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Biomedical subjects

B D Murphy

Publications and source records attributed to B D Murphy.

At least 91 records · Page 5Linked to original sources
PubMed1985

The limitations of atmospheric dispersion data and their contribution to uncertainties in dose assessment.

The calculation of atmospheric dispersion patterns is often an important component of radiation dose estimates. These dispersion calculations are a possible source of error and such errors or uncertainties need to be quantified. An important source of uncertainty is the meteorological data used in the calculations. Such data may be less than ideal because of constraints imposed by both availability and by the variances associated with population from which the data are obtained. We have studied a simple and much used model of atmospheric dispersion--the Gaussian plume. We discuss the uncertainties on the meteorological data which are input to the model and how these uncertainties could be used to estimate uncertainties for the modeling results. In doing this we have addressed both the uncertainty associated with a recorded climatology and the added uncertainty arising from the year-to-year variability at any given location.

Air Pollution, Radioactive↗
PubMed1985

Prolactin as a luteotrophin.

This review summarizes evidence suggesting a direct luteotrophic role for the hypophyseal hormone prolactin (PRL). This direct role consists of the capability to stimulate progesterone synthesis in vitro, the capability to maintain the membrane fluidity and receptors for luteinizing hormone and the capability to import substrate for progesterone synthesis. The time required for PRL-induced luteotrophic events is in the order of hours and sometimes days, and it appears that the effects are not associated with acute intracellular changes. The relatively slow responses and the stimulation of specific protein synthesis by PRL in target tissues other than the ovary suggest that PRL may function primarily through activation of the genome. PRL may induce the synthesis of specific luteal proteins, including enzymes for the regulation of intracellular substrate pools, membrane receptors for LH, or receptor proteins for lipoproteins, a major extracellular source of substrate.

Animals↗
PubMed1985

The effects of hypophysectomy and administration of pituitary hormones on luteal function and uptake of high density lipoproteins by luteinized ovaries and adrenals of the rat.

The role of plasma lipoproteins and hypophyseal hormones in the maintenance of progesterone secretion by the rat corpus luteum was investigated. In the first experiment, rats were treated daily from days 1-6 of pregnancy with 5 mg/kg 4-aminopyrozolopyramidine (4APP), a blocker of hepatic lipoprotein secretion, or with 5 mg/kg 4APP and 1 or 2 mg ovine PRL or 0.1 ml 0.5% phosphoric acid (4APP vehicle). The administration of 4APP reduced serum cholesterol and progesterone levels on days 2-6 of pregnancy and ovarian progesterone on day 6. The reduced progesterone secretion had no effect on embryo implantation. PRL, in the doses used, was incapable of abrogating the effects of 4APP on circulating or ovarian progesterone levels. Ovaries and adrenals, but not kidneys, of pseudopregnant rats exhibited specific and saturable uptake of porcine high density lipoprotein (HDL). Time-course studies indicated that the uptake of HDL was rapid in ovaries compared to that in adrenals. Ovaries from rats not only exhibited uptake of porcine HDL, but also were capable of using it for progesterone synthesis. Immature rats were assigned to 7 groups of 16 rats each; 8 rats from each group received 4 mg/kg 4APP, and 8 received 4APP vehicle from day 1 of pseudopregnancy. Four groups underwent hypophysectomy on day 1 and received one of the following: 0.1 mg (30 IU/mg) ovine PRL, 0.1 mg ovine LH or 0.1 mg synthetic ACTH daily, or no replacement therapy. Three sham-hypophysectomized groups received 0.1 mg PRL or LH twice daily or no hormone treatment. On day 5 of pseudopregnancy, rats received intravascular HDL, as described above, and were killed 1 h later. Treatment with 4APP increased the adrenal uptake of HDL, but ovarian uptake was not different from that in the control group. Hypophysectomy reduced both adrenal and ovarian uptake of HDL. In adrenals only ACTH at the dose employed ameliorated reduction of HDL uptake induced by hypophysectomy, while in the ovaries, both PRL and LH reversed the effect of hypophysectomy. The effect of PRL on uptake was specific to [125I]HDL and did not alter [125I]albumin uptake. It is concluded that: 1) hypophysectomy reduces HDL uptake in the luteinized rat ovary; and 2) PRL and LH replacement therapy maintain ovarian uptake of HDL, suggesting a direct effect of these luteotropins on lipoprotein uptake.

Adrenal Glands↗
PubMed1985

The effects of androgens and gonadotropins on testicular development in the prepubertal rat.

