Search Results

You are looking at 1 - 10 of 12 items for

  • Author: K. B. Smith x
  • Refine by access: All content x
Clear All Modify Search
K. B. Smith
Search for other papers by K. B. Smith in
Google Scholar
PubMed
Close
and
H. M. Fraser
Search for other papers by H. M. Fraser in
Google Scholar
PubMed
Close

ABSTRACT

We investigated the temporal relationship between serum concentrations of progesterone and immuno-reactive inhibin after treatment with an LHRH antagonist ([N-Ac-d-Nal(2)1,d-pCl-Phe2,d-Trp3,d-hArg(Et2)6,d-Ala10]-LHRH), during the mid-luteal phase in the macaque. Further, in an attempt to obtain a model of transitory suppression of luteal function, the effect of treatment with the LHRH antagonist for 1, 2 or 3 days during the mid-luteal phase on serum concentrations of progesterone and immunoreactive inhibin was compared. Differences in the pattern of decline of the two hormones were observed. Progesterone concentrations fell by 6 h after antagonist administration while inhibin was not significantly suppressed until 48 h. Treatment with three injections of LHRH antagonist caused a sustained suppression of luteal function as shown by low serum concentrations of progesterone and inhibin. Recovery of progesterone and inhibin secretion was observed in two out of six macaques treated with two injections of antagonist and in three out of six treated with a single injection. Therefore, with the regimens of LHRH antagonist which we employed this approach was not conducive to obtaining a reliable transitory suppression of luteal function. To elucidate further the gonadotrophin control of inhibin, six macaques were treated with three injections of the LHRH antagonist to induce a permanent suppression of luteal function but received concomitantly either human chorionic gonadotrophin (hCG) or human FSH daily for 5 days (n = 3 per group). FSH failed to prevent the antagonist-induced fall in progesterone and inhibin while hCG treatment completely reversed the inhibitory effects of the LHRH antagonist. These results give further support to the concept that the secretion of inhibin, like progesterone, is integrated with the LH control of the corpus luteum. The slower decline in inhibin after LHRH antagonist suggests that the gonadotrophic stimulus to the corpus luteum results in a more prolonged stimulus for inhibin than for progesterone secretion, or that inhibin has a longer metabolic clearance rate.

Journal of Endocrinology (1991) 128, 107–113

Restricted access
P. M. SMITH
Search for other papers by P. M. SMITH in
Google Scholar
PubMed
Close
and
B. K. FOLLETT
Search for other papers by B. K. FOLLETT in
Google Scholar
PubMed
Close

SUMMARY

Pituitaries from Japanese quail were superfused continuously for up to 12 h and the luteinizing hormone (LH) in the superfusate was measured by radioimmunoassay. After an initial period the release rate remained low and relatively constant. The introduction of hypothalamic extracts prepared from quail substantially increased immunoreactive LH release. The responses were dose-dependent. Cortical extracts caused a minor but significant response. Dopamine was inactive in the system. The technique is attractive because it allows for repetitive stimulation of the same pituitary glands with treatments being administered every 30–45 min.

Restricted access
B. J. A. FURR
Search for other papers by B. J. A. FURR in
Google Scholar
PubMed
Close
and
G. K. SMITH
Search for other papers by G. K. SMITH in
Google Scholar
PubMed
Close

* Department of Physiology & Biochemistry, The University, Whiteknights, Reading, RG6 2AJ, and † Imperial Chemical Industries Ltd, Pharmaceuticals Division, Mereside, Alderley Park, Macclesfield, Cheshire, SK104TG

(Received 4 April 1975)

Fraps (1961) proposed that in the hen an 'excitation' hormone secreted by the developing follicle initiated the release of the luteinizing hormone (LH) required for ovulation. Since progesterone induced premature ovulation in the hen (Fraps & Dury, 1943) it was considered the most likely candidate for such a role. Evidence showing that plasma progesterone rises either immediately before, or coincidentally with, the plasma LH surge is consistent with this hypothesis (Furr, Bonney, England & Cunningham, 1973). It has been demonstrated recently, however, that oestradiol (Senior & Cunningham, 1974) and testosterone (Etches, 1974) are also increased before the preovulatory rise in LH, which means that they cannot be precluded from consideration. Certainly there is ample evidence that oestradiol induces the LH

Restricted access
K. B. Smith
Search for other papers by K. B. Smith in
Google Scholar
PubMed
Close
,
S. F. Lunn
Search for other papers by S. F. Lunn in
Google Scholar
PubMed
Close
, and
H. M. Fraser
Search for other papers by H. M. Fraser in
Google Scholar
PubMed
Close

ABSTRACT

Changes in plasma concentrations of immunoreactive inhibin in the reproductively cyclic, pregnant and ovariectomized female marmoset monkey (Callithrix jacchus) were measured with a heterologous radioimmunoassay. The pattern of inhibin secretion in five marmosets studied individually during four consecutive cycles was shown to resemble that of progesterone. In these animals, data were pooled according to stage of cycle on the basis of plasma progesterone concentrations. Mean values for inhibin were 5465 and 4972 U/l during the early and late follicular phase. Concentrations rose during the luteal phase to 8431, 12 246 and 12 557 U/l for the early, mid- and late luteal phase respectively. The hormonal profile of inhibin during the normal cycle is similar in both marmoset and stumptailed macaque; however, the marmoset has a 28-fold greater level of inhibin during the luteal phase.

