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Biomedical subjects

R F Williams

Publications and source records attributed to R F Williams.

At least 19 recordsLinked to original sources

Characterization by electron paramagnetic resonance of the interactions of L-arginine and L-thiocitrulline with the heme cofactor region of nitric oxide synthase.

Nitric oxide synthase (NOS) catalyzes sequential NADPH- and O2-dependent mono-oxygenase reactions converting L-arginine to N omega-hydroxy-L-arginine and N omega-hydroxy-L-arginine to citrulline and nitric oxide. The homodimeric enzyme contains one heme/monomer, and that cofactor is thought to mediate both partial reactions. Here we show by electron paramagnetic resonance spectroscopy that binding of substrate L-arginine to neuronal NOS perturbs the heme cofactor binding pocket without directly interacting as a sixth axial heme ligand; heme iron is exclusively high spin. In contrast, binding of L-thiocitrulline, a NOS inhibitor, produces both high and low spin iron spectra; L-thiocitrulline sulfur is a sixth axial heme ligand in one, but not all, of the low spin forms. The high spin forms of the L-thiocitrulline NOS complex display a distortion in the opposite direction to that caused by L-arginine binding. The findings elucidate the binding interactions of L-arginine and L-thiocitrulline to neuronal NOS and demonstrate that each causes a unique perturbation to the heme cofactor pocket of NOS.

Animals

Lactational anovulation in non-human primates: restriction of nursing inhibits Prl secretion without precipitating the return of ovulatory menstrual cyclicity in cynomolgus monkeys.

To test the hypotheses that nighttime suckling and elevated nocturnal prolactin concentrations are essential for the continuation of lactational anovulation, the effects of restricting nursing to twelve h per day (either day or night) on maternal prolactin (Prl) levels and resumption of ovulatory menstrual cycles were studied in five groups of cynomolgus monkeys: Group 1: baby weaned: Group 2: baby fully nursed: Group 3: baby nursed night only; Group 4: baby nursed day only; and Group 5: baby housed with mother but not allowed to nurse. Restrictions were initiated at approximately 150 days postpartum and were achieved by placing a non-nursing jacket over the nursing jacket, which was worn 24 h/day. Fifteen out of seventeen monkeys remained anovulatory while housed with their infants, irrespective of the type of nursing restriction. First postpartum ovulations occurred approximately two months post-weaning. Plasma prolactin concentrations during both day and nighttime were significantly (p < 0.05) greater in the fully nursing group(s) than in all other groups. Fully nursing mothers had significantly (p < 0.01) greater prolactin concentrations at night than during the day. Among the restricted groups, the night only suckling group had significantly greater prolactin concentrations at night than the other restricted groups. There were no differences between daytime values, and within each restricted group there were no significant differences between day and night prolactin levels. We conclude that 1) nighttime suckling is not an absolute prerequisite for sustained lactational anovulation, and 2) suckling-induced hyperprolactinemia is not the principle mediator of lactational anovulation.

Animals

Antiovulatory actions of RU 486: the pituitary is not the primary site of action in vivo.