Treatment of male rat pups from five to 34 days of age with dihydrotestosterone or 5 alpha-androstane-3 alpha, 17 beta-diol, resulted in reduced testicular size at 35 days of age. This appeared to be due to decreased tubular diameters and reduced spermatocyte numbers, especially late pachytene cells in stages X to XIII. In rat pups treated with dihydrotestosterone or 5 alpha-androstane-3 alpha, 17 beta-diol, treatment with luteinizing hormone resulted in some restoration of tubular diameter and spermatocyte numbers. In 5 alpha-androstane-3 alpha, 17 beta-diol treated rat pups partial restoration of testes size resulted from follicle-stimulating hormone treatment, but tubular diameter and spermatocyte numbers were depressed. Single serum samples collected at 35 days of age were analysed for luteinizing and follicle-stimulating hormone concentrations. These data indicated that the effects of administered androgens were due primarily to depression of circulating gonadotropin concentrations but a direct inhibition at the level of the testis could not be ruled out.

Androstane-3,17-diol↗
PubMed1984

Role of lipoproteins and prolactin in luteal function in the ferret.

This study investigated luteal function in vitro during early pregnancy and pseudopregnancy in the ferret. Corpora lutea taken from animals on Day 13 following the ovulatory stimulus (mating or gonadotropin treatment) were dissociated with collagenase and incubated with ovine prolactin (Prl), ovine luteinizing hormone (LH), total lipoprotein fraction from canine serum, canine high-density lipoproteins (HDL), canine low-density lipoproteins (LDL) or combinations of Prl, LH, HDL, and LDL. Total lipoproteins produced statistically definable increases in progesterone accumulation in incubation media at 5 microliter (approx. 50 micrograms protein) through 25 microliter (250 micrograms protein) of the total lipoprotein solution. LDL in doses of 1 or more microgram protein stimulated progesterone accumulation in 2-h incubations and a similar stimulation was observed in the presence of 60 or more micrograms HDL. Prl, LH or the combination of Prl and LH had no apparent stimulatory influence on progesterone accumulation in vitro. Prl in combination with LDL further stimulated progesterone output by luteal cells in short-term incubation relative to LDL alone. Prl and LH together with LDL produced an increase in stimulation over LDL alone, but, for the most part, this augmentation did not exceed that recorded in the presence of the combination of Prl and LDL. No interactions between HDL and luteotropic hormones were present. The results indicate that lipoproteins increase progesterone output from ferret luteal cells, presumably by providing substrate for steroid hormone synthesis. No direct role for LH in ferret luteal function emerged from these experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Prolongation of the bovine estrous cycle with a gonadotropin-releasing hormone analog.

A series of in vitro and in vivo experiments was conducted to determine the effects of gonadotropin-releasing hormone (GnRH) on bovine luteal function. Biosynthesis of progesterone by bovine luteal cells during a 2-h incubation was determined following addition of 0, 10, 20, 40, 80 and 100 ng GnRH. Synthesis of progesterone was significantly depressed only by the 100-ng dose of GnRH. Luteal cells were incubated with 0.1 and 1.0 microgram GnRH in the presence and absence of 0, 1, 2 and 5 ng bovine luteinizing hormone (LH). Again, only the highest dose of GnRH significantly depressed LH-stimulated production of progesterone. Three experiments were conducted to assess the effects of repetitively administered GnRH. In the first, twice daily intrauterine infusions of 100 micrograms GnRH on Days 12, 13 and 14 of the bovine estrous cycle was without effect on plasma concentrations of progesterone and the functional life span of the corpus luteum (CL). In the second experiment, 10 micrograms of a highly potent GnRH analog (GnRH-A) was injected subcutaneously four times daily on Days 9-12 of the estrous cycle. GnRH-A-treated heifers had longer (P less than 0.05) mean estrous cycle lengths (26.2 +/- 0.72 days) when compared to control heifers (20.25 +/- 0.25 days). Plasma concentrations of progesterone were higher in the GnRH-A-treated group on Days 9-13 and Days 15-22 of the estrous cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Luteal contribution to the termination of preimplantation delay in mink.

