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Biomedical subjects

A Auzeby

Publications and source records attributed to A Auzeby.

15 recordsLinked to original sources
PubMed1996

Acute exposure to 50 Hz magnetic field does not affect hematologic or immunologic functions in healthy young men: a circadian study.

Some epidemiological studies report a relationship between magnetic field exposure and such human diseases as leukemia and immune system disturbances. The few published studies on animals do not demonstrate field exposure-related alterations in hematologic and immune systems. The data presented here are part of a broader study designed to investigate the possible effects of acute exposure to a 50 Hz linearly polarized magnetic field (10 microT) on hematologic and immunologic functions. Thirty-two young men (20-30 years old) were divided into two groups (control group i.e., sham-exposed. 16 subjects; exposed group, 16 subjects). All subjects participated in two 24 h experiments to evaluate the effects of both continuous and intermittent (1 h "off" and 1 h with the field switched "on" and "off" every 15 s) exposure to linearly polarized magnetic fields. The subjects were exposed to the magnetic field (generated by three Helmholtz coils per bed) from 23:00 to 08:00 while lying down. Blood samples were collected during each session at 3 h intervals from 11:00 to 20:00 and hourly from 22:00 to 08:00. No significant differences were observed between sham-exposed (control) and exposed men for hemoglobin concentration, hematocrit, red blood cells, platelets, total leukocytes, monocytes, lymphocytes, eosinophils, or neutrophils. Immunologic variables [CD3, CD4, CD8, natural killer (NK) cells and B cells] were unaltered. To our knowledge, this study is the first to document the effects of a 50 Hz magnetic field on the circadian rhythm of human hematologic and immune functions, and it suggests that acute exposure to either a continuous or an intermittent 50 Hz linearly polarized magnetic field of 10 microT, at least under the conditions of our experiment, does not affect either these function or their circadian rhythms in healthy young men.

Adult↗
PubMed1990

Cortisol and cortisone production in rat and mouse adrenal incubations.

The presence of 17 alpha-hydroxylase in rodent adrenals is debated. The presence in blood of mice of 11-deoxycortisol together with the absence of cortisol is well known. We demonstrated here the in vitro synthesis of 17 alpha-hydroxyprogesterone and cortisol from [3H]progesterone in rat and mouse adrenals. We have shown that these syntheses represented 45 and 28% of those of 11-deoxycorticosterone and corticosterone, respectively, from progesterone. These data clearly suggest the presence of a 17 alpha-hydroxylase activity in vitro in these rodents adrenals. In addition, a noticeable synthesis of cortisol (0.87-1.57% per mg tissue, i.e. 52-64% per incubation flask) from 11-deoxycortisol was also observed and was inhibited by 0.1-0.3 mumol of Metyrapone and SKF 12185. These results allow to underline that the adrenals of rat and mouse, two species commonly used in laboratory experiments, may be used for in vitro investigations on cortisol metabolism from exogenous radioactive precursors.

Adrenal Cortex Hormones↗
PubMed1989

Lack of effect in vivo of clofibrate on adrenal steroid secretion.

Clofibrate inhibits the synthesis of adrenal steroids when administered in vitro. In the present study the effect in vivo of clofibrate on adrenal steroid secretion has been investigated. Basal levels of plasma progesterone, corticosterone, aldosterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, dehydroepiandrosterone sulphate and dehydroepiandrosterone, and their response to ACTH 1 mg im, were not reduced by chronic administration of clofibrate 2 g per day p.o. for 8 to 34 days to 6 hyperlipidaemic men.

17-alpha-Hydroxyprogesterone↗
PubMed1989

Urinary neopterin in pulmonary sarcoidosis. Relationship to clinical and biologic assessment of the disease.

