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Biomedical subjects

V S Fang

Publications and source records attributed to V S Fang.

At least 91 records · Page 5Linked to original sources
PubMed1979

Behavioral and endocrine responses of schizophrenic patients to TRH (protirelin).

We studied the effects of intravenous protirelin (thyrotropin-releasing hormone) in 17 schizophrenic patients and 17 normal subjects. A total of 12 patients received protirelin, 0.5 mg, and, on another occasion, niacin, 2 mg, in a double-blind, crossover design. Both behavioral and endocrine data were collected. Five patients received protirelin in an open trial; only endocrine data were collected. Protirelin caused about a 50% prompt decrease in psychotic symptoms. Patients then tended slowly to experience a relapse. Side effects were about as infrequent after protirelin as after niacin. We assayed serum prolactin (PRL), growth hormone (GH), thyroid-stimulating hormone (TSH), L-triiodothyronine (T3) and thyroxine (T4). Free T4 (FT4) index was calculated. The values for PRL, GH, and TSH at baseline and after protirelin stimulation were normal. Patients showed lower T3 values at baseline, but a brisker T3 response to protirelin, than controls. Their FT4 indices were higher at baseline. Patients showed diminished T4 binding sites rather than increased total T4. The causes of these alterations in thyroid dynamics are unidentified.

Adult↗
PubMed1979

Extrapyramidal side effects and increased serum prolactin following fluoxetine, a new antidepressant.

Fluoxetine (Lilly 110140) is a potent, specific serotonin (5-HT) uptake blocker which is being tested in man for antidepressant activity. One of 9 depressed patients receiving this drug developed a dystonic reaction, parkinsonian rigidity, and increased serum prolactin levels, all signs of decreased dopaminergic activity. Homovanillic acid levels also decreased in the cerebrospinal fluid of this subject. We postulate that fluoxetine, via the increase in 5-HT activity resulting from 5-HT uptake blockade, inhibited both the nigro-striatal and tubero-infundibular dopaminergic neurons. These results provide additional evidence for a linkage between serotonergic and dopaminergic neurons in man.

Adult↗
PubMed1979

Serum prolactin levels following intramuscular chlorpromazine: two- and three-hour response as predictors of six-hour response.

Neuroendocrine studies that examine the changes in serum prolactin levels following intramuscular (im) neuroleptics have usually monitored prolactin levels before and for 90 minutes to 3 hours after neuroleptic injection. Recent studies have suggested that this may be an inadequate period of time. In the present study, six male and four female psychiatric inpatients, who had not received neuroleptic medication for at least 1 week before the study began, received an injection of chlorpromazine (CPZ) 25 mg im; serum prolactin levels were monitored for 6 hours after injection. Peak serum prolactin levels occurred at 60 minutes in one subject, 90 minutes in three subjects, 120 minutes in two subjects, 180 minutes in three subjects, and 240 minutes in one subject. Area under the serum prolactin curve at 2 hours and area under the curve at 3 hours after CPZ injection were found to be good predictors (r = 0.86; r = 0.95, respectively) of 6-hour area under the curve. Two-hour studies should therefore not be considered inadequate; however, a 3-hour study length results in more precise characterization of prolactin response to im CPZ.

Acute Disease↗
PubMed1979

Gonadotropin-releasing hormone infusion test in the distinction of hypopituitary patients from normal subjects.

We undertook a pilot study to determine whether infusion of gonadotropin-releasing hormone (GnRH) might improve the distinction of hypogonadotropinism from the normal state and might permit gonadotropin deficiency to be diagnosed in the prepubertal child. Normal prepubertal and pubertal boys had a greater luteinizing hormone (LH) reaction (delta LH 54 +/- 15 [SD] ng/ml and 165 +/- 23 ng/ml, respectively) to a 4-hour infusion (100 microgram/hour) than to a 100-microgram bolus of GnRH (19 +/- 9 and 52 +/- 35 ng/ml). These augmented responses were observed in boys with delayed puberty, but not in apparently hypogonadotropic males greater than or equal to 12 years old. LH (delta LH 445 to 1602 ng/ml) and FSH (delta FSH 718 to 2112 ng/ml) surges were induced consistently by GnRH infusion only in normal, postmenarchial females. In all, of 13 hypopituitary cases classified as hypogonadotropic on the basis of a subnormal response to GnRH infusion, 31% had a normal response to the GnRH bolus (P = 0.05). Thus, GnRH infusion testing seems to improve the distinction of hypogonadotropic patients from normal individuals, including boys with delayed puberty.

Adolescent↗
PubMed1979

Effect of clozapine on human serum prolactin levels.

The authors determined serum prolactin levels in 13 patients receiving clozapine, an antipsychotic drug that does not produce extrapyramidal side effects. Morning serum prolactin levels, 11 hours after the last dose, were not elevated during chronic treatment with clozapine in any subject despite its therapeutic effects. Serum prolactin levels were moderately increased between 90 minutes and 4 hours after administration of very high doses of oral clozapine in 4 patients but were smaller than those produced by chlorpromazine in other subjects. The authors suggest that clozapine in other subjects. The authors suggest that clozapine may achieve its antipsychotic effect differently than do classical neuroleptics and that sustained prolactin increases are not essential for antipsychotic action.

