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Biomedical subjects

A Steiger

Publications and source records attributed to A Steiger.

At least 109 records · Page 6Linked to original sources
PubMed1984

ACTH and multisteroid responses to corticotropin-releasing factor in depressive illness: relationship to multisteroid responses after ACTH stimulation and dexamethasone suppression.

One hundred micrograms of ovine-corticotropin releasing factor (o-CRF) was administered intravenously to eight unmedicated patients with severe endogenous depression. Responses of immunoreactive (ir)-ACTH and the adrenal glucocorticosteroids corticosterone (B), 11-deoxycortisol (S), cortisol (F) and cortisone (E) were measured and compared with those following synthetic corticotropin stimulation and dexamethasone suppression. A comparative evaluation of the three pituitary--adrenal function tests suggests that hypersecretion of ir-ACTH and adrenal corticosteroids (B, S, F, and E) in depression reflects a central dysfunction rather than an altered responsiveness of the pituitary or adrenal glands. The data illustrate that the o-CRF paradigm is a valuable instrument to further support the hypothesis that a limbic--hypothalamic overdrive is the basic mechanism underlying exaggerated adrenocortical output in the endogenous subgroup of depressed patients.

17-Hydroxycorticosteroids↗
PubMed1984

Mean 14.00-17.00 h plasma cortisol concentration and its relationship to the 1 mg-dexamethasone suppression response in depressives and controls.

Three-hour cortisol-profiles and cortisol responses to a 1 mg dose of dexamethasone were recorded in 31 depressed patients and nine controls. The data indicate that the likelihood of detecting non-suppressible cortisol concentrations after dexamethasone is significantly increased in depressed patients with a hypersecretion of cortisol. However, a considerable subsample of normosecretors shows abnormal DST results. Conversely, hypersecretion is often associated with dexamethasone suppression. In this study a 1 mg-DST did not reflect the adrenocortical activity with ultimate accuracy. Therefore any attempts which correlate psychopathological or biological data with pituitary-adrenal activity and use a DST-result as measure are criticizable . Data derived from volunteers illustrate that medical factors such as weight-loss, steroid-containing contraceptives and sleep deprivation can make a pituitary-adrenal activity test ambiguous.

Adult↗
PubMed1981

Structural alterations of tapetal cells in the retina of cats induced by prolonged treatment with chloroquine.

Cats were treated with high doses of chloroquine for one year during which the ocular fundus was periodically examined. After completion of the treatment, the tapetal cells were investigated by light and electron microscopy. Prolonged treatment with the retinotoxic drug chloroquine reduced the light reflection of the fundus, and examination by light and electron microscopy revealed a destruction of the rod-like structures in the cytoplasm of the tapetal cells.

Animals↗
PubMed1981

Lack of correlation between melanin affinity and retinopathy in mice and cats treated with chloroquine or flunitrazepam.

Flunitrazepam (Rohypnol, Roche, Basel, Switzerland), which is similar to chloroquine, has an affinity to melanin in retinal cells. However, in contrast to chloroquine, it does not induce structural alterations in these cells or in adjacent tissues of pigmented mice and cats even after treatment for 6 and 12 months with respectively, 2000-times (mice, or 130-times (cats) the effective human daily dose. Treatment with chloroquine (with a dose similar to that used in human anti-rheumatic therapy) over the same period, resulted in the appearance of numerous membranous cytoplasmic bodies in the retinal ganglion cells of mice and cats. In addition, in cats, an augmentation of lysosomal structures in the pigment epithelium, chiefly in the melanin-free region, and destruction of the tapetal cells were observed. Moreover, the pigment epithelium with the highest concentration of melanin was unaffected in mice and only slightly affected in cats. It was concluded that the retinotoxic effect of chloroquine is not the result of its affinity to melanin-containing tissues. Consequently, the affinity to melanin-containing cells per se is not sufficient to class a substance as potentially harmful to vision.

Animals↗
PubMed1981

[Pathologico-anatomical and histological studies with special reference to the tracheal mucus membrane of calves following exposure to an aerosol disinfectant (Wofasteril)].

Various morphological methods were used in examining calves, with the view to determining the action of Wofasteril, an aerosolic disinfectant, on their organism, particularly on their trachea. Calves were found to differ from animals with pneumonia and other pulmonary inflammations, in that no transformation and quality change occurred to the mucus of their tracheal goblet cells in response to peracetic acid. Pathologico-anatomic and histological alterations in various organs were not attributable either to the disinfectant. A contribution is made to a more general description of the normal tissue structure, in that data are presented on the length, width, and number of goblet cells in the trachea of calf.

Acetates↗
PubMedDate not supplied

Functional properties of deoxycorticosterone and spironolactone: molecular characterization and effects on sleep-endocrine activity.