Neopterin is a metabolite of guanosine-triphosphate, released in vitro by macrophages under the control of gamma-interferon and described as a marker of T cell activation in vivo. We have compared the urinary neopterin/creatinine ratio (mumol/mol) in patients with pulmonary sarcoidosis (n = 66), interstitial lung diseases other than sarcoidosis (nonsarcoid ILD, n = 35), and 45 normal control subjects. For the sarcoid population as a whole, urinary neopterin was higher (496 +/- 52 mumol/mol [mean +/- SEM]) than in control subjects (126 +/- 5 mumol/mol) (p less than 0.001). In patients with nonsarcoid ILD, urinary neopterin was frequently higher in granulomatous and/or lymphoproliferative diseases (hypersensitivity pneumonitis, tuberculosis, primitive Sjögren's syndrome, and malignant lymphomas) (781 +/- 193 mumol/mol, n = 10) but remained normal in other types of nonsarcoid ILD [( 163 +/- 14 mumol/mol, n = 25]: histiocytosis X, idiopathic pulmonary fibrosis, lung collagen-vascular diseases, diffuse neoplasms, pneumoconiosis; p less than 0.001 compared with sarcoidosis). We have also evaluated the relationship between urinary neopterin and the clinical or biologic markers currently used to assess sarcoidosis: alveolar lymphocytosis in lavage fluid (ALY), 67-gallium scan semiquantitative index (67Ga), or serum angiotensin-converting enzyme (SACE). Sarcoid patients with the highest urinary neopterin were those in whom mean values of these markers were the highest (p less than 0.05, all comparisons). Patients with positive markers (i.e., either clinical expression of sarcoidosis-ALY greater than 30%-67Ga greater than 20-SACE greater than 60 U/ml) had significantly higher urinary neopterin levels than did other sarcoid patients (p less than 0.05, all comparisons).

Adult↗
PubMed1988

[Specificity of CA 125 tumor marker. A study of 328 cases of internal medicine].

The sensitivity and specificity of CA 125 were evaluated retrospectively in 328 patients, some of them with several diseases, seen between January, 1985 and December, 1986. High levels of CA 125 were found in 110 assays performed in patients with solid tumour (43 cases), peritoneal, pleural or pericardial effusion (39 cases), infection (34 cases), malignant blood disease (3 cases) and various non-malignant and non-infective diseases (45 cases). High CA 125 levels were most frequently observed in patients with effusion. The frequency of cancer increased with the CA 125 titre. CA 125 levels were particularly high in ovarian, peritoneal and uterine carcinomas. It was higher in ovarian cancer than in other types of cancer and further elevated in the presence of effusion, irrespective of the primary cancer. All patients with ovarian carcinoma had ascites. The sensitivity of CA 125 was 59 per cent and its specificity 74 per cent in solid tumours and malignant blood diseases. The corresponding figures in solid tumours alone were 72 per cent and 75 per cent respectively. While there can be no doubt that CA 125 is valuable in the follow-up of patients with ovarian carcinoma, the clinical context and notably the presence of an effusion must be taken into account when asking for a CA 125 assay to evaluate the cause of an inflammatory syndrome or of an alteration of the general condition, since CA 125 levels may be raised in a wide variety of non-malignant diseases, and especially in effusions and infections. In this study, a CA 125 titre higher than 1,000 U/ml was always due to the presence of cancer; lower titres must be interpreted according to the clinical context and sometimes the course of the disease.

Adolescent↗
PubMed1987

Early rising or delayed bedtime: which is better for a short night's sleep?

The present study compares the effects on sleep and the subsequent period of wakefulness of delaying bedtime of 2 h or advancing rising time by 2 h in subjects clearly differentiated by morningness or eveningness in their circadian rhythms. Twelve young healthy good sleepers, six morning types (MT) and six evening types (ET), were selected. The data obtained from the second 24 h (night and day) with delayed bedtime (DB) and advanced rising time (AR) were compared with those obtained in the reference condition (R) with normal sleep schedules. Sleep was recorded polygraphically and rectal temperature was continuously monitored during the nights and during the day following the second night of each condition. Subjective estimations of alertness, performance tasks and urinary steroids were analysed. Early rising appeared to be more disturbing than a late bedtime. The second shortened night showed fewer characteristics of recovery sleep in AR than in DB. The decrease in self rated alertness was a function both of the type of condition (DB or AR) and of the morning-evening typology of the subject. The largest decrease was observed in AR and in the ET subjects. AR also resulted in the most pronounced decrease in performance tasks and in an increase in urinary 17 ketosteroids without changes in the 17 hydroxy-corticosteroids. The effects on rectal temperature were limited to short periods after bedtime in DB and rising time in AR.

17-Hydroxycorticosteroids↗
PubMed1987

Circadian rhythm in the membrane of circulating human blood cells: microviscosity and number of benzodiazepine binding sites. A search for regulation by plasma ions, nucleosides, proteins or hormones.

