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Featured researches published by S. L. Kaplan.


Journal of Clinical Investigation | 1972

Estradiol and Testosterone Secretion by Human, Simian, and Canine Testes, in Males with Hypogonadism and in Male Pseudohermaphrodites with the Feminizing Testes Syndrome

R. P. Kelch; M. R. Jenner; R. Weinstein; S. L. Kaplan; Melvin M. Grumbach

The role of the human testis in the production of 17beta-estradiol (E(2)) was investigated by determining the concentration of E(2) and testosterone in peripheral and spermatic vein plasma samples. Specimens were obtained from eight normal men, three men with hypogonadism, and two patients with the incomplete form of the feminizing testes syndrome. For comparison, similar studies were performed in four monkeys, 10 mongrel dogs, and 4 additional dogs who were given 1000 IU of human chorionic gonadotropin/day for 5 days. Plasma E(2) was measured by radioimmunoassay utilizing sheep anti-E(2) serum preceded by ether extraction and thin layer chromatographic separation of plasma steroids. Procedural blanks, which were subtracted from all reported values were 14.1+/-0.74 (SEM) pg for deionized water and 13.1+/-0.66 pg for charcoaladsorbed pooled male plasma. Pooled male and pooled female control plasmas averaged 17+/-0.71 pg/ml and 95+/-6.9 pg/ml, respectively; individual adult male specimens ranged between 8 and 28 with a mean of 18+/-1.4 pg/ml. In the eight normal men, the mean peripheral vein E(2) concentration was 20+/-1.6 pg/ml, while the spermatic vein concentration was 50 times as great, 1049+/-57 pg/ml. All three patients with testicular abnormalities had low spermatic vein E(2) concentrations (160, 280, and 416 pg/ml). Lesser E(2) gradients were found across the simian (3-fold) and canine (approximately 12-fold) testes. Testicular testosterone gradients (human 110-, simian 10-, and canine 77-fold) were greater than the E(2) gradients in all three species. In four dogs, HCG treatment elicited a 6-fold increase in peripheral and a 9-fold increase in spermatic vein testosterone concentrations; however, peripheral and spermatic vein E(2) concentrations did not differ from control values. Spermatic vein E(2) concentrations were > 4600 and 2210 pg/ml (post-HCG) in two patients with the incomplete form of the feminizing testes syndrome. Postorchiectomy, peripheral E(2) and testosterone concentrations fell precipitously in both patients, confirming the major contribution of the testes, in this syndrome, to circulating E(2) and testosterone. These studies provide direct evidence that the human testic secretes estradiol.


Journal of Clinical Investigation | 1974

Secretion of unconjugated androgens and estrogens by the normal and abnormal human testis before and after human chorionic gonadotropin.

R. Weinstein; R. P. Kelch; M. R. Jenner; S. L. Kaplan; Melvin M. Grumbach

The secretion of androgens and estrogens by normal and abnormal testes was compared by determining the concentrations of dehydroepiandrosterone (DHEA), androstenedione (Delta(4)A), testosterone (T), estrone (E(1)), and 17beta-estradiol (E(2)) in peripheral and spermatic venous plasma samples from 14 normal men and 5 men with unilateral testicular atrophy. Four normal men and one patient with unilateral atrophy of the testis were given human chorionic gonadotropin (HCG) before surgery. Plasma estrogens were determined by radioimmunoassay; plasma androgens were measured by the double-isotope dilution derivative technique. Peripheral concentrations of these steroids before and after HCG were similar in both the normal men and the patients with unilateral testicular atrophy. In normal men, the mean +/-SE spermatic venous concentrations were DHEA, 73.1+/-11.7 ng/ml; Delta(4)A, 30.7+/-7.9 ng/ml; T, 751+/-114 ng/ml; E(1), 306+/-55 pg/ml; and E(2), 1298+/-216 pg/ml. Three of four subjects with unilateral testicular atrophy had greatly diminished spermatic venous levels of androgens and estrogens. HCG treatment increased the testicular secretion of DHEA and T fivefold, Delta(4)A threefold, E(1) sixfold, and E(2) eightfold in normal men. In the single subject with an atrophic testis who received HCG, the spermatic venous concentrations of androgens and estrogens were much less than in normal men similarly treated. We conclude that: (a) E(1) is secreted by the human testis, but testicular secretion of E(1) accounts for less than 5% of E(1) production in normal men; (b) HCG stimulation produces increases in spermatic venous estrogens equal to or greater than the changes in androgens, including testosterone; and (c) strikingly decreased secretion of androgen and estrogen by unilateral atrophic human tests cannot be appreciated by analyses of peripheral steroid concentrations.


