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Biomedical subjects

H A Bern

Publications and source records attributed to H A Bern.

At least 55 records · Page 3Linked to original sources
PubMed1990

Growth responses of prostatic epithelial cells from male mice neonatally exposed to diethylstilbestrol in serum-free collagen gel culture.

Growth of anterior and ventral prostatic epithelial cells from mice neonatally exposed to diethylstilbestrol (DES) and from unexposed control mice was compared at different time points in serum-free collagen gel culture. A longer maintenance of the initial plating density (lag in growth) was observed in cultured DES-exposed ventral prostatic cells. Neonatal DES exposure resulted in two colony types: one similar to colonies arising from unexposed cells and one which appears to be non-growing. Keratinization was observed in some DES-exposed anterior prostatic cell colonies. Removal of epidermal growth factor from the serum-free medium significantly decreased growth in 3 of the 4 groups compared with their growth in the complete serum-free medium.

Animals↗
PubMed1990

Radioreceptor assay for growth hormone in coho salmon (Oncorhynchus kisutch) and its application to the study of stunting.

Binding sites for native chum salmon growth hormone (sGH) in coho salmon (Oncorhynchus kisutch) hepatic membranes were analyzed by radioreceptor assay. Displaceable (specific) binding represented up to 25% of total radiolabeled sGH added. Binding was dependent on buffer pH and membrane protein concentration, and was complete by 24 hours at 15 degrees C. Specific binding was greatest in liver membranes, and was also detected in muscle, ovary, gill, kidney, and brain. Scatchard analyses indicated a single class of hepatic binding sites that were specific for sGH. In stunts, abnormal seawater salmon with elevated plasma GH levels and inhibited growth, specific binding of sGH to liver membranes was three times lower than in normal seawater smolts. The concentration of salmon GH binding sites was decreased in stunt livers by 60%, while their affinity for sGH was unchanged. Down-regulation of hepatic GH receptors by high plasma GH levels may explain in part the low sGH binding in stunts.

Animals↗
PubMed1990

Serum-free culture of enriched mouse anterior and ventral prostatic epithelial cells in collagen gel.

Sustained growth of mouse ventral and anterior prostatic epithelial cells embedded within collagen gel matrix was achieved in a serum-free medium composed of Dulbecco's modified Eagle's medium and Ham's F12 medium, 1:1 (vol/vol), supplemented with bovine serum albumin fraction V, epidermal growth factor, transferrin, cholera toxin, prolactin, 5 alpha-dihydrotestosterone, cortisol, putrescine, fibroblast growth factor, and a trace element mixture. Three-dimensional growth of prostatic epithelial cells occurred inside the collagen gel matrix. This serum-free medium allowed cell growth greater than sevenfold over 10 d in culture. Tissue recombination and cell culture techniques were integrated to demonstrate that cultured cells retained prostatic characteristics. Following 10 d of culture, epithelial colonies from mouse ventral and anterior prostatic epithelial cell cultures were isolated and combined with rat fetal urogenital sinus mesenchyme and grown for 4 wk under the renal capsule of intact athymic male mice. These tissue recombinants showed distinctive prostatic histologic characteristics (alveoli and ducts lined with cuboidal or columnar epithelium surrounded by stroma). When histologic sections of recombinants were stained with the Hoechst 33258, epithelial cells of mouse origin were distinguishable from stromal cells of rat origin.

Animals↗
PubMed1990

Prolactin receptors in liver, kidney, and gill of the tilapia (Oreochromis mossambicus): characterization and effect of salinity on specific binding of iodinated ovine prolactin.

Specific binding of 125I-ovine prolactin (oPRL) to microsomal fractions from gill, kidney, and liver of adult tilapia was determined. Specific binding varied among tissues, the highest values being displayed by kidney membranes. In the liver, the binding of oPRL was not strongly displaced by tilapia prolactins (tPRL177 and tPRL188), although tPRL177 was six times more potent than tPRL188. On the other hand, in kidney and gill membranes, the two tPRLs were equipotent. Tilapia PRLs showed low potency in competing for oPRL-binding sites when pregnant rat liver membranes were utilized. Tilapia growth hormone (tGH) and human growth hormone (hGH) displaced 125I-oPRL from liver as well as did tPRL177 but were not recognized well by renal or branchial receptors. Two 125I-oPRL-binding sites were detected in every tissue tested. These binding sites are subject to physiological regulation since adaptation to seawater resulted in a significant decrease in specific binding.

