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R Leask

Publications and source records attributed to R Leask.

11 recordsLinked to original sources
PubMed1992

Choriodecidual production of interleukin-8 and mechanism of parturition.

Both prostaglandins and antiprogestagens can induce labour and ripen the cervix, but the mechanisms are unclear. The collagenases that bring about cervical ripening are neutrophil derived. We examined the potential of uterine tissues to control neutrophil attraction by measuring interleukin-8 production. Choriodecidual cells in culture produced substantial amounts of interleukin-8; release was inhibited by progesterone and stimulated by the antiprogestagen mifepristone. Interleukin-8 production was similar in cells from spontaneously delivered placentas and from those obtained at caesarean section. Since prostaglandin E and interleukin-8 have synergistic effects, we suggest that interleukin-8 activity is the final common step of prostaglandin and antiprogestagen action in parturition.

Cells, Cultured↗
PubMed1988

Comparison of inhibin immunological and in vitro biological activities in human serum.

A comparison of serum inhibin levels in men and women was undertaken using a sensitive sheep pituitary cell in vitro bioassay and a newly developed heterologous RIA. The RIA was based on an antiserum raised to bovine 31K inhibin using [125I]31K inhibin as tracer. Bovine inhibin alpha- and beta-subunits, bovine activin-A, transforming growth factor-beta, and Mullerian inhibitory substance did not cross-react in the RIA. In both assays, dilutions of serum gave response lines parallel to that of the partially purified human follicular fluid inhibin preparation used as standard. Negligible levels of both bio (B)- and immuno (I) activities were found in serum from women with premature ovarian failure or castrated men. In ovulation-induced cycles, serum B inhibin levels increased progressively from the early to the late follicular phase and remained at the late follicular phase level during the early and midluteal phases. Serum I inhibin levels also rose during the follicular phase, but declined during the early luteal phase before increasing again in the midluteal phase. As a consequence, inhibin B:I ratios varied during the treatment cycle, with high ratios in early follicular (2.86) and early luteal (2.25) phases and a low ratio in the midluteal phase (1.09). Similar changes in serum B:I ratios also occurred during the midcycle and midluteal phases of normal cycles. The B:I ratio was lower (0.35) in normal men. We conclude that the largely similar pattern of inhibin biological and immunological activities in serum obtained during a variety of physiological conditions support the validity of the RIA procedure, and the B:I ratio of serum inhibin varies during the follicular and luteal phases of the cycle and is low in men. Potential reasons for these changes in B:I ratio include the presence of interfering substances in either the bioassay or the RIA, the presence of inhibin isoforms, and/or modulation of secreted forms by sex steroids.

Adult↗
PubMed1988

The sheep corpus luteum secretes inhibin.

An experiment was performed in 20 Merino ewes in which ovarian venous blood was collected by venepuncture at surgery and at two stages of the oestrous cycle. The ovarian venous concentrations of inhibin, oestradiol-17 beta and progesterone were determined. The results demonstrate that during the luteal phase of the oestrous cycle the ovarian venous blood draining an ovary containing luteal tissue contains significantly more inhibin bioactivity than ovarian venous blood from an ovary not containing luteal tissue. During the follicular phase the concentration of inhibin bioactivity in ovarian venous blood was reduced compared with the luteal phase. From this data we conclude that the sheep corpus luteum secretes inhibin bioactivity into the ovarian venous blood.

Animals↗
PubMed1987

High activity of an unstable form of glucose phosphate isomerase in the mouse.

Quantitative electrophoretic studies of the three allozymes of glucose phosphate isomerase (GPI-1) produced by Gpi-1sa/Gpi-1sc heterozygous mice revealed two opposing influences on GPI-1 activity. First, the GPI-1AC heterodimer is less stable than GPI-1AA but more stable than the GPI-1CC homodimer. Second, a genetic determinant that maps close to or within the Gpi-1s structural gene causes elevated activity of GPI-1AC and probably also GPI-1CC dimers. The relative lability of these allozymes masks this elevated activity in some tissues but the effect is probably ubiquitous. The significance of these observations is discussed.

Alleles↗
PubMed1987

The effects of danazol, mefenamic acid, norethisterone and a progesterone-impregnated coil on endometrial prostaglandin concentrations in women with menorrhagia.