The Journal of Pediatrics | 1960

Amino acid and alpha-keto acid-induced hyperinsulinism in the leucine-sensitive type of infantile and childhood hypoglycemia.

Melvin M. Grumbach; S. L. Kaplan

Summary 1. Studies on 2 patients with leucine-induced “idiopathic” hypoglycemia showed that l -isoleucine also caused a striking fall in the concentration of blood glucose. d -leucine, l -valine, l -alanine, dl -threonine, and l -glycine did not have a significant effect. 2. The α-keto acid analogue of leucine, α-ketoisocaproic acid, induced hypoglycemia when injected intravenously but not its metabolite isovaleric acid. Its action was less effective orally. Pyruvic acid and α-ketoisovaleric acid failed to elicit a similar response. 3. No evidence of a defect in amino acid or α-keto acid metabolism was found, nor of a direct effect of leucine on glycolysis in whole blood. 4. It was shown that leucine caused increased peripheral utilization of glucose, suggesting an insulin-like action. Direct determinations of plasma insulin indicated a sharp rise in circulating insulin following the administration of leucine. 5. It is concluded that l -leucine, l -isoleucine, and their keto acid analogues induce an increase in the concentration of plasma insulin irrespective of the blood glucose level, an effect which may be attributed to their direct action on the mechanism of insulin secretion.


Journal of Clinical Investigation | 1975

The ontogenesis of human fetal hormones. III. Prolactin.

M J Aubert; Melvin M. Grumbach; S. L. Kaplan

The synthesis and release of human prolactin (hPRL) in the human fetus was assessed by radioimmunoassay analysis of the content and concentration of hPRL in 82 pituitary glands and the concentration of serum hPRL in 47 fetuses of gestational age 68 days to term. Fetal hPRL exhibited parallelism with the reference standard (Lewis 203-1). hPRL was detected by 68 days of gestation (10 wk), the earliest fetal pituitary gland studied; 8 out of 33 pituitaries had a prolactin (PRL) content above 2.0 ng between 10-15 wk gestation. The mean ocntent of PRL in the pituitary gland increased sharply from 14.8 plus or minus 4.6 ng at 15-19 wk to 405 plus or minus 142 ng at 20-24 wk and 542 plus or minus ng at 25-29 wk gestation. By term, the mean content was 2,039 plus or minus 459 (range 493-3,689) and the mean concentration 15.9 plus or minus 2.4 ng/mg (range 7-20). There was a significant positive correlation (P less than 0.001) between the hPRL and human growth hormone (hGH) content of fetal pituitary glands; at term the hPRL/hGH ratio was 1/290. The concentration of serum hPRL between 12 and 24 wk ranged from 2.9 to 67 ng/ml, mean 19.5 plus or minus 2.5 ng/ml )n = 21); by 26 wk fetal serum hPRL increased sharply and attained levels of 300-500 ng/ml in late gestation. At delivery, the mean plasma concentration of hPRL was 167 plus or minus 14.2 ng/ml in 36 umbilical venous specimens and 111.8 plus or minus 12.3 ng/ml in the matched maternal venous specimens. No correlation between serum hPRL and the pituitary content or concentration of hPRL was demonstrable in 12 matched fetal specimens. In five anencephalic infants, umbilical venous hPRL levels were between 65 and 283 ng/ml. In two anencephalic infants, thyrotropin releasing factor (TRF) (200 mug IV) evoked a rise in serum hPRL in one patient from 43 to 156 ng/ml at 30 min, and in the other from 65 to 404 ng/ml at 120 min. In both patients, plasma thyroid-stimulating hormone (TSH) rose from undetectable base-line levels to peak levels of 97 and 380 muU/ml, respectively. The pattern of change in serum hPRL in the human fetus contrasts sharply with that of serum hGH, luteinizing hormone, or follicle-stimulating hormone. These observations in the fetus and in anencephalic infants suggest that the striking elevation of serum PRL in the fetus is neither mediated by a putative PRL releasing factor or by TRF, nor is a consequence of suppression or absence of PRL release inhibiting factor alone, as a functional hypothalamus is not required to attain the high PRL concentration at term. Several lines of evidence support the view that high plasma estrogen levels characteristic of gestation act directly on the fetal anterior hypophysis to stimulate PRL secretion or to sensitize the secretory mechanism of the lactotrope, increasing its responsiveness to other stimuli.