Continuous administration of RU 486 impairs follicular development and inhibits ovulation in women. Yet, the mechanism of ovulation inhibition remains unknown. To characterize the mechanism(s) of ovulation inhibition, we studied six regularly menstruating cynomolgus monkeys for three consecutive (control-rest-treatment) cycles. Monkeys received 1 mg/kg.day RU 486 in between cycle days 2-22. Basal and GnRH-stimulated (1 and 50 micrograms GnRH, iv, 2 h apart) secretion of LH and FSH was assessed using serial blood samples (every 15 min for 12 h) collected on cycle day 10. Serum levels of estradiol (E2), progesterone (P4), RU 486, cortisol, LH, FSH, and PRL were analyzed by RIAs, the bioactivity of LH was assessed using a mouse Leydig cell assay. The mean cycle length was prolonged by RU 486 treatment from 31.8 to 69.8 days (P = 0.008). During RU 486 treatment, patterns of E2 secretion varied considerably; the mean +/- SD E2 level was 204 +/- 139 pmol/L. LH peaks and P4 profiles compatible with luteal function were seen only before resumption of menstruation. However, one monkey had an increase in P4 after the GnRH challenge-induced LH secretion. Basal levels of LH varied between suppressed and apparently normal values, whereas basal FSH seemed little affected by RU 486 treatment. In two monkeys with E2 secretion indicative of normal follicular development, minor peaks of LH, but no rises in serum P4, were seen. The ratio of bioactive/immunoactive LH was reduced in these monkeys during RU 486 treatment compared to that during the washout period of the treatment cycle. Surprisingly, the pituitary responsiveness to acute GnRH challenge was not affected by RU 486 administration. The individual levels of RU 486 were similar during the treatment period (mean, 40 nmol/L). A resumption of ovulatory cycles occurred when RU 486 concentrations were below 2.5 nmol/L. We conclude that in cynomolgus monkeys, inhibition of ovulation by RU 486 occurs mainly at the level of the hypothalamus, with possible additional effects on the granulosa cell function and alterations of LH bioactivity.

Animals

New magnetic resonance imaging techniques for the detection of breast cancer.

The importance of contrast agents in enhancing diagnoses from magnetic resonance images has been established in numerous cases. However, the development of a potent tissue-specific contrast agent, as a sensitive probe for early detection and investigation of the physiological characteristics of a tumor, has not yet been realized in MR imaging (MRI). In nuclear scintigraphy the technique has been demonstrated; however, the poor spacial resolution inherent to the modality and the substantial dose of radioactivity administered to the patient has hindered its widespread use. This article will review the different classes of contrast agents in MRI, with special focus on the strategies involved in the development of targeted tissue-specific MRI contrast agents for the early detection of breast cancer. The features of a new class of contrast agents for targeted MR imaging will be described. Gadolinium-containing melanin polymers (GMP's) have been synthesized as MR contrast agents in our laboratory. These GMP's demonstrate significantly higher relaxivities than any other paramagnetic contrast agents reported; consequently, they are extremely effective contrast enhancing, imaging agents by themselves. The successful coupling of these potent GMP's to a monoclonal antibody specific for breast carcinoma, the 323/A3 monoclonal antibody, suggests that in vivo tissue-specific MR imaging, at the receptor level, will become feasible in the near future.

Breast Neoplasms

Hypothalamo-pituitary effects of RU486: inhibition of progesterone-induced hyperprolactinaemia.

Monkeys given oestrogen priming at physiological levels for at least 1 week become hyperprolactinaemic upon the addition of physiological progesterone administration. Here, using RU486, we test whether that this oestrogen/progestin-induced hyperprolactinaemia results from classical progesterone actions at the hypothalamo-pituitary level. Blood samples were collected daily from study day 1-67. Each monkey (n = 2) received daily injections of 25 micrograms/kg oestradiol benzoate, i.m., on study days 5-60. Progesterone-filled silastic capsules (3 cm) were inserted on study day 14 and removed on day 53. On study days 39-45, each monkey received RU486 (25 mg/day, p.o.). Serum samples were stored at -20 degrees C until assayed for prolactin, oestradiol, progesterone and RU486 by radioimmunoassay. Hyperprolactinaemia was induced in all three monkeys upon insertion of progesterone capsules. Prolactin concentrations fell sharply during RU486 treatment to nadirs some 10-fold less than prior to RU486 treatment. The time series was modelled by the Box-Jenkins autoregressive-integrated moving average (ARIMA) method with progesterone producing a gradual increase in prolactin concentrations and RU486 producing a sudden decrease. Statistically significant effects of progesterone and RU486 were found. Thus, the addition of progesterone to an oestrogenized milieu significantly increased prolactin concentrations, and RU486 fully reversed this effect. This evidence indicates that the progesterone-induced hyperprolactinemia in an oestrogenized milieu results from classical progesterone effects.