The effects of four medical treatments have been assessed on menstrual blood loss (MBL) and endometrial prostaglandin (PG) concentrations in 30 women with objectively confirmed menorrhagia. Patients were randomly treated with danazol, 200 mg daily (n = 6), mefenamic acid, 500 mg three times daily during menses (n = 8), norethisterone, 5 mg twice daily from day 15-25 of the cycle (n = 8) or a progesterone-impregnated coil releasing 65 micrograms progesterone daily (n = 8). Endometrial biopsies were obtained in the mid-luteal phase before and after treatment in 23 cases, and assayed for PG content using radioimmunoassay. Treatment with norethisterone had no effect on either MBL or the concentration of PGs in the endometrium. MBL was significantly reduced after treatment with mefenamic acid (P = 0.05, n = 6) and the progesterone coil (P less than 0.05, n = 6), and was reduced in each of 4 cases treated with danazol in whom endometrial biopsies were available. Although there was no consistent change in endometrial PG concentrations in either the mefenamic acid or danazol groups, the lower MBL after insertion of the progesterone coil was associated with a reduced endometrial content of PGE, PGF2 alpha and "total" PG (6oxo PGF1 alpha + PGE + PGF2 alpha)-P = 0.05. Whereas the cyclooxygenase inhibitor mefenamic acid is likely to exert its effect on endometrial PGs at the time of menstruation itself, the continuous administration of progesterone throughout the menstrual cycle could result in both an impairment in estrogen receptor generation leading to reduced estrogen-mediated cyclooxygenase activity, and an increase in endometrial PG metabolism.

Biopsy↗
PubMed1987

Endometrial prostaglandins in women with abnormal menstrual bleeding.

Endogenous prostaglandin (PG) concentrations (6oxo PGF1 alpha, PGE, PGF2 alpha) have been measured by radioimmunoassay in the endometrium of women with objectively assessed menstrual blood loss (MBL). The concentration of PGE and "total" PG (6oxo PGF1 alpha + PGE + PGF2 alpha) was greater in the endometrium of those women with heavy menses (median MBL 152 ml (range 86,432) n = 16) than in those individuals with a normal menstrual loss (MBL 59 ml (18,78) n = 18). The concentrations of PGE and PGF2 alpha were similar in each group, but the concentration of 6oxo PGF1 alpha was significantly less than that of both PGE and PGF2 alpha. In 19 individuals, specimens of endometrium were incubated for 1 and 2 hours in modified 199 medium to assess PG release. There was a direct correlation between endogenous PG content and the production of 6oxo PGF1 alpha, PGE, PGF2 alpha and "total" PG in the first hour, which persisted for the second hour with PGF2 alpha and "total" PG. Endometrial PGs may play a role in the mechanism underlying menstruation; however the observed relationship between the prostanoids and MBL will vary with different experimental methods.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Quantification of the transition from oocyte-coded to embryo-coded glucose phosphate isomerase in mouse embryos.

A quantitative electrophoretic analysis of glucose phosphate isomerase (GPI-1) allozymes produced by heterozygous Gpi-1sa/Gpi-1sb mouse embryos has enabled us to estimate separately the contributions of GPI-1 enzyme that were oocyte coded, encoded by the embryonic, maternally derived Gpi-1sa allele and encoded by the embryonic, paternally derived Gpi-1sb allele. The oocyte-coded GPI-1 activity is stable until 2 1/2 days and then declines and is exhausted by 5 1/2 to 6 1/2 days post coitum (p.c.). The maternally and paternally derived Gpi-1s alleles are probably usually activated synchronously but several possible exceptions were observed. This activation was first detected in 2 1/2-day embryos. Total GPI-1 activity falls to a minimum around 3 1/2 to 4 1/2 days, even though embryonic gene expression has already begun. The profile of oocyte-coded GPI-1 activity is consistent with the suggestion (Harper & Monk, 1983) that there is a mechanism for the removal of oocyte-coded gene products at around 2 1/2 days p.c. The method of analysis described is applicable to other dimeric enzymes with electrophoretic variants.

Animals↗
PubMed1976

Plasma estrogen response to dehydroepiandrosterone sulphate injection in normal and complicated late pregnancy.

Dehydroepiandrosterone sulphate (DHAS) was administered intravenously to 70 women in the third trimester of pregnancy. By measuring the increase in the concentrations of estrogens in maternal plasma, it was hoped to assess the reserve capacity of the placenta. In normal pregnancies, unconjugated estradiol invariably showed a marked increase within 60 minutes of the injection of DHAS, reaching 174 to 478% above basal levels. Changes in unconjugated estrone were more variable, but significant increases usually occurred 2 to 3 hours after the peak concentration of estradiol. The concentrations of unconjugated estriol showed no significant change. Patients with preeclampsia, essential hypertension, retarded intrauterine growth, diabetes, and twin pregnancies did not show any major differences in response compared to the normal pregnancies. Two patients with intrauterine deaths had low basal concentrations of estrogens but responded to the DHAS injection by having significantly increased concentrations of unconjugated estradiol after 60 minutes. The only patient who did not show any increase in unconjugated estradiol levels after DHAS was thought to have a placental sulphatase deficiency. This test does not appear to have any advantage over existing methods of assessing the endocrine function of the placenta except in confirmation of placental sulphatase deficiency.

Dehydroepiandrosterone↗