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Biomedical subjects

L Laurian

Publications and source records attributed to L Laurian.

At least 19 recordsLinked to original sources

Migration decisions among settler families in the Ecuadorian Amazon: the second generation.

The authors use survey data collected in 1990 from 418 household heads of recent settlements in the Ecuadorian Amazon to study the extent of and reasons for out-migration of the settlers' children. "Our research identifies the types and incidence of out-migration of young adults from settler households in the Ecuadorian Amazon, as well as the effects of individual and household-level factors of out-migration. Important gender differences in both the levels and patterns of migration and in the factors affecting migration decisions are documented."

Adolescent↗

Dexamethasone suppression of the calcitonin induced beta-endorphin, ACTH and cortisol secretion.

Our previous observations have shown that calcitonin (CT) stimulates beta-endorphin, ACTH, and cortisol secretion. In order to give further information on the supposed hypothalamic pituitary involvement in this effect, we studied the influence of dexamethasone on this stimulative influence of CT. Six healthy women aged 50-65 years were investigated. All the subjects received 100 U CT salmon (Sandoz) i.v. at 0800 (0 time). Plasma beta-endorphin, ACTH, and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassays. The same subjects were evaluated a second time, at the same intervals, when 1 mg dexamethasone was administered per os at 11 PM the previous night and CT i.v. at 0800 the next morning. Beta-endorphin, ACTH, and cortisol levels (mean +/- SEM) rose significantly after 100 U CT from 5.6 +/- 0.17 to 16.75 +/- 1.8 pmol/L (p less than 0.001); from 39.6 +/- 6 to 88.0 +/- 3.1 pg/ml (p less than 0.0001) (from 8.7 +/- 1.3 to 19.4 +/- 0.7 pmol/L); and from 13.1 +/- 1.6 to 23.8 +/- 3.0 micrograms/dl (p less than 0.0001) [374 +/- 45 to 680 +/- 85 nmol/L], respectively. Dexamethasone suppressed almost completely the stimulatory effect of CT beta-endorphin rose from 4.9 +/- 0.12 to 6.3 +/- 1.3 pmol/L (n.s.), ACTH from 38.6 +/- 5.1 to 42.6 +/- 6.2 pg/ml (n.s.) (from 8.5 +/- 1.1 to 9.4 +/- 0.9 pmol/L) and cortisol from 0.88 +/- 0.23 to 0.88 +/- 0.18 microgram/dl (n.s.) (from 25.1 +/- 6.5 to 25.0 +/- 5.1 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Antiserotonergic inhibition of calcitonin-induced increase of beta-endorphin, ACTH, and cortisol secretion.

In a previous study we observed that calcitonin increases beta-endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor). Fourteen healthy subjects, aged 30-60 years were investigated. All the subjects received 100 IU Salmon calcitonin Sandoz i.v. at 8 a.m. (time 0). Plasma beta-endorphin, ACTH and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at -30 min and calcitonin i.v. at time 0. beta-endorphin, ACTH and cortisol levels (Mean +/- SEM) rose significantly after calcitonin (peak value at 30-90 min) from 5.2 +/- 0.7 to 15.1 +/- 2.6 pmol/l; from 43.0 +/- 2.7 to 70.7 +/- 4.1 pg/ml and from 10.6 +/- 1.5 to 19.6 +/- 2.1 micrograms/100 ml respectively (p less than 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time -30 did not alter the response of beta-endorphin, ACTH and cortisol to calcitonin (infused at time 0). Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin. We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.

Adrenocorticotropic Hormone↗

Delayed brainstem auditory evoked responses in diabetic patients.

The incidence of subclinical central diabetic neuropathy is unclear due to difficulty in detecting latent alterations of central neural transmission process. The aim of this study was to evaluate a central neuroconductive mechanism in diabetics by brainstem auditory evoked responses (BAER). We found increased latencies of peaks I, III, V in diabetics as compared to control subjects. These BAER abnormalities were demonstrated in 62 per cent of insulin-controlled diabetics and in 33 per cent o patients treated by diet, or peroral drugs. No alterations in brainstem responses were observed in patients with latent diabetes. We did not find any correlation between the BAER abnormalities and the duration of the disease, the blood glucose level or the level of control of the diabetes.