Animals↗
PubMed1979

Sex difference in the induction of lactogenic receptors in rat livers.

The relationship between serum levels of growth hormone (rGH), prolactin (rPRL), luteinizing hormone (rLH), follicle-stimulating hormone (rFSH), corticosterone, oestrogen, (oestradiol-17 beta) and testosterone and the hepatic binding sites specific to [125I]human-prolactin (h-PRL) were investigated in normal rats, in rats bearing the GH- and PRL-secreting tumour (GH3), and in rats 14 days after tumour removal. The presence of GH3 tumour elevated serum levels of rGH and rPRL and concomitantly increased the hepatic binding of [125I]h-PRL; the male rats had a greater increase than the female rats. The increased binding was due to an increase in the specific membrane binding sites, whereas the affinity constant (Ka) was not changed. In both male and female rats, there was a significant positive correlation between ser-m rGH levels (P less than 0.001) or serum rPRL (P less than 0.02) and specific binding of [125I]h-PRL in female rats only (P less than 0.02). In male rats, there was a significant negative correlation between serum testosterone levels and specific bindings of [125I]h-PRL (P less than 0.05). These results suggest that rGH and rPRL regulates the hepatic h-PRL receptors in female rats, and testosterone predominantly inhibits the induction of the hepatic lactogenic receptors in male rats.

Animals↗
PubMed1979

Cytotoxic activity of 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane (mitotane) and its analogs on feminizing adrenal neoplastic cells in culture.

Mitotane [1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane], an antineoplastic agent for inoperable adrenal carcinoma, was studied for its cytotoxic activity on a clonal line of feminizing human adrenal neoplastic cells (Fang-8 cells) in culture. At concentrations higher than 1.68 X 10(-4) M, mitotane produced a dose-related toxic effect on the cells. The effect of the drug was specific to Fang-8 cells because the same treatment produced little or no toxicity on lines of rat pituitary GH3 cells and human skin fibrocytes. The effect of mitotane to Fang-8 cells was a reversible one. Electron microscopic pictures revealed that the drug was causing mitochondrial degeneration. In this testing system, several isomers and analogs of mitotane were found equally or more toxic than was mitotane itself. The dichloro- or trichloroethylene structure was essential for the cytotoxic activity while the chloro substituents on phenyl rings appeared to be unimportant. This system appears to be useful in elucidating the biochemical mechanism of mitotane action on adrenal cancer.

Adrenal Gland Neoplasms↗
PubMed1978

Stimulation of rat prolactin secretion by indolealkylamine hallucinogens.

The hallucinogenic indoleamine drugs N,N-dimethyltryptamine (N,N-DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine, increased rat plasma prolactin (PRL) levels. The increase in plasma PRL produced by N,N-DMT, psilocybin, and bufotenin was inhibited by methysergide, a serotonin receptor blocker. Parachlorophenylalanine (PCPA), an inhibitor of serotonin synthesis, significantly potentiated the increase in PRL produced by N,N-DMT, and psilocybin. Parachloroamphetamine, a relatively selective toxin for serotonin neurons, also stimulated the increase in PRL produced by N,N-DMT. These results suggest that the indole hallucinogens stimulate PRL secretion by a serotonergic agonist mechanism. Bufotenin has been reported to pass the blood-brain barrier poorly, but of the indoles studied it had the most potent effect on PRL secretion. This raises the possibility that the serotonin receptors which promote PRL secretion may be outside the blood-brain barrier or that the central 5-HT receptors which mediate PRL secretion may be especially responsive to bufotenin.

Animals↗
PubMed1978

Cushing's syndrome due to adrenal adenoma with persistent diurnal cortisol secretory rhythm.

A 41-yr-old female with presumed Cushing's syndrome was found to have a diurnal cortisol rhythm characterized by low values of 8:00 a.m. and consistently high values at 4:00 p.m. and midnight. Hourly sampling of plasma cortisol over 24 hr confirmed this rhythm, as did measurement of urinary free cortisols in samples collected every 6 hr over 24 hr. Hypercortisolemia was not suppressed by 2 mg of dexamethasone given every 6 hr for 24 hr. The adrenal tissue was responsive to ACTH. Iodocholesterol scanning revealed unilateral activity, and the patient's syndrome was cured by resection of an adrenal adenoma. In this patient a diurnal cortisol secretory pattern was present due to the secretory activity of the adenoma. The cause of the abnormal but persistent diurnal pattern is unknown.

17-Hydroxycorticosteroids↗
PubMed1978

Enzymic, electrophoretic and immunoreactive properties of labeled MM and BB isoenzymes of human creatine kinase.

Purified MM and BB isoenzymes of human creatine kinase (CK) were labeled with Bolton-Hunter reagent. Labeling process did not affect their enzymic activity, although the labeled enzymes lost enzymic activity in storage. The labeled BB isoenzyme progressively changed its electrophoretic mobility, while labeled MM isoenzyme did not. Both labeled isoenzymes, however, maintained their immunoreactivity with their respective antisera. These results suggest that the enzymic and the immunoreactive sites of each CK isoenzyme are different and that BB isoenzyme, not MM isoenzyme, is electrophoretically unstable.