Animals↗
PubMed1990

Effect of hypophysectomy, replacement therapy with ovine prolactin, and cortisol and triiodothyronine treatment on prolactin receptors of the tilapia (Oreochromis mossambicus).

The effects of hypophysectomy and subsequent replacement therapy with ovine prolactin (oPRL) on specific binding of 125I-oPRL to gill, kidney, and liver membranes of male tilapia were examined. The possible control of prolactin receptors by cortisol (F) and triiodothyronine (T3) was also studied using intact animals. In gill and kidney, hypophysectomy resulted in a significant decrease in specific binding that was partially restored (threefold increase) by three injections of oPRL, suggesting a role of the pituitary in the control of prolactin receptors. However, removal of the pituitary and replacement therapy with oPRL had no effect on binding by liver membranes. Cortisol and T3 treatment, alone or in combination, did not significantly affect prolactin binding by any of the tissues tested.

Animals↗
PubMed1990

Effects of GnRH-associated peptide and its component peptides on prolactin secretion from the tilapia pituitary in vitro.

The rostral pars distalis (RPD), containing mainly prolactin (PRL)-secreting cells, of the pituitary from immature and mature tilapia was incubated for 16 hr at 27 degrees in hypoosmotic medium (300 mOsm/kg) in the presence (10(-8) and 10(-11) M) or absence of the human GnRH-associated peptide (GAP) molecule, a potent PRL-inhibiting factor in mammals (Nikolics et al., Nature (London) 316, 511, 1985), and of a series of its component peptides. The release of the two forms of PRL in tilapia into the medium was measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by densitometry. The variability inherent in this method was normalized by calculating PRL release as the percentage of the total hormone present in both tissue and medium. Newly synthesized PRL was detected by incorporation of [35S]methionine, introduced into the culture medium, by the PRL molecules. In immature tilapia, GAP inhibited the release of total PRL while stimulating the release of newly synthesized large PRL. Among the GAP fragments tested, 28-36 was the fragment that most significantly affected PRL secretion. Both concentrations of fragment 28-36 stimulated the release of newly synthesized PRL from immature rostral pars distalis (RPDs). This stimulation appears to be dependent on the osmotic pressure of the medium since this fragment did not affect PRL secretion in hyperosmotic medium (340 mOsm/kg). Fragment 38-49 inhibited total PRL release from mature RPDs. Fragment 51-66 stimulated the release of total PRL from mature RPDs. Examination of tissue and medium values in densitometric units after incubation with fragments 28-36 and 51-66 indicated that while the tissue content of PRL was decreased, the medium content of PRL was not affected. This suggests that fragments 28-36 and 51-66, in opposition to the situation found when the data are expressed as percentage release of PRL, may not stimulate PRL release but may instead decrease the tissue content of PRL. These results suggest that the entire human GAP molecule, as well as some of its fragments, may have direct effects on the PRL cells in the tilapia pituitary.

Animals↗
PubMed1990

Steroid binding alterations in tissue compartments of the vagina of control and neonatally diethylstilbestrol-treated adult mice.

Steroid binding in both the vaginal epithelium and the vaginal fibromuscular wall (FMW) was compared in control and neonatally estrogen-treated mice. Neonatal treatment with a low dose of the estrogen diethylstilbestrol (DES) had no significant effect on adult estrogen binding within the assayed vaginal compartments; however, this treatment caused a 2-fold increase in the level of cytosolic progestin binding in the vaginal FMW over that in vehicle-treated mice. This low neonatal dose did not affect the level of progestin binding in the vaginal epithelium. In contrast, neonatal treatment with a larger dose of DES caused marked increases in cytosolic progestin binding, decreases in cytosolic estrogen binding, and increases in nuclear estrogen binding within the FMW. Furthermore, as a result of the changes in specific binding induced by the neonatal DES treatment, the degree of the estrogen binding within in each tissue shifted from a predominantly cytosolic site to a nuclear one.

Animals↗
PubMed1990

Long-term genital tract changes in female mice treated neonatally with coumestrol.

