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Biomedical subjects

J D Wilson

Publications and source records attributed to J D Wilson.

At least 343 records · Page 19Linked to original sources
PubMed1979

Influence of prazosin on the development of antinuclear antibodies in hypertensive patients.

A recent publication suggested that antinuclear antibodies (ANA) occur in up to one third of patients treated with the hypotensive drug prazosin (Minipress). We have examined a large group of hypertensive patients and found ANA in 9.7% of 145 patients taking prazosin and in 12.2% of hypertensive patients on any treatment regimen. Excluding patients taking methyldopa (a drug associated with a high ANA incidence), the ANA incidence fell to 6.9% in the prazosin-treated group and to 7.2% of all treated hypertensives. Of over 350 untreated hypertensive patients, 6.0% had ANA. Prazosin did not increase the ANA incidence in patients on or off various drug combinations including beta blockers and diuretics. Analysis of the data by age and sex confirmed our conclusion that prazosin therapy is not accompanied by an increase in ANA.

Adrenergic beta-Antagonists↗
PubMed1979

The syndromes of primary hormone resistance.

The clinical features, genetics, pathophysiology, and management of endocrine diseases in which primary hormone resistance is the fundamental defect have been reviewed. Primary hormone resistance has been documented for nearly all hormones--vasopressin, parathyroid hormone, growth hormone, adrenocroticotropin, thyrotropin, gonadotropins, insulin, androgens, cortisol, aldosterone, progesterone, thyroid hormones, and vitamin D. A striking exception is estradiol, a steroid that may be vital for early embryonic development. Most of the hormone unresponsiveness syndromes represent only partial defects, and it is likely that most such patients go unrecognized. Therefore, hormone resistance should be suspected not only when a patient presents with hypofunction of particular endocrine system combined with high endogenous hormone levels but also whenever apparently normal function of an endocrine system is associated with inappropriately elevated levels of the corresponding hormone. The value of these defects in hormone responsiveness as a natural laboratory for the study of the normal mechanisms of hormone action is discussed.

Adrenocorticotropic Hormone↗
PubMed1979

3-Alpha-androstanediol and prostatic growth: comparison of 3-alpha-androstanediol formation in prostates from 8 species including man and dog.

To determine whether the formation of 3-alpha-androstanediol is critical for androgen-mediated growth of the prostate the conversion of dihydrotestosterone to 3-alpha-androstanediol was assessed in homogenates of 60 normal prostates from 8 species. Rates (nmol. times gm. tissue(-1) times hour(-1)) in the presence of reduced nicotinamide adenine dinucleotide phosphate as cofactor were as follows: dog 271, mouse 200, rat 160, opossum 109, rabbit 24, guinea pig 13, man 11 and cat 9. There was no correlation between prostate size and 3-alpha-androstanediol formation in the entire group. Therefore, either differences in the response to 3-alpha-androstanediol within the prostate or variations in the metabolism of 3-alpha-androstanediol must be more important than the rate of its formation for the development of prostatic hypertrophy in the dog.

Androstane-3,17-diol↗
PubMed1979

Regulation of cytoplasmic dihydrotestosterone binding in dog prostate by 17 beta-estradiol.

17 beta-estradiol enchances androgen-induced prostate growth in the castrate dog to a degree comparable to that seen in spontaneous prostatic hypertrophy. To investigate the mechanism of this synergism, cytosol androgen binding was measured by a density gradient technique in prostates of control and 17 beta-estradiol-treated castrate dogs. [3H]Dihydrotestosterone was bound principally to a moiety that averaged 8.6S in size. Approximately twofold enhancement of this binding by 17 beta-estradiol was demonstrable after 1 wk of treatment with 750 microgram/wk and after 3 wk with 75 microgram/wk. Under conditions in which binding in the 8S region was demonstrable with dihydrotestosterone and testosterone no binding of 3 alpha-androstanediol or progesterone was detectable. Thus, enhancement by 17 beta-estradiol of a prostate cytosol androgen-binding protein occurs under circumstances in which 17 beta-estradiol enhances androgen-mediated prostatic growth.

Animals↗
PubMed1979

Concentration of dihydrotestosterone and 3 alpha-androstanediol in naturally occurring and androgen-induced prostatic hyperplasia in the dog.

Previous studies have suggested that dihydrotestosterone accumulation in the prostate may be involved in the pathogenesis of prostatic hyperplasia in man and dog. However, the fact that the administration of 10 mg dihydrotestosterone/d to castrated, mongrel dogs (0.5 mg/kg body wt) causes little growth in the prostate, whereas identical doses of 3alpha- androstanediol regularly induce prostatic hyperplasia (> 14 g weight) has raised the possibility that the dihydrotestosterone accumulation may be the result rather than the cause of the pathology. To investigate the mechanism of this phenomenon, we measured the levels of dihydrotestosterone and 3alpha-androstanediol in prostates from 75 dogs. In both naturally occurring and 3alpha-androstanediol-induced prostatic hyperplasia, the levels of dihydrotestosterone were high (>5 ng/g), whereas in immature glands and glands from dihydrotestosterone-treated animals, levels were similar (2.1 and 2.6 ng/g, respectively). 3alpha-Androstanediol levels were no different in animals treated with dihydrotestosterone or 3alpha-androstanediol.Therefore, because exogenous 3alpha-androstanediol is a better precursor of prostatic dihydrotestosterone than exogenous dihydrotestosterone itself, the effects of treatment with larger doses (2.5 mg/kg per d) of dihydrotestosterone and 3alpha-androstanediol for 12 wk were examined. In these amounts, dihydrotestosterone was as effective as 3alpha-androstanediol in inducing the development of prostatic hyperplasia and in elevating prostatic dihydrotestosterone concentration. Because dihydrotestosterone accumulates in spontaneous prostatic hyperplasia, because the administration of sufficient amounts of dihydrotestosterone to the castrated dog can induce the development of prostatic hyperplasia, and because 3alpha-androstanediol induces the development of hyperplasia via conversion to dihydrotestosterone, we conclude that accumulation of dihydrotestosterone is the cause of canine prostatic hyperplasia.