Five groups of mink were mated once between March 17-19 (Day O), Group 1, designated intact controls, received no further treatment. The remaining four groups of mink underwent unilateral ovariectomy on the day following mating. At that time, preovulatory follicles were transplanted to the ipsilateral kidney capsule of two groups (3 and 5) to become ectopic corpora lutea (CL). The second ovary was removed from all of the animals in Groups 2-5 on Day 8 after mating. At that time animals in Groups 4 (ovariectomized) and 5 (ovariectomized + ectopic CL) received 1-g Silastic implants releasing progesterone. Similar Silastic implants without progesterone were administered to Groups 2 (ovariectomized only) and 3 (ovariectomized + ectopic CL). Blood samples were taken for progesterone analysis and laparotomies performed on all mink through Day 44 of the experiment. Embryos implanted in all (7/7) of the animals in Group 1 (intact controls) at an average of 23.7 days after mating. In Group 5 (ectopic CL + progesterone implant) 6/8 mink were found to have embryos which were calculated to have implanted at an average of 36.3 days after mating. No embryo implantation occurred in Groups 2, 3 and 4 although some unattached blastocysts were recovered from the uteri of the latter two groups. Progesterone was elevated by implants to levels typical of mink gestation. Ectopic corpora lutea further increased progesterone levels in the presence of a progesterone-releasing Silastic implant. The results demonstrate the absolute necessity of the ovary for embryo implantation in mink. Further, the hormonal requirements for implantation consist of progesterone as well as some other factor or factors of luteal origin.

Animals↗
PubMed1983

Precocious induction of luteal activation and termination of delayed implantation in mink with the dopamine antagonist pimozide.

The effects of the dopamine antagonist pimozide on the preimplantation delay phase of mink gestation were investigated in field and laboratory trials. Three doses of 0.1 mg pimozide in acetic acid administered on the 7th, 9th and 11th days after mating abbreviated gestation in Pastel kit female mink to a mean (+/- SEM) of 45.5 +/- 0.5 days, 10 days less than that observed in mink treated with vehicle only (55.6 +/- 0.6 days). In laboratory trials, four doses of 0.1 mg pimozide on the 7th, 9th, 11th and 13th day after mating resulted in embryo implantation at a mean of 25 +/- 4.3 days after mating while vehicle-treated control animals had mean preimplantation delay of 37 +/- 3.1 days. Luteal activation in the pimozide-treated group, as indicated by a rapid increase in circulating progesterone, began within 2 days after the first pimozide injection. No increase was observed in vehicle-treated mink until 6 or more days after the initiation of injections or 13 days after mating. It was concluded that pimozide, presumably by permitting endogenous secretion of prolactin, can induce precocious luteal activation and embryo implantation in the mink.

Animals↗
PubMed1982

Effects of medroxyprogesterone acetate on gestation in mink.

Mink ovariectomized 14 days after the first of two matings received injections of 2 mg MPA, the same MPA treatment + an oestradiol-17 beta implant or no replacement therapy. Some mink were ovariectomized after implantation and given a single dose of 2 mg MPA or no replacement therapy. MPA persisted in the serum at detectable levels for 13 or more days in all mink treated. MPA and MPA + oestradiol induced uterine growth but neither treatment was capable of inducing embryo implantation. More embryos were retained in mink treated with MPA alone and these appeared to be viable. Implanted embryos persisted for a longer period in animals that were ovariectomized and treated with MPA. MPA neither supported pregnancy nor permitted parturition. Serum LH was elevated by 1 week after ovariectomy and elevations persisted for a further 20 or more days. While MPA alone had no apparent negative feedback effects on LH, animals that received MPA + oestradiol did not display any elevation of LH, suggesting that oestradiol or a combination of MPA and oestradiol has a potent negative feedback in mink.

Animals↗
PubMed1981

Luteolysis in the hamster: abrogation by gonadotropin and prolactin pretreatment.

The luteolysis which terminated pseudopregnancy (PSP) in superovulated hamsters was studied. Spontaneous luteolysis occurred before 1100 on Day 7 of PSP and was characterized by a rapid decline in circulating progesterone levels. Luteolysis induced by prostaglandin F2 alpha (PGF2 alpha) on Day 5 of PSP displayed a similar rapid reduction in progesterone over 24 hours. In both cases levels of the progesterone metabolite 20 alpha hydroxypregn-4-ene-3-one (20 alpha-OHP) were less than 2 percent of progesterone levels and declined in a manner similar to progesterone. This suggests that conversion of progesterone or its precursors to 20 alpha-OHP was not a functional aspect of luteolysis in the hamster. Pretreatment with either prolactin (PRL), luteinizing hormone (LH) or follicle stimulating hormone (FSH) failed to prevent PGF2 alpha-induced luteolysis on Day 5 in the superovulated PSP hamster. Combinations of PRL and LH, LH and FSH or PRL and FSH were also unsuccessful in abrogating luteolysis. However, pretreatment with a combination of PRL, FSH and LH prevented luteolysis in 11/14 animals. These results suggest that luteotropic agents can reverse the luteolytic effects of PGF2 alpha in the hamster.