The neonatal mouse model has proven to be an effective system to examine long-term reproductive tract abnormalities resulting from early exposure to estrogens. Newborn C57BL/Crgl mice received 8 x 10(-2) micrograms diethylstilbestrol (DES) or 100 micrograms coumestrol (a plant estrogen) in 0.005 mL dimethyl sulfoxide (DMSO) or DMSO alone or received no treatment for the first 5 days of life. Half of the animals were ovariectomized at 40 days of age. Vaginal lavages were examined for 15 consecutive days before termination at 13 months of age, at which time genital tracts and mammary glands were removed for histological examination. Diethylstilbestrol- and coumestrol-treated animals exhibited ovary-independent persistent vaginal cornification as well as cervico-vaginal pegs and downgrowths, uterine squamous metaplasia, and an enhancement of age-related changes in the ovary including hemorrhagic follicles. In general, neonatal exposure to the naturally occurring plant estrogen, coumestrol, has long-term effects similar to those seen following exposure to natural and synthetic estrogens.

Animals↗
PubMed1990

Reproductive abnormalities in female mice exposed neonatally to various doses of coumestrol.

Female C57BL/Crgl mice were neonatally exposed to various doses of coumestrol to determine the threshold doses required for the occurrence of reproductive tract abnormalities. Newborn mice received daily subcutaneous injections of 10(-3), 10(-2), 8 X 10(-2), 10(-1), 1, 5, 25, 50, and 100 micrograms coumestrol in 0.005 ml dimethyl sulfoxide (DMSO) or DMSO alone, or received no treatment for the first 5 d of life. Some of the animals were ovariectomized at 40 d of age. Mice were killed at 20-22 mo of age. All neonatal doses of coumestrol advanced vaginal opening before that of controls. At 2 and 20-22 mo of age, doses greater than or equal to 25 micrograms consistently resulted in ovary-independent persistent vaginal cornification as judged by vaginal smears. Intact untreated and DMSO-treated control mice exhibited aging changes in the genital tract, some cervical adenosis and early cervicovaginal pegs and downgrowths, uterine cystic glandular hyperplasia, corpora lutea, and scattered areas of ovarian ceroid deposition. Intact mice receiving neonatal coumestrol exhibited cervicovaginal pegs and downgrowths (at all doses with the exception of 25 and 50 micrograms), cervical adenosis (at doses greater than or equal to 8 X 10(-2) micrograms), uterine squamous metaplasia (significant at doses greater than or equal to 50 micrograms), and a decrease in uterine cystic glandular hyperplasia (significant at doses greater than or equal to 25 micrograms). The levels of 10(-1), 5, and 100 micrograms neonatal coumestrol daily resulted in hemorrhagic follicles. An increase in ovarian ceroid deposition (significant at doses greater than or equal to 5 micrograms) was observed. At 40 d and 20-22 mo of age, corpora lutea were consistently absent from the 100-micrograms-treated animals. Most of the ovariectomized untreated and DMSO-treated control animals showed typical castrate-like morphology of the genital tract, with the majority of the control mice exhibiting uterine cystic glandular hyperplasia. Ovariectomized mice receiving coumestrol neonatally exhibited various degrees of cervicovaginal alterations: pegs and downgrowths (significant at all doses with the exception of 10(-1) micrograms), endometrial collagen deposition (significant at greater than or equal to 25 micrograms), and reduced or absent uterine glands (significant at 10(-3), and 10(-11), and at all doses greater than or equal to 5 micrograms).

Age Factors↗
PubMed1990

Influence of neonatal diethylstilbestrol treatment on prolactin receptor levels in the mouse male reproductive system.

Neonatal exposure to the synthetic estrogen, diethylstilbestrol, is known to affect the structure of the male reproductive system; thus, changes may also occur in the levels of hormone receptors. Prolactin receptor levels from the reproductive systems of male BALB/c mice exposed neonatally to diethylstilbestrol were analyzed. Neonatal exposure to diethylstilbestrol caused significant decreases (i) in prolactin receptor levels in the seminal vesicle, ductus deferens, and anterior and ventral prostates and (ii) in tissue weight and protein content in reproductive organs other than the ventral prostate.

Animals↗
PubMed1990

Effects of early exposure to diethylstilbestrol on cellular protein expression by mouse vaginal epithelium and fibromuscular wall.