Androstenediols↗
PubMed1979

Origin of estrogen in normal men and in women with testicular feminization.

The purpose of this study was to quantify the various sources of estrone (E1) and 17 beta-estradiol (E2) production in normal men and in women with testicular feminization. The mean production rate of E1 in four young adult men was 58 micrograms/24 h, while that of E2 was 44 micrograms/24 h. In these men, E1 production could be accounted for totally by extraglandular formation through 1) aromatization of plasma androstenedione, 2) conversion of E2 which was formed from the aromatization of plasma testosterone, and 3) conversion of secreted E2. In these men, only 12 micrograms or less of E2 production could not be accounted for by extraglandular formation from plasma C19 precursors, and is presumed to have arisen by testicular secretion. In six women with testicular feminization, the mean production rate of E1 was 99 micrograms/24 h, while that of E2 was 77 micrograms/24 h. THe amount of E2 production that arose by glandular secretion could be computed in four of these women and was considerably greater than that found in the young adult men. In these women with testicular feminization, an average of 44 micrograms/24 h E2 could not be accounted for by extraglandular formation and is presumed to have arisen by testicular secretion. The mean plasma production rate of testosterone in the normal men was 5.7 mg/24 h, while that in the women with testicular feminization was 8.3 mg/24 h. However, the range of plasma production rates of testosterone in the women with testicular feminization was large (1.3--17.0 mg/24 h).

Adolescent↗
PubMed1979

Transfer factor and hepatitis B: a double blind study.

A prospective, double blind placebo-controlled trial was carried out on twenty-nine patients with hepatitis B. Thirteen received transfer factor and sixteen placebo. There were no significant differences between the two groups in any clinical or laboratory measurements made, although a rapid early reduction of serum aspartate transaminase levels by transfer factor is possible. Similarly, no significant changes were delineated by the in vitro measurements of lymphocyte function. Transfer factor did not alter the natural course of hepatitis B.

Adult↗
PubMed1978

Estrogen formation in the early rabbit embryo.

Androgen formation (3beta-hydroxysteroid dehydrogenase activity) was detectable in the rabbit blastocyst on day 5 of gestation (before implantation); estrogen formation was first detectable on day 7. The capacity to form estrogen on the day of implantation suggests that estrogen formation in the blastocyst may play a role in the implantation process.

3-Hydroxysteroid Dehydrogenases↗
PubMed1978

Antinuclear antibodies in patients receiving non-practolol beta-blockers.

Antinuclear antibodies (ANA) were found in 54 (7.0%) out of 767 treated hypertensive patients compared with 59 (2.4%) out of 2470 healthy controls. Inclusion of a non-practolol beta-blocker in the treatment regimen did not significantly affect the incidence of ANA. ANA was found in significantly more patients being treated with methyldopa (13.0%) than patients receiving other hypotensive agents (3.8%). Non-practolol beta-blockers in combination with methyldopa did not increase the incidence of ANA further.

Adrenergic beta-Antagonists↗
PubMed1978

Clinical and endocrinological evaluation of patients with congenital microphallus.

Eight patients with congenital microphallus were investigated. Plasma luteinizing hormone, follicle-stimulating hormone, testosterone and androstenedione levels were obtained in all cases. In addition, the response to the administration of human chorionic gonadotropin, luteinizing horomone-releasing hormone and adrenocorticotropic hormone, the assessment of testicular histology by electron microscopy and the measurement of dihydrotestosterone formation by preputial skin were determined in some patients. The results of these studies were compared to similar studies in 6 normal prepubertal boys, 4 boys with bilateral cryptorchidism, 1 male infant with anorchia and 1 adult with hypogonadotropic hypogonadism. The clinical and endocrinological findings in the 8 patients with microphallus can be divided into 2 distinct categories. In 5 patients the disorder is familial, gonadotropin levels are low and there is a normal response to stimulation with chorionic gonadotropin. The data are compatible with the possibility that 3 (possibly 5) of the 8 patients with microphallus have hypogonadotropic hypogonadism. In the other group the cases are sporadic, serum luteinizing hormone and follicle-stimulating hormone levels are elevated and plasma testosterone failed to increase after short-term treatment with chorionic gonadotropin. In these patients a primary testicular disorder appears to be responsible. Experimental and clinical evidence suggests that microphallus results from defective testicular function during the second and third trimesters of pregnancy, either as the result of defective gonadotropin secretion or defective androgen synthesis.

Adolescent↗
PubMed1978

Location on chromosome 1 of Rnr, a gene that regulates renin in the submaxillary gland of the mouse.

Renin activity (EC 3.4.99.19) was measured in submaxillary gland extracts from four sets of recombinant inbred mouse strains. Recombination between Rnr, a gene that mediates the susceptibility of submaxillary gland renin to induction by androgen, and Dip-1, a chromosome 1 marker, was found in only 1 of 51 recombinant inbred strains, indicating that the two genes are closely linked on chromosome 1. Renin activity in androgen-treated female mice of all recombinant inbred strains resembled that of one or the other progenitor strains, as expected if a single gene is responsible. Documentation that a single gene can have major effects on renin in the submaxillary gland of the mouse implies that single gene differences might explain known variations in renin in other species.

Animals↗