Brain↗
PubMed1978

Hormone receptors in livers of GH3 tumor-bearing rats: the predominant effect of growth hormone and testosterone.

The relationship between serum levels of rat GH (rGH), rat PRL (rPRL), corticosterone, estrogen, and testosterone and the liver-binding sites specific to [125I]iodo-human GH (hGH), -human PRL (hPRL), and -rPRL were investigated in normal rats, in rats bearing the GH- and PRL-secreting tumor (GH3), and in rats 14 days after tumor removal. The GH3 tumor elevated serum levels of rGH and rPRL and concomitantly increased the hepatic binding of radioiodinated hGH, hPRL, and rPRL; male rats had a greater increase than female rats. The increased binding was due to an increase in the specific membrane-binding sites, the receptors, whereas the affinity constant of binding (Ka) was not altered. In both male and female rats, the specific binding of receptors and the total binding capacities of livers correlated positively with serum levels of rGH (P less than 0.02) and inversely with serum levels of testosterone (P less than 0.05). There was insignificant or no correlation between rPRL or other steroids and the total liver-binding capacities. These results suggested that GH was the primary inducer and testosterone was the predominant regulator of the hepatic receptors in rats. The observed sex difference in the increase of receptors by GH3 tumor indicated that in normal and tumor-removed male rats, testosterone had suppressed the induction of hepatic receptors.

Animals↗
PubMed1978

Heterogeneous human prolactin from a giant pituitary tumor in a patient with panhypopituitarism.

A patient with hypopituitarism and an unusually large chromophobe adenoma which secreted an enormous amount of human PRL (hPRL) provided us with a unique opportunity to study the heterogeneity of hPRL. Serum samples obtained before and after surgery as well as pituitary extract were studied. Each sample contained three distinct hPRL peaks on gel filtration designated as big medium, and small. The hPRL moiety of each peak fraction was stable in size, immunoreactivity, and bioreactivity, indicating that the polymorphic hPRL components, once formed, were not interconvertible. As the relative proportion of medium and small hPRL components in all blood samples obtained before surgery and in the pituitary tumor extracts were similar, it seems that these two forms of hPRL originate from the tumor. However, there was a lack of correlation between big, medium, and small hPRL in samples obtained before and 1 yr after surgery. Also, increasing amounts of radioactive substance similar to increasing amounts of radioactive substance similar to big PRL were formed by exposure of 125I-labeled small PRL to progressively larger concentrations of serum. Thus, only small and possibly medium PRL are secretory products.

Adenoma, Chromophobe↗
PubMed1978

Direct inhibition of Leydig cell function by estradiol.

Suppression of plasma testosterone levels from a mean of 760 ng/dl to a mean of 295 ng/dl could be induced in normal young adult men 24 h after a single injection of 2 mg aqueous 17 beta-estradiol. Maximum suppression to 123 ng/dl was noted 36 h after estradiol administration. Neither LH nor FSH levels were similarly affected. After administration of 5000 IU hCG to a similar group of subjects, daily blood samples were obtained for testosterone and estrogen. Maximum testosterone levels of 2060 ng/dl (basal, 784 ng/dl) were seen 96 h after hCG administration. Maximum estrogen levels of 13 pg/ml (basal 73 pg/ml) were seen 36 h after hCG administration. The testosterone response to hCG could be attenuated by preceding hCG administration with an injection of 17 beta-estradiol. These results can be explained by the concept of enzyme inhibition; estrogen acts directly on the Leydig cell to effect changes in the activities of certain enzymes important for testosterone synthesis. Whether endogenous estrogen production by the Leydig cell may be important in this postulated short loop feedback is as yet unclear.

Adult↗
PubMed1978

Partial gonadotrophin-resistance in pseudohypoparathyroidism.

A patient with classical Albright's pseudohypoparathyroidism was investigated because of oligomenorrhoea. Hypo-oestrogenism was associated with elevated basal gonadotrophin values [mean basal serum LH and FSH were 272 +/- 84 (SD) ng/ml and 593 +/- 83 ng/ml, resplectively (normal less than or equal to 220 and less than or equal to 400, respectively)]. The response to gonadotrophin releasing hormone (Gn-RH) was exaggerated, with maximal LH and FSH increments of 1688 and 458 ng/ml, respectively. These results and the findings on ovarian biopsy were compatible with partial ovarian resistance to gonadotrophins. This resistance could be overcome by administration of human menopausal gonadotrophins. This is the first evidence for gonadotrophin resistance in pseudohypoparathyroidism. The plasma cyclic adenosine-3',5'-monophosphate response to glucagon administration by two different protocols was about 70% that of normal control subjects. Other endocrine glands whose responses to hormones are mediated via the adenylate cyclase system evidenced minor abnormalities of questionable significance. This indirect evidence is compatible with a more extensive defect in the adenylate cyclase system in pseudohypoparathyroidism than has hitherto been suspected.

Adenylyl Cyclases↗