Circadian rhythms in both the number of peripheral type binding sites for benzodiazepines in platelet membranes and the microviscosity of the erythrocyte membrane were demonstrated in 7 healthy men. Neither variable appeared to be linked to each other, or regulated by the plasma concentrations of total or free cortisol, testosterone, potassium, magnesium, calcium, cAMP, cGMP or proteins or by the erythrocytic concentration of magnesium or potassium or by the plasma cAMP:cGMP ratio or by the ratio of intra-erythrocyte:plasma concentrations of potassium or magnesium. A highly significant negative correlation was found between the microviscosity of the erythrocyte membrane and the activity of the membrane-bound enzyme, methyltransferase I. Such a correlation was validated both on raw data and on 24 hr-means (r = 0.84; P less than 0.01). A circadian rhythm in the activity of this enzyme was also demonstrated. Moreover, a highly significant correlation was also found between plasma transcortin concentration (TRC) and microviscosity (r = 0.50, P less than 0.01), and between TRC and methyltransferase I activity (r = 0.61, P less than 0.01). Such findings may constitute clues towards the understanding of the regulation of the circadian rhythm in the fluidity of the red blood cell membrane in man and guide future steps with regard to the role of this rhythm upon the availability of drug binding sites at the cell surface.

Adult↗
PubMed1986

Decreased nocturnal plasma melatonin peak in patients with a functional alteration of the retina in relation with uveitis.

A functional alteration of the retina is present in patients suffering from uveitis. Because of the relation between the pineal gland and the retina we documented possible modifications of melatonin secretion in patients with uveitis. Plasma melatonin was assayed in 19 patients and 16 age-matched controls. Blood samples were drawn at the known high and low points of the circadian rhythm of the hormone, i.e. 02.00 and 11.00 h, respectively. We found that the nocturnal peak of plasma melatonin was greatly decreased (45%) in patients with uveitis. These data cannot be related to the impairment of retinal melatonin synthesis alone. The possibility exists that the decline of the nocturnal peak of melatonin we have reported is due to a pineal inflammation in patients with uveitis, as observed in the experimental autoimmune uveitis induced in rats by retinal S-antigen.

Adolescent↗
PubMed1986

Lack of circadian rhythm in plasma levels of 3,4-dihydroxyphenylethyleneglycol in healthy human subjects.

In order to investigate the possible existence of a circadian rhythm in plasma free and sulfate-conjugated 3,4-dihydroxyphenylethyleneglycol (DOPEG), the plasma levels of this metabolite (and for comparison, of melatonin and cortisol) were measured in seven healthy volunteers at 4-h intervals over a period of 24 h. Plasma concentrations of melatonin and cortisol showed distinct diurnal variations with acrophases at 2.5 h and 8.5 h, respectively. In contrast, plasma free DOPEG levels were relatively stable over the 24-h period studied. Sulfate-conjugated and free + sulfate-conjugated DOPEG levels showed a slight, non-significant increase in the early afternoon. These results indicate that in contrast to plasma 3-methoxy 4-hydroxyphenylethyleneglycol, plasma free and conjugated DOPEG levels do not exhibit a circadian rhythm.

Adult↗
PubMed1986

Differences between young and elderly subjects in seasonal and circadian variations of total plasma proteins and blood volume as reflected by hemoglobin, hematocrit, and erythrocyte counts.

Circadian and seasonal rhythms in total plasma proteins were documented in healthy young men (around 24 years old), and in elderly subjects (both sexes), including senile-dementia patients in their eighties. The concentration of plasma proteins within a given group changed predictably (7-13%), depending on the hour of sampling and the season. Concentrations decreased noticeably around 04:00 h, then peaked around 08:00 h (shortly after waking). The 24-h mean concentrations of total plasma proteins were lower in the elderly groups than in the young men. But the seasonal variations of the 24-h mean values were strikingly larger in the elderly groups (7-8 g/L) than in the young men (2-5 g/L). Moreover, the circadian profiles of plasma proteins differed from the profiles of hematocrit, hemoglobin, and erythrocyte counts. Evidently, circadian variations of blood volume may not be the only element accounting for the variations of plasma protein concentrations. We suggest that the rhythms in plasma protein concentrations be taken into account when reference values are set. Circadian and seasonal variations in plasma proteins may also significantly affect the transport and binding of drugs, especially in the aged.