Epithelia and fibromuscular walls were dissociated from the vaginae of ovariectomized BALB/cCrgl mice (ca. 41 days old) exposed neonatally to diethylstilbestrol (DES) or sesame oil and purified by centrifugation through Percoll density gradients. Neonatal exposure to DES caused the vaginal epithelium to become permanently proliferated and partially keratinized; the control epithelium was low cuboidal. The major cellular proteins expressed in each tissue compartment were examined by two-dimensional gel electrophoresis of [35S]methionine-labeled tissues. The epithelia and fibromuscular walls displayed distinctive two-dimensional protein patterns. In the DES-exposed vaginal epithelium, the expression of two proteins (one had a molecular size of 65 kDa and a pl of 6.0, and the other had a molecular size of 38 kDa and a pl of 6.3) was increased, while the expression of three proteins with molecular sizes of 25, 30, and 140 kDa and pls of 5.6, 5.6 and 6.7, respectively, was reduced, relative to the control epithelium. In the DES-exposed vaginal fibromuscular walls, the expression of 9 proteins was increased whereas the levels of 21 specific proteins, distinct from those in the epithelium, were decreased. Thus, long-term tissue-specific alterations in the synthesis of a select number of cellular proteins occur in the DES-exposed vagina.

Animals↗
PubMed1989

Influence of neonatal diethylstilbestrol treatment on androgen and estrogen receptor levels in the mouse anterior prostate, ventral prostate and seminal vesicle.

Perinatal exposure to the synthetic estrogen, diethylstilbestrol (DES), affects the structure of both male and female reproductive systems. Changes may also occur in the levels of steroid hormone receptors. Cytosolic and nuclear androgen and estrogen receptor levels (expressed per mg DNA) from the sex accessory glands of male BALB/c mice exposed neonatally to DES were analyzed by exchange assays. Neonatal DES exposure caused significant decreases in: (1) cytosolic androgen and cytosolic and nuclear estrogen receptor levels in the anterior prostate and (2) cytosolic estrogen receptor levels in the ventral prostate. A significant increase was seen in the cytosolic estrogen receptor levels in the seminal vesicle. Significant decreases in cytosolic protein levels occurred in all DES-exposed glands.

Animals↗
PubMed1989

Reproductive alterations in female C57BL/Crgl mice exposed neonatally to zearalenone, an estrogenic mycotoxin.

Newborn female mice were injected daily for 5 days with 1 microgram zearalenone (Z, a weakly estrogenic mycotoxin present in cereal grains), resulting in ovary-dependent reproductive tract alterations at 8 months of age. Corpora lutea were absent from 25 of 34 (74%) Z-treated mice, indicating ovarian dysfunction. Fifty-six percent of Z-treated mice had dense collagen deposition in the uterine stroma and lacked uterine glands. Squamous metaplasia of the uterine luminal epithelium was found in 59% of Z-treated mice, and altered vaginal epithelium was found in 32% (2 mice had dysplastic lesions). Ovariectomized Z-treated mice were indistinguishable from ovariectomized controls.

Animals↗
PubMed1989

Smoltification and seawater adaptation in coho salmon (Oncorhynchus kisutch): plasma prolactin, growth hormone, thyroid hormones, and cortisol.

The status of circulating growth hormone and prolactin during the parr-smolt transformation and during seawater adaptation of coho salmon (Oncorhynchus kisutch) was investigated in relation to changes in plasma levels of thyroxine, triiodothyronine, and cortisol, and in hypoosmoregulatory ability. Sampling (biweekly or monthly) occurred between early February and October. When peak hypoosmoregulatory ability was achieved (mid-April), one group of fish was acclimated to seawater over a period of 18 hr and was sampled 1, 3, and 7 days after the introduction of fish to seawater and biweekly thereafter. Plasma prolactin levels rose steadily from the first sampling date to a peak of 15 ng/ml in early April, declined rapidly, and remained low until June when a second increase occurred. Prolactin declined to 2 ng/ml within 1 day of the beginning of seawater adaptation. Growth hormone increased twofold from February to late March, and achieved plateau levels of 20 ng/ml in the period from mid-April to July and then gradually declined to 10 ng/ml in September and October. Plasma levels of growth hormone in seawater-acclimated fish were similar to those of freshwater coho, but with larger fluctuations; no increase was apparent during the first week of seawater acclimation. Plasma cortisol and plasma triiodothyronine increased at the same time as plasma growth hormone; increases in plasma thyroxine occurred later. In general, both growth hormone and cortisol levels were elevated when hypoosmoregulatory ability was high. Conversely, prolactin levels generally showed a negative relationship with hypoosmoregulatory ability.