In six marmosets in which pregnancy occurred, inhibin concentrations showed no decline at the end of the conceptual cycle and remained increased with respect to the follicular phase throughout the subsequent gestation. Inhibin levels were non-detectable (< 1000 U/l) in ovariectomized and acyclic marmosets.

These results suggest that the corpus luteum is the major source of inhibin in this New World monkey, in common with man and the Old World primates.

Journal of Endocrinology (1990) 126, 489–495

Restricted access
J. J. Smith
Search for other papers by J. J. Smith in
Google Scholar
PubMed
Close
,
A. V. Capuco
Search for other papers by A. V. Capuco in
Google Scholar
PubMed
Close
,
I. H. Mather
Search for other papers by I. H. Mather in
Google Scholar
PubMed
Close
, and
B. K. Vonderhaar
Search for other papers by B. K. Vonderhaar in
Google Scholar
PubMed
Close

ABSTRACT

Developmental variation in the expression of the prolactin receptor in the ruminant mammary gland was investigated. Affinity chromatography revealed that bovine prolactin and human GH each bound to the same mammary gland proteins, yielding fractions enriched in binding activity and a protein of M r 36 000, assumed to be a bovine prolactin receptor. Affinity cross-linking of 125I-labelled human GH to mammary microsomes confirmed that the M r 36 000 protein was a bovine prolactin receptor. Binding assays of receptors in microsomes from the mammary tissue of cows and ewes at various stages of the lactational/reproductive cycle indicated developmental regulation of receptor concentration, but not receptor type, as no other bovine prolactin receptor type was detected by affinity cross-linking. These results suggest that differences in the response to prolactin in the mammary gland at various developmental stages in ruminants are not due to the expression of different forms of the prolactin receptor, and the lack of a prolactin effect on established lactation in ruminants is not due to the absence of the M r 36 000 form of the prolactin receptor.

Journal of Endocrinology (1993) 139, 37–49

Restricted access
K. A. MUNDAY
Search for other papers by K. A. MUNDAY in
Google Scholar
PubMed
Close
,
B. J. PARSONS
Search for other papers by B. J. PARSONS in
Google Scholar
PubMed
Close
,
JUDITH A. POAT
Search for other papers by JUDITH A. POAT in
Google Scholar
PubMed
Close
, and
D. J. SMITH
Search for other papers by D. J. SMITH in
Google Scholar
PubMed
Close

The presence of calcium in the fluid in which intestinal or kidney tissue is incubated is required for the tissue to respond to angiotensin. Everted sacs of rat colonic mucosa exhibited an increased rate of fluid transport in the presence of angiotensin; this response was lost when the serosal fluid, but not the mucosal fluid, was calcium-free. Angiotensin-stimulated transport was maintained when calcium was replaced with strontium or barium, but was lost when calcium was exchanged for magnesium. Similarly, calcium ions were required in the incubation fluid of rat kidney cortex slices to demonstrate angiotensin-enhanced sodium transport. These observations are discussed in relation to the possible roles of divalent cations in the mechanism of action of angiotensin.

Restricted access
E Hendry
Search for other papers by E Hendry in
Google Scholar
PubMed
Close
,
G Taylor
Search for other papers by G Taylor in
Google Scholar
PubMed
Close
,
K Ziemnicka
Search for other papers by K Ziemnicka in
Google Scholar
PubMed
Close
,
F Grennan Jones
Search for other papers by F Grennan Jones in
Google Scholar
PubMed
Close
,
J Furmaniak
Search for other papers by J Furmaniak in
Google Scholar
PubMed
Close
, and
B Rees Smith
Search for other papers by B Rees Smith in
Google Scholar
PubMed
Close

Human thyroid peroxidase (TPO), the key enzyme in thyroid hormone synthesis, can be produced in active form in the High Five insect cell line and when purified from the cell culture medium is soluble at concentrations of up to 18 mg/ml. This contrasts to a recent report in which human TPO produced in insect cells was found to be insoluble at high concentrations. Our concentrated TPO grows trigonal trapezohedral crystals of up to 0.5 mm in length in a vapour diffusion apparatus using polyethelene glycol as a precipitant. The crystals diffract X-rays to a 6 A resolution and the diffraction data from the crystals have been analysed giving unit cell dimensions. A potential molecular replacement solution has been identified using myeloperoxidase (MPO) as a phasing model.