Animals

Non-competitive anti-oestrogenic activity of progesterone antagonists in primate models.

We have summarized some of the studies containing basic biological data suggesting potential therapeutic utility of the anti-proliferative activity of antiprogestins on uterine tissues. The non-competitive anti-oestrogenic effects of RU486 were examined using oestradiol-treated ovariectomized monkeys given RU486, progesterone or both. The oestradiol-induced luteinizing hormone surge of control animals was abrogated by progesterone and/or RU486. Secretory transformation by progesterone was inhibited by RU486 co-administration. RU486 alone (1 mg/kg) induced endometrial secretory transformation, but higher doses (5 mg/kg) induced inhibited proliferation and secretory activity. Thus, in the presence of progesterone, RU486 is antagonistic but, in its absence, RU486 exhibits endometrial progestational effects at low doses and an anti-proliferative (anti-oestrogenic) effect at higher doses. These data encourage continued evaluation of RU486 as a potential contraceptive agent acting at the pituitary and/or endometrial level. Our study also demonstrates that after physiological oestradiol replacement therapy, oestradiol receptor concentrations rise dramatically following antiprogestin treatment; this effect was dose-dependent.

Animals

Postpartum anovulation in non-nursing monkeys: hypothalamic-pituitary-ovarian refractoriness is not induced by the milieu of early pregnancy.

To evaluate the role of the early pregnancy milieu in inducing postpartum refractoriness of the hypothalamic-pituitary-ovarian axis, pregnancies in rhesus monkeys were terminated on either day 35 of gestation or near term at 162 days. Non-nursing mothers with gestations interrupted near term resumed ovulation at a mean of 56 +/- 12 (mean +/- SE) days postpartum, in contrast to the 17 +/- 2 days required for the females having had abortions at day 35. These results demonstrate that the early pregnancy milieu is not determinant of the hypothalamic-pituitary-ovarian refractoriness observed in non-nursing mothers delivering at term.

Abortion, Induced

Hypothalamo-anterior pituitary gonadotropin-releasing hormone and substance-P systems during the 17 beta-estradiol-induced plasma luteinizing hormone surge in the ovariectomized female monkey.

The present study examined the effects of 17 beta-estradiol benzoate (E2B) on the hypothalamic (HT) and anterior pituitary (AP) content of GnRH precursor (pro-GnRH-GAP), GnRH, GnRH-associated peptide (GAP), and substance-P (SP) during the various phases of the E2B-induced LH surge in cynomolgus monkeys. Changes in GnRH and GnRH-associated peptide (GAP) at both hypothalamic and AP levels were closely related at all times after E2B treatment. However, the pattern of change in the AP was very different from that in the HT. In the HT, pro-GnRH-GAP levels did not change significantly throughout the experimental period. In the AP, the pro-GnRH-GAP increased 48 h post-E2B treatment, the time of initiation of the LH surge. An 8-fold increase in AP GnRH occurred 30 h post-E2B treatment. There were no significant changes in the HT content of SP at any time after E2B treatment. However, there was a depletion of AP content by 48 h post-E2B, the time of the LH surge. These results demonstrate that E2 activates and deactivates in a coordinated manner the GnRH and SP systems of the HT-AP complex during initiation of the E2-induced LH surge. The observation that more significant changes occur in the AP than in the HT suggests that an important component of the E2 effect in inducing the LH surge may be directly at the AP level. This action involves changes in the contents of GnRH and SP in the AP.

Animals

Amniotic fluid epidermal growth factor concentrations. The effect of intra-amniotic thyroxine for acceleration of fetal maturation.