Brain Stem↗

Primary tissue cultures of benign and malignant human thyroid tumors: effect of TSH.

Many thyroid carcinomas seem to be dependent upon the thyroid growth-promoting properties of the thyroid stimulating hormone (TSH). The purpose of the present investigation was to compare the in vitro effect of TSH on tissue cultures derived from malignant and benign thyroid tumors. The results indicate that TSH can affect the morphology and protein synthesis of primary tissue cultures derived from benign and malignant thyroid tumors differently. The addition of TSH to cultures derived from benign tumors resulted in a reorganization of follicle-like structures of the monolayer and in a reduction of protein synthesis. In contrast to this, monolayers derived from carcinomas of the thyroid were not able to reorganize and their protein synthesis was not inhibited in the presence of TSH. For a better understanding of TSH suppressive therapy, we suggest testing the influence of TSH on a large number of tissue cultures derived from benign and malignant tumors of the thyroid.

Culture Techniques↗

Delayed brainstem auditory evoked responses in experimental diabetes mellitus.

The brainstem auditory evoked responses (BAER) were utilized for the evaluation of central neural transmission in alloxan-induced diabetes in rats. The mean latencies of waves I, III, V and the interpeak latencies III-V and I-V were prolonged in diabetic rats as compared to the same rats before alloxan administration. The incidence of abnormal BAER was more frequent in the group of rats with severe diabetes (82 per cent) than in mildly diabetic animals (42 per cent). Our results may suggest the presence of a central neuropathy in experimental diabetes, which can be detected by the method of BAER.

Animals↗

Calcitonin induced increase in ACTH, beta-endorphin and cortisol secretion.

The response of ACTH, beta-endorphin and cortisol to calcitonin administration was investigated in 8 subjects with recent fractures of the vertebrae due to postmenopausal or senile osteoporosis (Ost) and in seven normal healthy controls (NC). A significant increase of the three hormones was observed in 13 subjects. The maximum increase was observed between 15 and 60 min.: the cortisol level (microgram/100 ml) rose from 14.3 +/- 1.9 to 24.8 +/- 3.2 (P less than 0.05) in Ost and from 7.7 +/- 0.6 to 21.7 +/- 1.7 (P less than 0.001) in NC, the beta-endorphin (pmol/l) from 5.8 +/- 0.6 and to 21.2 +/- 1.3 in OST (P less than 0.001) and from 5.9 +/- 0.4 to 21.9 +/- 4.5 (P less than 0.01) in NC and the ACTH levels (pg/ml) from 21.3 +/- 5.7 to 61.7 +/- 3.6 (P less than 0.001) in OST and from 30.0 +/- 6.2 to 58.8 +/- 7.5 (P less than 0.05) in NC. The results indicate a possible role of calcitonin in modulating the anterior pituitary function. It also suggests that the analgesic effect of calcitonin might be mediated by the increase of beta-endorphin. The possibility that this analgesic effect of calcitonin is due to its direct binding to the opiate receptors was excluded in the present study by in vitro binding assay.

Adrenocorticotropic Hormone↗

Observations on the chemical and physiological properties of urodiolenone, an urinary compound found in hypertension.

Urodiolenone is a substance that appears as the glucuronide in the urine of 1 in 3 hypertensive subjects. It is a potent inhibitor of Na+, K+-ATPase in kidney tissue of the guinea pig, as measured by cytochemical assay. Chemical and mass spectrometric evidence is presented, from which it is concluded that urodiolenone is a sesquiterpenoid substance, is a bicyclic enone with a vicinal diol side chain, and has molecular formula C15H24O3.

Female↗

Auditory brain stem response in experimentally induced hypothyroidism in albino rats.

In order to elucidate the relationship between the auditory function and the thyroid state, experiments were designed to study the effect of hypothyroidism on the onset of auditory brain stem response (ABR) in 26 adult myxedematous albino rats. A state of hypothyroidism was induced by daily oral administration of 6-N-propyl-2-thiouracil (PTU). In 23 out of 26 rats we found minor changes in the amplitudes of all ABR waves without any correlation with the rats' T4 variation. We noted a conspicuous, dynamic, and reversible change in the amplitude of the third wave (N3) of ABR which correlates directly with the thyroxin (T4) levels in the rats' blood. The electrophysiological finding in this report indicates a lesion in the auditory tracts in the brain stem but mainly in the second main relay station of the central auditory pathway, i.e., the superior olivary complex.

