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Biomedical subjects

S Marshall

Publications and source records attributed to S Marshall.

At least 217 records · Page 12Linked to original sources
PubMed1977

Infertility in male pesticide workers.

A number of cases of infertility were discovered among men working in a California pesticide factory. The suspected cause was exposure to the chemical 1,2-dibromo-3-chloropropane (D.B.C.P.). The major effects, seen in 14 of 25 non-vasectomised men, were azoospermia or oligospermia and raised serum-levels of follicle-stimulating hormone and luteinising hormone. No other major abnormalities were detected, and testosterone levels were normal. Although a quantitative estimation of exposure could not be obtained, the observed effects appeared to be related to duration of exposure to D.B.C.P.

Adult↗
PubMed1977

Carcinoma within urethral diverticula.

Because diagnosis of urethral diverticulum is often elusive the presence of a tumor within the diverticular cavity may be overlooked until it has grown beyond the confines of the diverticulum. A search of the medical records from 1940 to 1975 at the University of California Medical Center in San Francisco and Alta Bates Hospital in Berkeley has revealed only 3 cases of carcinoma within a urethral diverticulum. Two are presented here and the third was reported by Hinman in 1960. The paucity of cases in the literature reflects the rarity of such location for the tumor--or, perhaps, rather its evasive diagnostic nature. Undoubtedly, many cases are unreported but the important message for the clinician is that he suspect a urethral diverticulum (with the possibility of underlying neoplasm) in any patient with unexplained persistent irritative symptoms of the lower genitourinary tract.

Adenocarcinoma↗
PubMed1977

Ureterovesicoplasty: selection of patients, incidence and avoidance of complications. A review of 3,527 cases.

The procedure of ureteral reimplantation has certainly come of age. The incidence of complications can be kept low by careful selection of patients for operation along clear and definite guide lines, by close attention to detail in the surgical procedures and by rigorous followup care. When surgical intervention is deemed advisable the expected cure rate should be more than 94%. While complications do occur resultant damage to the upper urinary tracts should be minimized by its prompt recognition and by institution of appropriate therapy.

California↗
PubMed1977

Relation of gonadotropin secretion by pituitary grafts to spermatogenesis in hypophysectomized rats.

In hypophysectomized male rats, 2 anterior pituitary (AP) grafts placed underneath the kidney capsule partially prevented atrophy of the testes and ventral prostate during a 17 day post-implantation period. Spermatogenesis was partially maintained as revealed by histological examination of the testes. The AP grafts released small amounts of LH and FSH and substantial amounts of prolactin as determined by radioimmunoassay. Serum LH and FSH were undetectable in the hypophysectomized rats with no AP grafts. Inhibition of prolactin release by daily injections of ergocornine methanesulfonate (ERG) did not significantly alter serum levels of FSH and LH, spermatogenesis or testes and ventral prostate weights, indicating that circulating levels of prolactin were not responsible for the partial maintenance of spermatogenesis and prostate weight in these rats. Daily injections of ovine prolactin also had no effect on spermatogenesis or prolactin also had no effect on spermatogenesis or prostate weight in the hypophysectomized rats, and there was no change in the histological appearance of the testes and prostate. These observations indicate that secretion of gonadotropins and not prolactin by AP grafts accounts for the partial maintenance of spermatogenesis and prostate weight in hypophysectomized, AP-grafted male rats during the experimental period studied.

Animals↗
PubMed1977

Effects of starvation in rats on serum levels of follicle stimulating hormone, luteinizing hormone, thyrotropin, growth hormone and prolactin; response to LH-releasing hormone and thyrotropin-releasing hormone.

Adult male Sprague-Dawley rats averaging 300 g each were subjected to complete food removal for 7 days (acutely starved), 7 days complete food removal followed by 2 weeks of 1/4 ad libitum food intake (chronically strved), 7 days complete food removal and 2 weeks of 1/4 ad libitum intake followed by ad libitum feeding for 7 days (refed), or fed ad libitum throughout (controls). Serum LH, FSH, TSH, PRL, and GH levels were measured by radioimmunoassays for each group of rats. The in vivo response to the combination of synthetic LHRH and TRH also was tested in each group of rats. Circulating LH, TSH, GH, and PRL were significantly depressed in acutely and chronically starved rats, and FSH was lowered only in acutely starved rats. After 7 days of refeeding, serum levels of LH and FSH were significantly greater than in ad libitum fed controls, PRL returned to control levels, and TSH and GH increased but were still below control levels. After LHRH + TRH injection serum LH and TSH were increased significantly in all groups of rats, FSH and PRL rose in acutely but not in chronically starved rats, and GH was not elevated in any group. The increases in serum LH, FSH, TSH and prolactin in response to LHRH + TRH injection in acutely or chronically starved rats were equal to or greater than in the ad libitum fed controls. These data indicate that severe reductions in food intake result in decreased release of at least 5 anterior pituitary hormones, and this is due primarily to reduced hypothalamic stimulation rather than to inability of the pituitary to secrete hormones.

Adrenal Glands↗
PubMed1976

Effects of estrogen and testosterone on specific prolactin binding in the kidneys and adrenal of rats.