Adrenal steroid hormones are capable of interfering with a variety of behavioral phenomena including sleep. The mechanisms appear to involve effects at the cell membrane as well as nuclear actions mediated by intracellular mineralo- and glucocorticosteroid receptors (MR and GR). We employed the MR agonist deoxycorticosterone (DOC) and the MR antagonist spironolactone (SP) to study the role of MRs in the regulation of human sleep. We also tested whether the effects of DOC upon the sleep EEG and nocturnal hormone secretion (growth hormone and cortisol) are compatible with those predicted for its major metabolite tetrahydro-DOC (THDOC): electrophysiological and animal experiments had suggested that THDOC would act as a hypnotic via positive modulation of the GABAA receptor. Because neither DOC nor SP affected the sleep EEG substantially, the involvement of MRs in the regulation of sleep needs further study. The sleep-endocrine data showed a suppressive effect of DOC upon plasma cortisol concentrations and an earlier occurrence of nocturnal GH maxima, which can be plausibly explained by GR or sigma receptor-mediated effects. Molecular characterization of DOC and SP confirmed a relatively strong effect of DOC upon transactivation via MR and no effect of SP on the GR-mediated transcription rate. In addition, the possibility that a low dose of the mineralocorticoid DOC may serve as a prodrug for the potential hypnotic THDOC is not supported by the current data.

Adult↗
PubMedDate not supplied

Growth hormone-releasing hormone (GHRH)-induced effects on sleep EEG and nocturnal secretion of growth hormone, cortisol and ACTH in patients with major depression.

Studies in normal human subjects and animals suggest that the neuropeptide growth hormone-releasing hormone (GHRH) is a common regulator of the sleep EEG and nocturnal hormone secretion. In healthy volunteers GHRH prompts an increase in the amount of slow wave sleep (SWS) and in growth hormone (GH) secretion and blunting of cortisol release. Inhibition of GHRH may contribute to sleep-endocrine aberrances during depression. We tested the effects of pulsatile application of 4 x 50 micrograms GHRH on the sleep EEG and simultaneously investigated nocturnal hormone secretion in 10 inpatients (four females, six males) with the acute episode of major depression. In contrast to the effects of placebo, GH secretion increased distinctly and rapid-eye-movement (REM) density decreased during the second half of night. No other significant changes in sleep-endocrine activity, including SWS, cortisol and ACTH secretion, could be observed. We assume that hypothalamic-pituitary-adrenocortical system activity and slow wave sleep are inert to the influence of GHRH during acute depression. Cortisol and ACTH remained unchanged even in a subsample of five younger (aged 19-28 years) patients. This observation is in contrast to our recent finding that cortisol secretion is blunted in young normal volunteers after GHRH. But on the other hand, GHRH is capable of stimulating GH and inducing a decrease in REM density in these subjects.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Multisteroid analysis after DST in depressed patients--a controlled study.

111 consecutively admitted in-patients with a depressive syndrome received a dexamethasone suppression test (DST) after all known factors which might confound the test results had been carefully excluded. Plasma concentrations of cortisol, corticosterone and dexamethasone were compared with several diagnostic evaluations (RDC, DSM-III, ICD-9) in a controlled study. The positive predictive value of nonsuppressed corticosteroid levels was only moderate for each diagnostic category. Diagnostic specificities were 84.6% for major depression, endogenous subtype (RDC), 71.2% for melancholia (DSM-III) and 86.8% for endogenous depression (IDC-9) when using a post-DST cortisol value above 50 ng/ml (5 micrograms/dl) as the referent value to define DST nonsuppression. Combined determination of cortisol and corticosterone as an index of dexamethasone-induced suppression raised the sensitivity rate considerably at the cost of the predictive value for major diagnostic categories. Dexamethasone plasma levels were reciprocally correlated with cortisol levels and neglect of samples with low plasma dexamethasone contents improved the diagnostic performance for endogenous depression according to RDC and ICD-9, but not for DSM-III melancholia. Although it would be speculative to suppose that the observed low dexamethasone levels are involved in DST nonsuppression, the present findings emphasize that multisteroid analysis which includes dexamethasone is important in future studies designed to explore the clinical utility of the DST.

Adult↗
PubMedDate not supplied

Sleep EEG and nocturnal secretion of cortisol and growth hormone in male patients with endogenous depression before treatment and after recovery.

The authors conducted a sleep-endocrine evaluation among 10 unmedicated male patients with major endogenous depression during their depressive episode and following full clinical remission and drug withdrawal. While abnormally high values for cortisol secretory activity normalized after return to euthymia, growth hormone release and characteristic disturbances of EEG sleep remained unchanged. Whether or not neuroendocrine and sleep EEG abnormalities, which are present in remission, are trait markers remains undecided until premorbid sleep-endocrine data are available.

Adult↗
PubMedDate not supplied

Effects of an ACTH/MSH(4-9) analog (HOE 427) on the sleep EEG and nocturnal hormonal secretion in humans.

The synthetic ACTH/MSH(4-9) analog HOE 427 ("ebiratide"), which is behaviorally the most potent ACTH-derived peptide but which is devoid of endocrine activity, was administered intravenously in a pulsatile mode 4 times (120 micrograms each) at 2200, 2300, 2400 and 0100 to study its effect on the sleep EEG and on concomitant hormonal secretion of cortisol and growth hormone. In comparison to placebo, the peptide produced signs of general activation associated with specific deteriorating effects on the quality of sleep. Sleep onset latency and intermittent wakefulness were increased, slow wave sleep was reduced, but only during the first 3 hours of the sleep period. The nocturnal secretory patterns of cortisol and growth hormone were unaffected by HOE 427. These effects are different from those reported in similar studies in which corticotropin-releasing hormone (CRH) was applied in humans, and they suggest that peripherally administered neuropeptides have specific nonendocrine behavioral effects.

Adrenocorticotropic Hormone↗