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Biomedical subjects

S Solomon

Publications and source records attributed to S Solomon.

At least 271 records · Page 15Linked to original sources
PubMed1983

Human phosphoserine 31 corticotropin1-39. Isolation and characterization.

Two distinct forms of corticotropin1-39 (ACTH) were isolated and purified from an extract of three adult human pituitaries by reversed-phase chromatographic techniques. Structural studies indicated that the more polar form of ACTH was phosphorylated at serine residue 31. Approximately 30% of the ACTH was found in the phosphorylated form. A similar proportion of phosphorylated ACTH was observed in extracts of three pituitaries from human fetuses of 15, 17, and 20 weeks gestation. Phosphorylated and nonphosphorylated human ACTH1-39 were found to be steroidogenically equipotent using both an isolated rat adrenal cell bioassay and a cultured human fetal adrenal cell bioassay.

Adrenocorticotropic Hormone↗
PubMed1983

Impairment of memory function by antihypertensive medication.

This study describes a specific memory impairment in subjects taking either of two kinds of centrally active anti-hypertensive agents. Verbal memory impairment was present in hypertensive and normotensive patients taking methyldopa or propranolol hydrochloride, while hypertensive patients receiving only a diuretic did not show this deficit. Visual memory impairment was not seen in any of the groups tested. The majority of the subjects were unaware of their memory deficit, even when test results clearly revealed impairment. An earlier pilot study of 12 hypertensive patients receiving methyldopa or propranolol used a broad range of cognitive tests and also demonstrated impairment in verbal memory only, while other cognitive measures remained relatively unaffected.

Diuretics↗
PubMed1983

alpha-N-acetyl-beta-endorphin1-26 from the neurointermediary lobe of the rat pituitary: isolation, purification, and characterization by high-performance liquid chromatography.

The neurointermediary lobes from 190 rat pituitaries were homogenized in an acidic medium which inhibits peptidase activity and maximizes the solubilization of undamaged peptides. Octadecylsilyl-silica (ODS-silica) was used to extract the supernatant of the tissue homogenate. The ODS-silica eluate, now largely protein and salt free, was subjected to reversed-phase high-performance liquid chromatography (HPLC) employing 0.1% trifluoroacetic as counter ion. The column eluates were monitored for beta-endorphin immunoreactivity. Five immunoreactive components were observed. The most hydrophobic of these was repurified on the same HPLC column using 0.13% heptafluorobutyric acid as counter ion. Characterization of the purified peptide by gel permeation HPLC, amino acid analysis, and tryptic fragmentation indicated that it corresponded in structure to alpha-N-acetyl-beta-endorphin1-26. Amino acid analysis of the native peptide and its trypsin and carboxypeptidase fragments indicated that an alanyl residue occupies position 26. This finding is in contrast to the sequence predicted for the beta-lipotropin/corticotropin precursor by recombinant DNA techniques which suggests that the 26th residue of the beta-endorphin molecule should be valine.

Amino Acid Sequence↗
PubMed1983

Androstenedione-mediated inhibition of 11 beta-hydroxylation in monolayer cell cultures of fetal calf adrenals.

The possibility that the formation of androstenedione by fetal calf adrenal cells in culture is linked to their decreased ability to form cortisol and corticosterone was investigated. Fetal calf adrenal cells metabolise radioactive adrostenedione to two major products which coelute on thin layer chromatography with 11 beta-hydroxyandrostenedione and 11 beta-hydroxytestosterone. When the cells are incubated with 11-deoxycortisol or 11-deoxycorticosterone in the presence of androstenedione there is a dose dependant inhibition of cortisol and corticosterone formation. Further studies with progesterone showed an accumulation of 11-deoxycortisol and 11-deoxycorticosterone in cells incubated simultaneously with androstenedione. The results demonstrate that exogenous androstenedione can have dramatic effects on steroidogenesis in the fetal calf adrenal and suggest that the accumulation of androstenedione in the medium of cultured andrenocortical cells is responsible, at least in part, for the decreased formation of cortisol and corticosterone.