Journal of Clinical Investigation | 1986

Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men.

Stephen M. Rosenthal; J A Hulse; S. L. Kaplan; Melvin M. Grumbach

Previous studies from this laboratory and by others in rats, monkeys, and humans support the concept that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism. With the availability of human growth hormone-releasing factor (GRF), the possible existence of such a mechanism was reexplored by examining the effect of exogenous GH on the GH response induced by GRF-44-NH2 in six normal men (mean age, 32.4 yr). In all subjects the plasma GH response evoked by GRF-44-NH2 (1 microgram/kg i.v. bolus) was studied before and after 5 d of placebo (1 ml normal saline i.m. every 12 h), and then before and 12 h after 5 d of biosynthetic methionyl human GH (5 U i.m. every 12 h). The GH response to GRF (maximal increment over time 0 value) was significantly inhibited after GH treatment (0-1.3 vs. 2.3-11.2 ng/ml before treatment, P = 0.05), but was not significantly affected by placebo. This impaired pituitary response to GRF persisted for at least 24 h following exogenous GH treatment in two subjects who underwent further study. Serum somatomedin-C concentrations were significantly increased after 5 d of GH treatment (2.66-5.00 vs. 0.92-1.91 U/ml before treatment, P = less than 0.01). The impaired pituitary response to GRF may be mediated indirectly through somatomedin, somatostatin, by a direct effect of GH on the pituitary somatotropes, or by all of these mechanisms. These data suggest that after GH treatment, the blunted GH response to synthetic GRF is not solely a consequence of the inhibition of hypothalamic GRF secretion.


Experimental Biology and Medicine | 1964

PREPARATION OF HUMAN CHORIONIC "GROWTH HORMONE-PROLACTIN".

Herman Cohen; Melvin M. Grumbach; S. L. Kaplan

Summary A simple procedure for partial purification of human chorionic “growth hor-mone-prolactin” is described utilizing DEAE-cellulose chromatography and Sephadex G-75 filtration. The preparation has a high degree of homogeneity. However, small amounts of serum protein contaminants were detected. The electrophoretic mobility in starch gel of the isolated hormone, utilizing a modified discontinuous buffer system was comparable to that of the “native” hormone in a freshly prepared crude placental extract.


The Lancet | 1970

SEPTO-OPTIC DYSPLASIA AND PITUITARY DWARFISM

W.F Hoyt; S. L. Kaplan; Melvin M. Grumbach; J.S Glaser


The Journal of Clinical Endocrinology and Metabolism | 1972

Hormonal Changes in Puberty: IV. Plasma Estradiol, LH, and FSH in Prepubertal Children, Pubertal Females, and in Precocious Puberty, Premature Thelarche, Hypogonadism, and in a Child with a Feminizing Ovarian Tumor

M. R Jenner; R.P. Kelch; S. L. Kaplan; Melvin M. Grumbach


The Journal of Clinical Endocrinology and Metabolism | 1964

STUDIES OF A HUMAN AND SIMIAN PLACENTAL HORMONE WITH GROWTH HORMONE-LIKE AND PROLACTIN-LIKE ACTIVITIES.

S. L. Kaplan; Melvin M. Grumbach


The Journal of Clinical Endocrinology and Metabolism | 1965

Serum Chorionic “Growth Hormone-Prolactin” and Serum Pituitary Growth Hormone in Mother and Fetus at Term

S. L. Kaplan; Melvin M. Grumbach

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Felix A. Conte

University of California

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Stephen M. Rosenthal

University of Connecticut Health Center

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J.S Glaser

University of California

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