20-alpha-Dihydroprogesterone↗
PubMed1981

Influence of GnRH infusion on endocrine parameters and duration of postpartum anestrus in beef cows.

The effect of an intravenous infusion of gonadotrophin releasing hormone (GnRH) on the duration of postpartum anestrus in suckled beef cows was studied. Twenty-eight, mature, suckled beef cows were assigned in equal numbers to one of four treatment groups which were based on infusion with saline or GnRH (15ug/hour for 12 hours) and stage postpartum (pp) (20 or 35 days). Serum LH and progesterone were determined by radioimmunoassay for the period which began 5 days pre-infusion and ended at 55 days postpartum (ie: 35 or 20 days post-infusion). Serum LH remained below 5ng/ml during infusion in all control cows. Peak serum LH values, times of LH peaks, and duration of LH responses (means +/- SE) during infusion were 49 +/- 12 ng/ml, 162 +/- 42 minutes and 7.8 +/- 1.3 hours for the 20 day group and 44 +/- ng/ml, 144 +/- 6 minutes, and 8.2 +/- 1.1 hours for the 35 day group respectively. Serum progesterone levels indicated that the proportion of cows showing the onset of estrous cycles within 10 days of infusion was greater in the 20 day pp GnRH group (4/7) than the 20 day pp saline group (0/7) (p < .05) but was not significantly different between the 35 day pp GnRH (4/7) and 35 day pp saline (2/6) groups. The incidence of estrus was not affected by GnRH treatment and was 37% in all cows prior to 55 days pp. It was concluded that infusions of GnRH for 12 hours at a rate of 15 ug/hour could induce estrous cycles in suckled beef cows treated at 20 days postpartum.

Journal Article↗
PubMed1981

Prolactin in maintenance of the corpus luteum of early pseudopregnancy in the golden hamster.

The role of prolactin in the maintenance of the corpus luteum of pseudopregnancy was studied in the golden hamster. Nine groups of seven to fourteen animals each received 1 mg bromocriptine at 11.00 h on days 1, 2 or 3 of pseudopregnancy (three groups for each day). On each day of treatment with bromocriptine, one group of hamsters was injected with bovine prolactin 4 h before bromocriptine, and one group received prolactin 4 h before bromocriptine for three consecutive days following treatment with bromocriptine. One group received bromocriptine only. These nine groups were compared with a control group of animals given 0.85% saline instead of bromocriptine and prolactin. Peripheral blood samples were taken from all hamsters at 11.00 h on days 3, 4, 5 and 6 of pseudopregnancy and plasma levels of progesterone were determined by radioimmunoassay. Luteolysis, indicated by a decline in progesterone level by 24 or 48 h after treatment with bromocriptine, occurred in all hamsters given bromocriptine alone, whether it was administered on day 1, 2 or 3. Pretreatment with a single dose of prolactin did not mitigate the bromocriptine-induced fall in progesterone. In the majority of cases, pretreatment with prolactin plus daily doses of prolactin maintained the progesterone at levels not different from saline-treated hamsters. These data suggest that prolactin is a necessary luteotrophin during early pseudopregnancy without which luteolysis ensues.

Animals↗
PubMed1977

Failure of exogenous LH to prevent PGF2alpha-induced luteolysis in beef cows.

Henderson and McNatty (Prostaglandins 9:779, 1975) proposed that LH from the preovulatory LH surge attached to receptors on luteal cells and that this attachment might protect the early corpus luteum from PGF2alpha induced luteolysis. To test this hypothesis, experiments were performed on heifers at day 10-12 of the cycle. Both jugular veins were catheterized and infusions of either saline (0.64 ml/min) or LH-NIH-B9 (10 microgram/min; 0.64 ml/min) were given. Saline infusions were from 0-12 h; LH infusions were for 10 h and were preceded by a 2 h saline infusion. All animals were given 25 mg PGF2alpha im at 6 h (6 h into the saline infusion and 4 h into the LH infusion). Blood samples were taken at 0.5 h, 1 h and 4 h intervals from 0-12h, 13-18 h and 12-42 h respectively. Serum was assayed for LH and progesterone by radioimmunoassay methods. Two animals received saline and two received LH in each experiment. Each treatment was replicated 6 times. LH infusion resulted in a mean serum LH of 75 ng/ml compared to 0.90 ng/ml in saline infused animals. This elevation of LH did not alter PGF2alpha induced luteolysis as indicated by decline in serum progesterone. This experiment does not support the hypothesis that the newly formed corpus luteum is resistant to PGF2alpha because of protection afforded by the proestrus LH surge.

Animals↗