Adrenal Glands↗
PubMed1983

Effect of Transcendental Meditation versus resting on physiological and subjective arousal.

On four successive days, 10 highly trained and experienced meditators were asked to relax for 5 minutes, meditate for 20 minutes, and then relax for 5 minutes. In contrast, 10 other subjects who had no training or experience with meditation were asked to relax for 5 minutes, rest for 20 minutes, and then relax for 5 minutes. Physiological arousal (heart rate, skin resistance, respiration rate, systolic blood pressure, diastolic blood pressure) and subjective arousal (cognitive, somatic, relaxation) were measured throughout the experiment. Results indicated that (a) prior to meditating or resting, meditators tended to have higher heart rates and diastolic blood pressure than did nonmeditators, (b) meditation was associated with generally reduced arousal, but (c) while meditating, meditators did not evidence lower levels of arousal than nonmeditators did while resting. This investigation employed controls, which were not used in previous investigations, and the results place qualifications on previously reported results. The results have implications for the study of personality functioning, stress management, and psychotherapy.

Adult↗
PubMed1983

Gestational changes in the metabolism of progesterone by the fetal calf adrenal.

The metabolism of [3H]progesterone by the fetal calf adrenal was examined in homogenates and microsomal fractions of adrenals obtained from mid- or late gestational fetal calves. Throughout the course of gestation, there was no detectable difference in the formation of corticosterone from progesterone by adrenal homogenates. In contrast, cortisol production in these same homogenates increased 7-fold from 0.3-2.2% at the end of gestation. Similar results were obtained using microsomal fractions prepared from these homogenates: the 17 alpha-hydroxylation of progesterone (i.e. 17 alpha-hydroxyprogesterone and 11-deoxycortisol) increased from 0.7% to 26% at the end of gestation. The results suggest that the increased cortisol observed in the fetal circulation toward the end of gestation is the result of a rapid increase in the capacity of the fetal calf adrenal to form 17 alpha-hydroxycorticosteroids. The underlying mechanism for this change is discussed.

17-alpha-Hydroxyprogesterone↗
PubMed1983

Determination of plasma dexamethasone in the mother and the newborn after administration of the hormone in a clinical trial.

A RIA method is described for the measurement of dexamethasone in maternal, cord, and neonate plasma in a collaborative multicenter clinical trial to evaluate the efficacy of antenatal steroid therapy in the prevention of respiratory distress syndrome. The antiserum raised against dexamethasone-3-carboxymethyloxime-BSA conjugate was highly specific in that the endogenous steroids and 11-dehydrodexamethasone, a metabolite of dexamethasone, had a cross-reaction of less than 2.0%. Both pregnancy and cord plasma had to be purified by either gel filtration and/or paper chromatography. The overall recoveries of dexamethasone were 75.3 +/- 6.7% and 48.9 +/-6.7% for maternal and cord plasma samples, respectively. The intra- and interassay coefficients of variance for maternal plasma were 8.4% ad 9.1%, respectively, and for cord plasma were 11.9% and 10.9%, respectively. There was a good correlation between the dexamethasone values obtained by RIA when compared with those obtained by performance liquid chromatography in some cord plasma specimens. The recoveries of added dexamethasone and its metabolite by high performance liquid chromatography were also found to be good. The average maternal plasma dexamethasone level was 37 ng/ml 2 h after im injections of 5 mg dexamethasone phosphate every 12 h. The half-life of dexamethasone measured after the discontinuation of the drug was 216 min. Dexamethasone appeared too be cleared very rapidly from the circulation of the fetus and neonate. Because 11-dehydrodexamethasone was not present in significant amounts in the neonate, it was concluded that other factors in addition to the conversion of dexamethasone to its 11 dehydro metabolite were responsible for the rapid clearance of dexamethasone from fetal and neonatal circulation.

Antibody Specificity↗
PubMed1983

Regulation of vitamin D metabolism in normal human pregnancy.