The effects of estradiol benzoate in the female rat, testosterone propionate in the male rat, and castration in both sexes on specific prolactin binding sites in the particulate membranes of the kidneys and adrenals were studied. Castration resulted in a significant increase in PRL binding activity in the kidneys of both males and females, and in a significant increase in PRL binding activity in the adrenals of the females. The increase in PRL binding with castration and the decrease seen with testosterone treatment were similar in both immature and mature rats. Progesterone administration to castrate females failed to alter PRL binding in both tissues. The present results suggest that estrogen and testosterone participate in the PRL osmoregulatory system in rat.

Adrenal Glands↗
PubMed1976

Induction of estrous cycles in old non-cyclic rats by progesterone, ACTH, ether stress or L-dopa.

Cycling was induced in old non-cyclic, constant estrous rats by daily injections of progesterone, ACTH or L-dopa or by subjection to ether stress. Progesterone and ACTH were the most effective agents used for re-establishing estrous cycles in these rats. Most of the progesterone- and ACTH-treated rats showed regular cycles, and their ovaries had many corpora lutea; they also showed proestrous serum LH surges. Ether stress and L-dopa mostly induced irregular cycles and fewer corpora lutea in the ovaries; a smaller number of these rats showed proestrous LH surges. After treatment with each of these agents was discontinued, most of the rats returned to constant estrus or irregular cycling.

Adrenocorticotropic Hormone↗
PubMed1976

Effects of castration, testosterone, estradiol, and prolactin on specific prolactin-binding activity in ventral prostate of male rats.

Lactoperoxidase-catalyzed 125I-labeled ovine prolactin (PRL) was found to bind specifically to particulate membrane fractions of rat ventral prostate. Unlabeled PRL readily displaced the labeled PRL, whereas ovine GH, LH, FSH, or TSH showed no such competition. Castration reduced the binding of 125I-labeled PRL to about 1/6 of that in intact rats, and injections of testosterone propionate (TP) increased PRL binding to values as great or greater than those in intact controls. Injections of TP into intact immature and mature rats also increased PRL binding. In vitro binding of labeled PRL was inhibited in prostatic tissue removed from intact immature rats 2 h after injecting unlabeled PRL, but not in ventral prostates from rats killed 26 or 74 h after injecting unlabeled prolactin. PRL injected together with TP in castrated rats produced no greater increase in prolactin binding than TP alone, while estrogen appeared to decrease PRL binding beyond that produced by castration alone.

Animals↗
PubMed1976

Relation between prolactin and gonadotrophin secretion in post-partum lactating rats.

In post-partum lactating rats, sucking by the young was associated with high prolactin release and maintenance of lactation but severe inhibition of LH and FSH release and suspension of oestrous cycles. Shortly after the pups were removed on day 22 post partum LH and FSH release returned to normal and oestrous cycles resumed. Twice-daily injections of ergocornine methanesulphonate (ERG) into mothers beginning at 5 or 7 days post partum, resulted in sustained inhibition of prolactin release and diminished mild secretion. By frequent exchange of pups between control and ERG-treated mothers, it was possible to maintain vigorous sucking and almost normal pup growth despite low serum prolactin levels and diminished lactation. In these rats, serum levels of LH remained low during 11 or more days of treatment with ERG, but serum FSH was consistently higher than in untreated control mothers. After 11 or more days of ERG treatment, most rats showed a return to normal LH and FSH release and resumption of oestrous cycles. These results suggest (a) that the sucking stimulus rather than high prolactin levels in the circulation is mainly responsible for inhibition of LH and FSH release during the first 11 days post partum, (b) that the sucking stimulus acts to increase prolactin and inhibit LH release by separate hypothalamic mechanisms, and (c) that administration of ERG results in diminished prolactin release and lactation, and in increased release of FSH and subsequently of LH with earlier resumption of oestrous cycles.

Animals↗
PubMed1976

Estrogen and prolactin receptor concentrations in rat mammary tumors and response to endocrine ablation.

Estrogen and prolactin receptor concentrations were measured in 24 carcinogen-induced rat mammary tumors and correlated with the tumor response to host ovariectomy or hypophysectomy. It was found that essentially all of the tumors contained some specific estrogen receptor, and all but three contained prolactin receptor. The values for each receptor comprised a continuum from very low to relatively high concentrations, suggesting that previous considerations of hormone dependence on the basis of presence or absence of hormone receptors may be oversimplified. The concentration of each receptor tended to be lower in the hormone-independent than in the hormone-dependent tumors, but there were a number of hormone-independent tumors with higher receptor levels than some of the hormone-dependent tumors had. A better correlation of tumor response to endocrine ablation resulted from a combination of the 2 receptor levels than from either receptor concentration alone. These results suggest that there is a complex relationship between mammary tumor response to endocrine ablatin and levels of estrogen and prolactin receptors and that some tumors may be dependent upon 1 or both of these hormones for growth.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Effects of high hoses of estrogen on prolactin-binding activity and growth of carcinogen-induced mammary cancers in rats.

Specific binding sites for prolactin (PRL) were present in membrane preparations from 7,12-dimethylbenz(a)-anthracene-induced rat mammary tumors. The specific binding of PRL was time and temperature dependent. A significant negative correlation was noted between administered doses of estrogen and the subsequent binding of PRL to tumor cell membranes. Injections of 10 or 25 mug estradiol benzoate daily for 10 days effectively inhibited mammary tumor growth and significantly reduced specific PRL binding to mammary tumor cell membranes.

9,10-Dimethyl-1,2-benzanthracene↗