Adult↗
PubMed1984

11 beta-Hydroxy-11-ketosteroids equilibrium, a source of misinterpretation in steroid synthesis: evidence through the effects of trilostane on 11 beta-hydroxysteroid dehydrogenase in sheep and human adrenals in vitro.

Trilostane is known as an inhibitor of 3 beta-hydroxysteroid dehydrogenase. Conflicting data published on this drug led us to look for the effects of 0.02 to 0.5 mM of trilostane on the in vitro steroid synthesis in sheep adrenals and human adrenals (Cushing's or Conn's syndrome) in the presence of an NADPH-generating system. The synthesis of 4-androstenedione, 11 beta-hydroxyandrostenedione and 11-ketoandrostenedione were studied either from dehydroepiandrosterone or 4-androstenedione or 11 beta-hydroxyandrostenedione. The synthesis of 11-deoxycortisol, cortisol, cortisone, 4-androstenedione, 11 beta-hydroxyandrostenedione and 11-ketoandrostenedione were studied either from 17-hydroxyprogesterone or 11-deoxycortisol or cortisol. This study showed that trilostane inhibited 3 beta-hydroxysteroid dehydrogenase whereas it had no effect on 21-, 11- and 17-hydroxylase. Trilostane was responsible for an increased 11 beta-hydroxysteroid dehydrogenase activity in vitro, resulting in low yields of cortisol and 11 beta-hydroxyandrostenedione, and high yields of cortisone and 11-ketoandrostenedione. This unexpected effect of trilostane allowed us to show that erroneous conclusions (in this case: pseudo inhibition of 11 beta-hydroxylase) can be drawn if all the metabolic pathways from a determined precursor are not exhaustively documented when studying the effects of drugs on steroid synthesis in vitro. The decrease of cortisol synthesis by trilostane may thus be related to the effects of the drug on both 3 beta-hydroxysteroid-dehydrogenase (inhibitory effect) and 11 beta-hydroxysteroid-dehydrogenase (stimulatory effect). This latter effect was found to be species-dependent.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1983

Experimental evidence for biosynthesis of steroids in metastatic tissue originating from a primitive adrenocortical carcinoma.

1. Cortisol, cortisone, 11-deoxycortisol and deoxycorticosterone were synthesized in large amounts in vitro by a metastatic tissue from an adrenocortical carcinoma. 2. Both 11 beta- and 21-hydroxylase were very active. 3. A secreting metastasis can be thus responsible for a biological relapse. 4. A metastasis originating from another secreting adrenocortical carcinoma was found to be non-secreting.

Adrenal Cortex Neoplasms↗
PubMed1979

Glucocorticoid and mineralocorticoid pathways in two adrenocortical carcinomas: comparison of the effects of o,p'-dichlorodiphenyldichloroethane, aminoglutethimide and 2-p-aminophenyl-2-phenylethylamine in vitro.

The synthesis of glucocorticoids and mineralocorticoids in vitro was studied in an adrenocortical carcinoma after alblation from an 11.5-year-old boy. This patient had been unsuccessfully treated with high doses of o,p'-dichlorodiphenyldichloroethane (o,p'-DDD) and aminoglutethimide. These in-vitro results were compared with those obtained with another adrenocortical carcinoma removed from a 26-year-old woman who had received no preoperative treatment. The sensitivity of these adrenocortical carcinomas to o,p'-DDD, aminoglutethimide and 2-(p-aminophenyl)-2-phenylethylamine (SKF 12185) was investigated. Synthesis of cortisol (47%) and corticosterone (45%) in control incubations showed that 11 beta-hydroxylase activity was not affected by the treatment. This explains the raised level of plasma cortisol in the treated child. All three compounds inhibited both 11 beta-hydroxylase and 18-hydroxylase activities up to 95%, depending on the inhibitor. This study shows (a) an inhibitory effect of o,p'-DDD on the steroidogenesis of an adrenocortical carcinoma in vitro, an effect not previously reported in man or laboratory animals, and (b) the in-vitro efficacy of o,p-DDD and aminoglutethimide on corticosteroidogenesis by a carcinoma unresponsive to treatment in vivo. This discrepancy between data obtained in vivo and in vitro could possibly be explained by either an insufficient ratio of ingested dose: tumour mass, or a malabsorption of the drugs in this patient.

Adrenal Cortex Neoplasms↗