The increasing serum concentrations of various hormones (PTH, PRL, estrogens, and human placental lactogen) are hypothesized to regulate 1,25-dihydroxyvitamin D [1,25(OH)2D] and possibly 24,25-dihydroxyvitamin D [24,25(OH)2D] production during pregnancy. We examined the correlation between the serum levels of 1,25(OH)2D and the pregnancy-related hormones in 25 normal pregnant women, followed throughout gestation and postpartum. Maternal serum levels of 1,25(OH)2D were high during the first trimester (mean +/- SE, 74 +/- 8 pg/ml), remained high until the time of delivery (95 +/- 14 pg/ml), and then fell to almost normal levels (50 +/- 9 pg/ml) on the third postpartum day. The serum levels of 1,25(OH)2D do not correlate with the serum levels of any of the aforementioned hormones. The increase in serum 1,25(OH)2D in pregnancy has been postulated to be related to the stressed calcium homeostatic mechanisms known to occur in the mother. In twin pregnancy, this maternal calcium homeostatic mechanism(s) conceivably may be stressed to a greater extent. However, serum 1,25(OH)2D levels, measured in 27 women with a twin pregnancy in both the second and third trimesters as well as at delivery, did not differ from the levels observed in women with a singleton pregnancy. There were no significant changes in the serum levels of 24,24(OH)2D or 25-hydroxyvitamin D as pregnancy progressed. However, serum 24,25(OH)2D correlated significantly with both serum 1,25(OH)2D (r - 0.51; p less than 0.001, n = 83) and serum 25-hydroxyvitamin D (r = 0.37; P less than 0.001, n = 94). In conclusion, serum levels of 1,25(OH)2D rise early in the first trimester of pregnancy, fall acutely to normal levels soon after delivery, and are similar in singleton and twin pregnancies. The changes in the serum levels of 1,25(OH)2D do not relate to the changes in the serum levels of any of the pregnancy-related hormones.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Influence of streptozotocin-induced diabetes in pregnant rats on plasma corticosterone and progesterone levels and on cytoplasmic glucocorticoid receptors in fetal tissues.

Administration of a dose of 45 mg streptozotocin/kg on day 2 of gestation produced a diabetic state in pregnant rats and was associated with fetal hyperinsulinaemia. Although there was no evidence of fetal macrosomia, the ratio of fetal liver and lung weight to body weight was greater in fetuses of diabetic rats, suggesting an increase in the size of these organs relative to the body weight. Maternal and fetal plasma corticosterone levels of diabetic rats between 19 and 22 days of gestation was significantly lower than the corresponding control values. Maternal plasma progesterone levels of diabetic rats were lower than controls on days 19 and 20 of gestation, but higher than controls on day 21 of gestation. The absence of pregnancy-related changes in maternal and fetal plasma corticosterone levels and maternal progesterone levels in diabetic rats suggest that adrenocortical function as well as ovarian and/or placental function may be impaired, which may in turn be related to the observed delay in parturition of approximately 18 h as well as to the low survival rate of the pups. There was a small increase in the cytoplasmic glucocorticoid receptor concentration in the lung but not in the liver of fetuses of diabetic mothers when compared with fetuses of controls, suggesting that the increased receptor concentration may be a compensatory mechanism to overcome the effect of decreased corticosterone levels and increased insulin levels in the fetuses of diabetic rats.

Animals↗
PubMed1983

Role of pro-opiomelanocortin-derived peptides in the regulation of steroid production by human fetal adrenal cells in culture.

Synthetic (1-39)ACTH, (1-24)ACTH, (18-39)ACTH, alpha-MSH, met-enkephalin and alpha-, beta- and gamma-endorphin were tested for their ability to stimulate steroidogenesis by human fetal adrenal cells in culture. Adrenal cells were incubated with peptide hormones for two periods of 24h. On the third day of the experiment the cells were incubated with progesterone (4 micrograms/2 ml) for 8 h. At the doses tested only (1-39)ACTH, (1-24)ACTH and alpha-MSH stimulated steroidogenesis. None of the other peptides had any corticotrophic effect on the formation of cortisol, corticosterone or dehydroepiandrosterone sulphate (DHAS). At the highest doses tested, alpha-MSH (100 micrograms/2 ml) had a corticotrophic effect that was not different from that obtained with 20 ng (1-39)ACTH or (1-24)ACTH. At the lower doses (0.2-2 micrograms/2 ml), alpha-MSH stimulated the formation of DHAS (P less than 0.01) without stimulating the formation of cortisol.