Animals↗

New clinical applications of the stapedial reflex.

Stapedial reflex data were obtained from 11 myasthenic, 18 hyperthyroid and six hypothyroid patients. Data were studied with respect to reflex threshold, amplitude and decay. Elevated threshold, decreased amplitude, and high and low frequency reflex decay were observed in myasthenic and hyperthyroid patients. Hypothyroidism merely increases stapedial reflex amplitude but causes no significant threshold or decay changes.

Adult↗

Changes in serum dopamine-beta-hydroxylase activity during cold pressor test in subjects with high and low basal activity of this enzyme.

Twenty-seven healthy subjects, eight with high levels, eight with low levels and eleven with intermediate levels of serum dopamine-beta-hydroxylase (DBH) activity, were investigated. Serum DBH activity and blood pressure were measured in their response to the cold pressure test (CPT). Plasma renin activity (PRA) was also estimated. Blood pressure, systolic and dyastolic, increased equally in the three groups. PRA did not change significantly throughout the test in any of the groups. Serum DBH activity increased significantly in the group with low initial levels. No significant changes were seen in the controls and in the group with high initial serum DBH activity. It is suggested that subjects with high basal serum DBH activity might have a genetically-determined high sympathetic tone and therefore would hardly respond to a mild stress like CPT; the opposite might be true for the subjects with low basal DBH activity levels.

Adolescent↗

Growth hormone response to L-dopa in the thinned obese.

The response of plasma growth hormone (GH) to 0.5 g L-dopa was studied in 17 obese nondiabetic subjects and in 6 normal-weight subjects, aged 16 to 46 yr. The test was repeated after the obese subjects were thinned 12 to 50 kg, either with a hypocaloric diet or by a jejunoileal shunt. All the obese subjects had a blunted response to L-dopa stimulation. Nine of the thinned obese continued to exhibit the same blunted GH response, while the other eight responded with a significant GH rise after L-dopa stimulation, although the increase was smaller than that in the controls. No correlation between the initial or final weight or the extent of weight loss and the response to L-dopa was observed. It is assumed that a hypothalamic underresponsiveness is responsible for the blunted response in the obese subjects and its persistence in some of the thinned obese.

Adolescent↗

Failure of naloxone to antagonize metoclopramide induced prolactin rise.

Seven subjects aged 21--54 years were investigated. Serum PRL and DBH were estimated before and at 30, 60, 90 and 120 min after the administration of 20 mg clopropamide. The same parameters were estimated a second time when 0.4 mg naloxone was associated. PRL level increased and DBH decreased in all the patients in both investigations and no significant differences between the two occasions were detected. It is suggested that probably the two substances do not act on identical receptors.

Adult↗

Selective IgA deficiency with multiple autoimmune disorders.

A case of an IgA deficient child who developed several autoimmune diseases namely, celiac disease, pernicious anemia, autoimmune thyroiditis and autoimmune thrombocytopenic purpura is reported; the possible connections and etiology of these phenomena is briefly discussed. Individuals with selective IgA deficiency should no longer be considered "normal".

Autoimmune Diseases↗

Low cortisol and growth hormone secretion in response to methoxamine administration in obese subjects.

To investigate the hypothalamic responsiveness in obesity, changes in the levels of plasma cortisol and growth hormone (GH) were studied in 11 obese and six normal-weight subjects after hypothalamic alpha-adrenergic stimulation with methoxamine, 20 mg i.v. To allow for dose/body weight differences, five additional obese subjects received 30 mg methoxamine. Plasma GH, cortisol, insulin, free fatty acid and glucose levels were determined during the 3-h infusion of methoxamine. The responses of cortisol and GH were reduced in the obese subjects as compared with the normal-weight subjects. No significant changes in plasma glucose, free fatty acids or insulin were observed in any of the groups. The reduced responses of plasma cortisol ang GH in the obese subjects are considered to be an expression of hypothalamic underresponsiveness, since the stimuli for the secretion of these hormones are at least partially controlled by an alpha-adrenergic mechanism.

Adult↗