Free access
H. M. Fraser
Search for other papers by H. M. Fraser in
Google Scholar
PubMed
Close
,
K. B. Smith
Search for other papers by K. B. Smith in
Google Scholar
PubMed
Close
,
S. F. Lunn
Search for other papers by S. F. Lunn in
Google Scholar
PubMed
Close
,
G. M. Cowen
Search for other papers by G. M. Cowen in
Google Scholar
PubMed
Close
,
K. Morris
Search for other papers by K. Morris in
Google Scholar
PubMed
Close
, and
A. S. McNeilly
Search for other papers by A. S. McNeilly in
Google Scholar
PubMed
Close

ABSTRACT

The putative endocrine role of inhibin in the control of FSH secretion during the luteal phase in the primate was investigated by immunoneutralization. Antisera against the 1–23 amino acid sequence of the N-terminus of the human inhibin α subunit were raised in a ewe and three macaques. Antisera (10–20 ml) were administered to macaques on day 8/9 of the luteal phase and serum samples collected during the treatment cycle and post-treatment cycle for determination of FSH, oestradiol and progesterone. In addition, localization of inhibin within the macaque ovary at this stage of the luteal phase was investigated using the ovine antiserum. Intense immunostaining was localized within the granulosa-lutein cells of the corpus luteum with absence of staining in the thecalutein cells or other ovarian compartments. Administration of antisera was without significant effect on serum concentrations of FSH when compared with control animals, either during the first 24 h of detailed observation or for the following 10-day period of the late luteal phase and subsequent early follicular phase. These results provide further evidence that the corpus luteum is the major source of inhibin immunoreactivity during the primate menstrual cycle, but fail to support an endocrine role for inhibin in the suppression of FSH secretion.

Journal of Endocrinology (1992) 133, 341–347

Restricted access
F. K. HABIB
Search for other papers by F. K. HABIB in
Google Scholar
PubMed
Close
,
G. L. HAMMOND
Search for other papers by G. L. HAMMOND in
Google Scholar
PubMed
Close
,
I. R. LEE
Search for other papers by I. R. LEE in
Google Scholar
PubMed
Close
,
J. B. DAWSON
Search for other papers by J. B. DAWSON in
Google Scholar
PubMed
Close
,
M. K. MASON
Search for other papers by M. K. MASON in
Google Scholar
PubMed
Close
,
P. H. SMITH
Search for other papers by P. H. SMITH in
Google Scholar
PubMed
Close
, and
S. R. STITCH
Search for other papers by S. R. STITCH in
Google Scholar
PubMed
Close

SUMMARY

Zinc and cadmium concentrations were measured by atomic absorption spectroscopy in normal and pathological human prostates. Our studies confirm that the values of zinc in normal tissue [6·84 ± 1·21 (s.e.m.) μmol/g] and benign prostatic hypertrophy (BPH) (6·91 ± 1·19 μmol/g) are similar, while in neoplastic tissues zinc concentrations were significantly lower (2·61 ± 0·45 μmol/g). The Cd2+ levels in BPH (23·11 ± 3·28 nmol/g) were, on the other hand, considerably higher than those found for normal tissues (5·15 ± 0·62 nmol/g). In agreement with other published reports, Cd2+ concentrations were found to be markedly increased in carcinomatous tissue (129·79 ± 22·22 nmol/g). No correlation was however established between the values for the two metals in either type of prostatic tissue.

An established specific radioimmunoassay was used for the measurement of testosterone and dihydrotestosterone (DHT) and a distinct pattern emerged upon comparing these results with those for the zinc and cadmium concentrations. It appears that the concentrations of DHT in benign hypertrophy and of testosterone and DHT in carcinoma were inversely proportional to the levels of Zn2+ in abnormal tissue. In contrast, the DHT levels in the hypertrophied and malignant tissue were proportional to the Cd2+ concentrations.

Restricted access
K. B. Smith
Search for other papers by K. B. Smith in
Google Scholar
PubMed
Close
,
M. R. Millar
Search for other papers by M. R. Millar in
Google Scholar
PubMed
Close
,
A. S. McNeilly
Search for other papers by A. S. McNeilly in
Google Scholar
PubMed
Close
,
P. J. Illingworth
Search for other papers by P. J. Illingworth in
Google Scholar
PubMed
Close
,
H. M. Fraser
Search for other papers by H. M. Fraser in
Google Scholar
PubMed
Close
, and
D. T. Baird
Search for other papers by D. T. Baird in
Google Scholar
PubMed
Close

ABSTRACT

The localization of inhibin α-subunit within the human corpus luteum was investigated. The antiserum used was raised in sheep against the first 1–23 amino acid sequence of the N-terminus of the human inhibin α-subunit. Using the avidin-biotin immunoperoxidase technique, intense immunostaining was localized within the granulosa-lutein cells of the corpus luteum, with absence of staining in the theca-lutein cells and surrounding ovarian tissue. Similar distribution of inhibin α-subunit immunostaining was observed in 12 corpora lutea obtained during the early, mid- and late-luteal phases and no changes in intensity were apparent at these different stages. Negative controls were obtained by applying antiserum which had been preabsorbed overnight with excess inhibin peptide in place of primary antiserum and also normal non-immune sheep serum as a substitute for primary antiserum. These results provide further evidence that the human corpus luteum is a significant source of immunoreactive inhibin during the normal human menstrual cycle. The specific localization within the granulosalutein cells of the corpus luteum suggests that inhibin α-subunit production may originate from a discrete cell population within the human corpus luteum.

Journal of Endocrinology (1991) 129, 155–160

Restricted access