Adrenal Glands↗
PubMed1983

Influence of maternal diabetes on fetal rat development: alteration of insulin receptors in fetal liver and lung.

The influence of maternal diabetes on fetal development was studied in rats made diabetic by administration of streptozotocin on day 2 of gestation as well as in genetically diabetic BB Wistar rats. A dose of 65 mg streptozotocin/kg produced severe diabetes with plasma glucose levels of approximately 36 mmol/l, this was associated with fetal growth retardation but not fetal hyperinsulinaemia. In contrast, a smaller dose of streptozotocin (45 mg/kg) produced moderate diabetes with plasma glucose levels of approximately 20 mmol/l and was associated with fetal hyperinsulinaemia but only a marginal effect on fetal size. In both groups of diabetic animals, maternal body weight gain was decreased, maternal plasma insulin levels were low and fetal glucose levels were similar. In a small group of genetically diabetic BB rats on insulin therapy the fetuses were macrosomic and hyperinsulinaemic. The specific binding of 125I-labelled insulin to partially purified liver and lung membranes of fetuses of both groups of streptozotocin-induced diabetic rats was significantly lower than the binding to membranes from fetuses of control animals. The specific binding of 125I-labelled insulin to fetal liver and lung membranes from the diabetic BB Wistar rats also appeared to be reduced when compared to tissues from controls. Decreased insulin receptors in fetal lung and liver of diabetic rats suggest a role for insulin in the development of these organs during the fetal and neonatal period.

Animals↗
PubMed1982

Characterization of eight forms of corticotropin-like intermediary lobe peptide from the rat intermediary pituitary.

The isolation and characterization of eight forms of corticotropin-like intermediary lobe peptide (CLIP, adrenocorticotropin18-39) from the intermediary lobe of the rat pituitary has been accomplished by using reversed phase high performance liquid chromatography. The eight forms are the result of all combinations of the presence or absence of three post-translational modifications. These are glycosylation, phosphorylation, and removal of the carboxyl-terminal amino acid. The sites of phosphorylation and glycosylation are at serine 31 and asparagine 29, respectively. The eight forms (in order of elution from the reversed high performance liquid chromatography column) are glycosylated, phosphorylated CLIP18-38; glycosylated, nonphosphorylated CLIP18-38; nonglycosylated, phosphorylated CLIP18-38; nonglycosylated, nonphosphorylated CLIP18-38; glycosylated, phosphorylated CLIP18-39; glycosylated, nonphosphorylated CLIP18-39; nonglycosylated, phosphorylated CLIP18-39; and nonglycosylated, nonphosphorylated CLIP18-39.

Adrenocorticotropic Hormone↗
PubMed1982

Hypothalamic-pituitary dopaminergic function in hepatic failure in man.

The growth hormone (GH) response to apomorphine HCl (Apo) (0.75 mg sc), a dopamine (DA) receptor agonist, was assessed in healthy chronic alcoholics without cirrhosis (N = 20) and in patients with alcoholic cirrhosis both with (N = 5) and without (N = 14) hepatic encephalopathy (HE). A significant number of cirrhotic patients with (P less than 0.004) and without (P less than 0.002) HE had an impaired GH response (peak increment less than 5 ng/ml) compared with non-cirrhotic individuals. An impaired GH response was independent of the presence of HE. The magnitude of the GH response was unrelated to plasma oestrone, oestradiol, or progesterone concentrations but was significantly correlated with plasma testosterone levels (P less than 0.01). None of the patients with an abnormally low testosterone concentration showed a normal GH response. None of the subjects with HE showed an arousal response to Apo. These results suggest that DA receptor sensitivity is decreased in liver cirrhosis and that this decrease is related to inadequate circulating levels of testosterone. The occurrence of HE is independent of impaired DA function. The present study only evaluates DA function in the hypothalamic-pituitary axis and therefore may not reflect changes in other regions of brain.

Alcoholism↗