Intra-amniotic thyroxine (200-500 ug) was administered weekly to 29 women in the third trimester to enhance fetal maturation. Lecithin-sphingomyelin ratio (L/S) and epidermal growth factor (EGF) were measured in amniotic fluid (AF) before (n = 58) and after (n = 92) administration of thyroxine. The AF L/S ratio and EGF concentration increased linearly with increasing gestational age both before (r = 0.76, p < 0.0001; r = 0.41, p < 0.001, respectively) and after (r = 0.62, p < 0.0001; r = 0.43, p < 0.001 respectively) initiation of thyroxine treatment. The slopes of gestational age vs L/S (0.07) and EGF (0.004) before T4 increased significantly after initiation of T4 therapy (L/S:0.23, p < 0.001; EGF:0.015, p < 0.01, respectively). L/S ratios correlated with AF EGF levels before (r = 0.77, p < 0.001) and after (r = 0.63, p < 0.001) initiation of T4 therapy. These results demonstrate that intra-amniotic thyroxine accelerates not only the progression of the amniotic fluid L/S ratio, but the appearance of EGF.

Adult

Antide bioavailability: single dose administration for suppression of testosterone and inhibin in male monkeys.

The pharmacokinetics and pharmacodynamics of a single sc injection of Antide on testosterone (T) and inhibin secretion in intact male cynomolgus monkeys were examined. Fifteen primates were randomized to three groups receiving: propylene glycol and water vehicle, 3 mg/kg Antide, and 10 mg/kg of Antide. Antide at the 10 mg/kg dose caused long-term suppression of T ranging from 24-56 days. At the 3 mg/kg dose, suppression of T was of shorter duration. Serum Antide levels were significantly greater in the 10 mg/kg group than the 3 mg/kg group (p less than 0.02), both initially and through 35 days post-treatment. The duration of testosterone inhibition and sustained Antide levels were significantly correlated (p less than 0.01). Inhibin concentrations followed the same general pattern as testosterone reaching a nadir on day 21 post-treatment before subsequent recovery. The prolonged suppressive effect of Antide on T without detectable side effects makes this compound an excellent candidate for clinical evaluation.

Animals

GnRH antagonists suppress prolactin release in non-human primates.

GnRH antagonists, such as Antide, are being evaluated for potential contraceptive applications. Although their contraceptive efficacy clearly results from their rapid inhibitory effects on gonadotropin release, there remains the possibility of other incidental effects. Under certain physiological conditions, the release of prolactin (Prl) appears to be temporally related to the secretion of luteinizing hormone (LH) and hence by inference to the secretion of GnRH. Here, we examined the effects of the GnRH antagonist Antide on the release of LH and Prl. Under agonadal conditions, a remarkable concordance was seen between LH and Prl pulses with up to 100% of pulses being coincident. Administration of Antide resulted in a rapid parallel decline in both LH and Prl with LH levels falling by 50% within 2 h and Prl levels falling by 30-40%. At this dose of Antide (1.0 mg/kg, sc), pulsatile release of LH and Prl continued albeit at a much reduced amplitude. The administration of a bolus of exogenous GnRH in the face of GnRHant-induced suppression resulted in prompt release of LH and Prl in all 3 monkeys. Since Antide inhibits the release of LH and Prl in a parallel fashion, and GnRH re-stimulates the release of both hormones in a parallel fashion, we conclude that the synchronous pulsatile release of LH and Prl observed in the agonadal monkey is due to a direct action of GnRH. What this action is for Prl release, and how it relates to the control of dopamine or other neuroendocrine mechanisms normally controlling the release of Prl remains unclear. It also remains to be seen whether this GnRH antagonist-induced suppression of Prl will have physiologic significance.

Animals

Magnetic resonance spectroscopy of inflammation associated with the temporomandibular joint.