Acclimatization↗
PubMed1989

Smoltification and seawater adaptation in coho salmon (Oncorhynchus kisutch): plasma calcium regulation, osmoregulation, and calcitonin.

In order to examine the dynamics of ion regulation, osmoregulation, and plasma calcitonin during the parr-smolt transformation (smoltification), blood and gill tissue were collected from yearling coho salmon, Oncorhynchus kisutch, from February to October. Fish were kept in fresh water (FW) throughout this period. In addition, fish were exposed to seawater (SW) at the peak of smoltification in mid-April, and samples from these fish were collected until July. Plasma osmolality, gill Na+,K+-ATPase activity, plasma levels of calcitonin, and free and total calcium and magnesium were measured. SW adaptability of FW fish was assessed throughout the study by measurements of plasma osmolality following a 24-hr exposure to seawater. The greatest hypoosmoregulatory ability occurred in April-May, although SW-adapted fish had higher plasma osmolality than FW-adapted fish at all times. Gill Na+,K+-ATPase activity in FW-adapted fish increased from April to June and increased rapidly following exposure of fish to SW, and remained elevated in SW-adapted fish. Free plasma calcium and magnesium levels increased following SW exposure, but returned to prior levels within 1 week. Netting and confinement stress during sampling caused an increase in plasma osmolality and free calcium and magnesium levels in both FW- and SW-adapted fish. Changes in hypoosmoregulatory ability during smoltification and SW adaptation were correlated with changes in gill Na+,K+-ATPase activity. A sharp transitory peak in plasma calcitonin levels occurred early in smoltification (March) and in SW-adapted fish in June. Plasma calcitonin levels gradually increased in FW-adapted fish during the period of desmoltification. However, no change in plasma calcitonin levels occurred during SW-induced hypercalcemia, suggesting that the hormone does not play a major role in short-term plasma calcium regulation in coho salmon.

Acclimatization↗
PubMed1989

In vitro stimulation of Na+-K+-ATPase activity and ouabain binding by cortisol in coho salmon gill.

To investigate the hormonal control of gill Na+-K+-adenosinetriphosphatase (ATPase) (the sodium pump) in coho salmon, a technique for the culture of primary gill filaments for up to 4 days was developed. Trypan blue exclusion was greater than 99.9%, histological appearance of the cells was normal, and total [Na+], [K+], and protein content of gill filaments cultured for 2-4 days was unchanged from initial levels (measured immediately after isolation). In fish with initially low gill Na+-K+-ATPase activity (presmolts), cortisol (0.1, 1.0, and 10.0 micrograms/ml) caused a significant dose-dependent increase in gill Na+-K+-ATPase activity over initial (41%) and control levels (45%) after 4 days in culture. In fish with initially high gill Na+-K+-ATPase activity (postsmolts), cortisol partially prevented the decline in activity that occurred during 4 days of culture. The relative ability of steroids to increase gill Na+-K+-ATPase activity was dexamethasone greater than cortisol = 11-deoxycortisol greater than cortisone. Insulin (0.1, 1.0, and 10.0 micrograms/ml), alone or in combination with cortisol, had no significant effect on gill Na+-K+-ATPase activity. Cortisol treatment significantly increased maximum binding capacity of [3H]ouabain in gill tissue (from 2.92 to 5.22 pmol/mg dry wt) but had no significant effect on the dissociation constant. These results demonstrate that cortisol has direct effects on the osmoregulatory physiology of the teleost gill.

Animals↗
PubMed1989

Effects of testosterone on morphology and on progestin and estrogen receptor levels in the mouse uterus and mammary gland.

The effects of androgen on the morphology and levels of cytosolic estrogen and progestin receptors (ER and PR) were studied in the mouse uterus and mammary gland. Testosterone neonatally and/or continuously in the adult lowers ER and PR levels particularly at early ages (40-60 days of age) in both the uterus and mammary gland. At older ages, less prominent changes in ER and PR levels are observed. Neonatal androgen treatment appears to exert both direct effects on the uterus and mammary gland and indirect effects (via the hypothalamo-hypophysio-ovarian axis). At all ages, neonatal testosterone in combination with continuous adult testosterone consistently depressed PR levels in both uterus and mammary gland, indicating that testosterone is a negative modulator of PR in these tissues.

Animals↗