretion is severely impaired after hepatectomy in rat, dog and man.

In 90%-hepatectomized rats, the plasma testosterone level (0.34 +/- 0.07 ng.ml, mean +/- SEM) is significantly lower (P less than 0.001) than in sham operated male rats (1.7 +/- 0.26 ng.ml, mean +/- SEM). In dogs, after 90% hepatectomy, the mean plasma testosterone concentration fell to 1/10 of the plasma testosterone level measured in sham operated animals either 24 or 72 h after surgery. In hepatectomized men, plasma testosterone is markedly decreased in contrast to what is observed after duodeno-pancreatectomy performed under the same conditions of anesthesia. These results suggest that 90% hepatectomy severely alters the Leydig cell function.

Animals

[Prolonged functional disturbance of prolactin secretion after surgery under neuroleptanalgesia].

Plasma level of prolactin and its response to the injection of haloperidol were measured in nine women before and after elective gynecological surgery under neuroleptanalgesia using dextromoramidedroperidol combination. The day before the operation, the injection of haloperidol 0.25 mg intramuscularly increases the concentration of PRL by 5.4 +/- 1.9 mg/ml, while this response is completely abolished the day following the operation. Two days later, a tenfold increase in the dose of haloperidol (2.5 mg I.M.) is necessary to obtain a PRL response that equals that observed pre-operatively (5.8 +/- 1.2 ng/ml). The low plasma levels observed 24 and 48 hours post-operatively compared to the pre-operative level, illustrate a prolonged functional disturbance of the secretion of PRL.

Adult

Increase in sleep related GH and Prl secretion after chronic arginine aspartate administration in man.

Arginine aspartate was administered orally (250 mg/dg/day) for one week to 5 healthy male human volunteers aged 20-35. After this period, the 24 h patterns of growth hormone (GH) and prolactin (Prl) secretion were determined by radioimmunoassay on blood samples withdrawn every 20 min and correlated with the polygraphic recordings of electroencephalogram, electromyogram and electrooculogram. the results were compared to data obtained in identical conditions with the same subjects but after a week of placebo administration. In all 5 subjects the slow wave sleep related GH peak was about 60% higher after a week of arginine aspartate administration than in the control period, with individual changes of +24, +25, +42, +47 and +162%. The nocturnal mean plasma Prl of each subject was higher after arginine aspartate than before. The nocturnal rise of plasma Prl increased from a mean value of +21.5% during the placebo period to +95% at the end of the arginine aspartate treatment. These hormonal modifications were not accompanied by any detectable alteration of sleep organization and specially of the slow wave sleep pattern, suggesting a direct neuroendocrine action of the drug.

Adult

[Decrease in BSP clearance during epidural anesthesia at a constant flow rate. Clinical implications].

The fractional clearance K1 of bromsulphthalein was measured in twelve surgical patients at an interval of a least 48 hours. The first measurement was performed pre-operatively and the second postoperatively 24 hours after the operation, whilst the patients were receiving analgesia by the epidural injection of lignocaine at a constant flow rate. Between the two determinations there was a fall in BSP clearance of 25 +/- 11 p. 100 (range: -8 and -40 p. 100) P less than or equal to 0.0001. The clinical implications are discussed on the basis of concrete examples.

Adult

[Comparison of postoperative blood levels of prolactin and somatotropin after two methods of anesthesia].

Prolactin and somatotrophin were measured during the postoperative period in two series of 15 patients after gynaecological surgery. Samples were collected for four days at the same times during the 24 hours period. The anesthetic given in the first group was a neuroleptanalgesia of dextromoramide-droperidol type followed by postoperative analagesia using a noramidopyrine compound. In the second group, epidural anaesthesia was given, followed postoperatively by the injection of lidocain at constant rate interrupted between the final two samples. In the neuroleptanalgesia group, from a basal levels of 11 micrograms.l-1, prolactin rose to 22 micrograms.l-1 on the evening after surgery (p less than 0.001) to subsequently stay on a plateau between 6 and 8 micrograms.l-1 (p less than 0.025 to p less than 0.005). From a basal level of 2.8 micrograms.l-1, somatotrophin rose to 9 micrograms.l-1 (p less than 0.05) then fell progressively from 7.5 to 2 micrograms.l-1 (NS on D1, D2, D3). In the epidural group, from a basal level of 13.5 micrograms.l-1, prolactin rose to 23 micrograms.l-1 on the evening after surgery (NS) to fall sharply on D1 to 5.6 micrograms.l-1 (p less than 0.01) and then follow a plateau on D2 and D3 of the order of 11 to 12 micrograms.l-1 (NS). From a basal level of 1.9 micrograms.l-1, somatotrophin rose to 10 micrograms.l-1 (p less than 0.001) to fall again to 4.5 micrograms.l-1 on D1 (p less than 0.01) and to 2 micrograms.l-1 on D2 and D3 (NS). Comparison of these two groups showed a difference only on D2 with regard to somatotrophin (p less than 0.05) and on D2 and D3 with regard to prolactin (p less than 0.025 and p less than 0.05). These results are discussed. They do not indicate any fundamental difference in the endocrine response to aggression in relation to the two types of anaesthetic studies.

Anesthesia

[Prolactin secretion during sleep at puberty. Preliminary results (author's transl)].

Plasma prolactin was measured in six normal boys, during night sleep, with simultaneous recording of EEG for determination of the various stages of sleep. Peaks of prolactin appear clearly during cycles of rapid sleep: in prepuberty, the average of night peaks of prolactin is higher than that in post-puberty subjects. These results suggest indirectly, a participation of prolactin in prepuberty adrenal maturation.

Adolescent

[Nycterohemeral variations of growth hormone and prolactin in 6 Parkinson's sufferers treated with bromocriptine (author's transl)].

Secretions of GH and of PRL studied over a period of 24 hours in 6 untreated Parkinson's patients showed slight changes. The normal secretion of PRL in the female shows no nocturnal increase in the male. The secretion of GH linked to sleep is identified in the male and not in the female. These variations related to sex are interpreted as an increase in those normally found in the adult and facilitated by age. Bromocriptine given continuously at a dose of 10 to 20 mg/day for periods of 20 days to 6 months, results in suppression or a marked decrease in the 24-hour secretion of PRL. It has virtually no effect upon the secretion of GH. These results show that the dopaminergic regulation of PRL is preserved in Parkinson's disease.

Aged

[Plasma prolactin levels in normal children from birth to adolescence].

Plasma prolactin levels were determined by an homologous radio-immuno assay in normal children: in cord blood, at the first day of life, during childhood and along puberty. 1. In both sexes, there is a very important secretion of prolactin during the neonatal period. 2. Longitudinal studies make obvious a different pattern of plasma prolactin in boys and in girls at puberty.

Adolescent

[Secretions of GH, FSH and LH during sleep of the normal child and the child with retarded growth].

In normal children the major GH release begins during NREM sleep of first cycle. At puberty secretion of gonadotropins is enhanced and secretion of LH occurs with the same periodicity as the sleep cycles. Two groups of dwarfish are seen: the first lacks both GH secretion during sleep and the increase of gonadotropins at puberty. The second group exhibits GH, LH and FSH secretion patterns similar to normal children. Study of secretion patterns of GH, FSH and LH during sleep in children can document the degree of maturation of the hypothalamic pituitary hormonal system.

Adolescent