Noninvasive early recognition and treatment of temporomandibular joint dysfunction remains a diagnostic challenge. This pilot study evaluated the use of phosphorus 31 magnetic resonance spectroscopy with magnetic resonance imaging to measure alterations in pH and high-energy phosphate metabolite ratios of muscle that is adjacent to an inflamed temporomandibular joint. Ten New Zealand white rabbits were used in this study. Two animals were used to develop signal acquisition protocols and to ensure that stable baseline data could be measured. In each of the eight animals used in the experiment, one temporomandibular joint was injected with a suspension of silica particles and the contralateral joint served as a control. Data were collected from control and experimental joints on days 0, 7, 14, 21, and 28, after the injection. At the end of the study, temporomandibular joints were block resected and histologically examined to confirm the presence of an inflammatory response. Results indicated that pH and metabolite ratios could be obtained by 31P-magnetic resonance spectroscopy. Changes in pH and some metabolite ratios in experimental joints showed statistical significance (p < 0.001). Differences were seen on day 2 and day 7 (p = 0.040 and p = 0.008, respectively) in the phosphocreatine/alpha-adenosine triphosphate ratios. This contrasts with phosphocreatine/beta adenosine triphosphate ratios that showed significance that began at day 7 (p = 0.022) and continued to day 14 (p = 0.025). Histologic examination indicated that the tissue response within the joint capsule was less than the granulomatous reaction expected.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate

Interval required for gonadotropin-releasing hormone-agonist-induced down regulation of the pituitary in cynomolgus monkeys and duration of the refractory state.

OBJECTIVES: To determine the minimal interval of gonadotropin-releasing hormone agonist (GnRH-a) administration required to induce pituitary refractoriness to the positive feedback effects of estradiol (E2) and to determine the duration of the induced refractory state in a nonhuman primate model. SETTING: Research laboratories of The Jones Institute for Reproductive Medicine. SUBJECTS: Cynomolgus monkeys with documented regular menstrual cycles. INTERVENTIONS: Part 1. Groups of four monkeys treated with leuprolide acetate (LA) for increasing intervals (0, 2, 4, 6, and 8 days), then challenged with E2 benzoate to induce a gonadotropin surge. Part 2. Groups of four monkeys treated with LA for the minimal time required to induce pituitary refractoriness (6 days), then challenged with E2 benzoate 2, 4, or 7 days after cessation of LA treatment. MAIN OUTCOME MEASURE(S): Pituitary luteinizing hormone and follicle-stimulating hormone and E2 levels were monitored. RESULTS: A minimum of 5 days of treatment is required for LA to induce pituitary refractoriness to the positive feedback effects of E2 benzoate. Once the down regulated condition is achieved, the refractory state lasts for at least 4 but not more than 6 days. CONCLUSION: The minimal treatment interval required for a GnRH-a to induce pituitary refractoriness to the positive feedback effects of estrogen and the duration of the induced refractory state are determined to be 5 days for these primates.

Animals

Controlled study of Pseudomonas cepacia and Pseudomonas maltophilia in cystic fibrosis.

In a retrospective study, children with cystic fibrosis who were colonised with Pseudomonas cepacia were compared with a control group who were colonised with Pseudomonas maltophilia. Out of 216 children with cystic fibrosis seen between 1983 and 1990, P cepacia was recovered from 13 (median age at colonisation 12.2 years) and P maltophilia from 23 (median age at first colonisation 6.1 years), and both organisms were recovered in five cases. With the exception of two patients with P cepacia in whom no other pathogens were found, all the patients with P cepacia or P maltophilia had co-colonisation with Pseudomonas aeruginosa. The lack of spread of P cepacia to siblings with cystic fibrosis, and the relative lack of inpatient contact between colonised and uncolonised patients suggest that cross infection is not the sole route whereby patients with cystic fibrosis become infected, but the possibility of cross infection cannot be excluded from our data. Three patients with P cepacia died, but two of these had shown appreciable respiratory deterioration before colonisation with P cepacia; there was no evidence of unexpected deterioration in the remainder or in the controls with P maltophilia. By 1990, the prevalence of P cepacia was 9/133 (7%) and that of P maltophilia was 13/133 (10%), but it was impossible to determine to what extent this increase was due to the introduction of the routine use of selective media. Further studies are required to establish whether patients with and without P cepacia should be segregated.

Adolescent