Search Results
You are looking at 1 - 10 of 11 items for
- Author: D. B. Ramsden x
- Refine by access: All content x
Search for other papers by D. L. INGRAM in
Google Scholar
PubMed
Search for other papers by D. B. RAMSDEN in
Google Scholar
PubMed
The disappearance rates of radioactive 3,5,3′-tri-iodothyronine (T3) and 3,3′,5′-tri-iodothyronine (reverse T3) from plasma were investigated in young pigs receiving various levels of food intake. The rate of utilization of reverse T3 decreased when intake was decreased to zero, whilst the rate of utilization of T3 was unaffected.
Search for other papers by S. G. Ball in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
ABSTRACT
The uptake of 3,5,3′-tri-iodothyronine (T3) by human erythrocytes was shown to occur by two saturable processes. System I (Michaelis constant (K m) 109 ± 40 (mean ± s.d.) nmol/l; maximal velocity (V max) = 43 ± 16 pmol/min per 109 cells) was observed over the range 1–50 nmol T3/l whilst system II (K m = 8·8 ± 8·0 pmol/l; V max = 29 ± 6 fmol/min per 109 cells) was observed over the range 1–500 pmol T3/l. At low concentrations (1–500 pmol/l) uptake processes equivalent to system II could be demonstrated for thyroxine and 3,3′,5′-tri-iodothyronine also. System II had the properties of a carrier-mediated process.
Journal of Endocrinology (1989) 123, 143–148
Search for other papers by Susan G. Daniel in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
The release of immunoreactive β-endorphin from rat anterior pituitary cells in culture was studied by radioimmunoassay and gel-filtration chromatography. Two forms of immunoreactivity were detected corresponding to β-lipotrophin (β-LPH) and β-endorphin. Cells were found to release β-endorphin-like immunoreactivity (β-endorphin LIR) into the culture medium for up to 10 days with a trough in release occurring between days 2–4. The ratio of β-LPH to β-endorphin released remained constant during the course of culture. After 4 days in culture β-endorphin LIR release was constant and responsive to modulation. Incubation with lysine-vasopressin (0·1 units/ml) produced a two- to threefold increase in release and dexamethasone (10−6 mol/l) suppressed release to 33% of controls. Neither stimulation nor suppression resulted in a change in the ratio of β-LPH to β-endorphin released. Dexamethasone suppression was not overcome by removal of dexamethasone or addition of vasopressin.
Search for other papers by N. J. S. Fitch in
Google Scholar
PubMed
Search for other papers by M. T. Akbari in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
ABSTRACT
Amplification and sequencing of the four transthyretin (TTR) exons of a subject with a variant TTR with four-fold increased affinity for thyroxine revealed a heterozygous G to A point mutation at base 7 of exon 2. This results in a serine for glycine change at residue 6 of the mature TTR monomer. No other mutations were found in any exon. Amplification and MspI digestion of TTR exon 2 from the leucocyte DNA of eight members of the subject's family revealed that all but one member were also heterozygous for [Ser6]-TTR.
Journal of Endocrinology (1991) 129, 309–313
Search for other papers by D. F. Wood in
Google Scholar
PubMed
Search for other papers by J. A. Franklyn in
Google Scholar
PubMed
Search for other papers by K. Docherty in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
Search for other papers by M. C. Sheppard in
Google Scholar
PubMed
ABSTRACT
Thyroid hormones are important regulators of GH synthesis and secretion. In this study we have made a detailed examination of the time-course of the effects of hypothyroidism and tri-iodothyronine (T3) replacement in the intact rat on GH gene expression in the anterior pituitary gland. Changes in pituitary cytoplasmic GH messenger (m)RNA levels were compared with total pituitary GH content and serum GH concentration during the development of hypothyroidism and following short-term T3 replacement in vivo. Hypothyroidism was associated with a fall in pituitary GH mRNA levels. Treatment of hypothyroid animals with T3 rapidly stimulated GH mRNA levels to values above those seen in euthyroid controls. The reduction in GH mRNA levels seen during the development of hypothyroidism was accompanied by a fall in serum GH and pituitary GH content, both of which were partially restored by T3 replacement. Thus thyroid hormone replacement in hypothyroidism rapidly stimulates GH mRNA synthesis, which is followed by the gradual restoration of pituitary GH stores and serum GH concentration.
J. Endocr. (1987) 112, 459–463
Search for other papers by D. F. Wood in
Google Scholar
PubMed
Search for other papers by K. Docherty in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
Search for other papers by K. I. J. Shennan in
Google Scholar
PubMed
Search for other papers by M. C. Sheppard in
Google Scholar
PubMed
ABSTRACT
The effects of tri-iodothyronine (T3) and TRH on prolactin mRNA accumulation in monolayer pituitary cell cultures prepared from both euthyroid and hypothyroid rats were investigated. Basal prolactin mRNA concentrations and prolactin release into culture medium were increased in hypothyroid cultures, the increase being related to the duration of hypothyroidism in vivo. The inhibitory effects of T3 seen in euthyroid cells were preserved in cells derived from hypothyroid animals, and the degree of inhibition was greater in cells from the most severely hypothyroid rats. However, the stimulation of prolactin synthesis and secretion induced by TRH in euthyroid cultures was not found in the hypothyroid cells. Hypothalamic and anterior pituitary TRH content were measured in similarly hypothyroid and euthyroid rats. A large hypothalamic pool of TRH was found, which was unchanged in hypothyroidism, whereas anterior pituitary TRH content was increased in the hypothyroid rats. The consequent down-regulation of anterior pituitary TRH receptors may explain the poor response of prolactin to TRH seen in vitro.
J. Endocr. (1987) 115, 497–503
Search for other papers by J. A. Franklyn in
Google Scholar
PubMed
Search for other papers by J. R. E. Davis in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
Search for other papers by M. C. Sheppard in
Google Scholar
PubMed
ABSTRACT
Circulating free thyroid hormone concentrations are reduced in subjects taking long-term phenytoin, a finding at variance with their euthyroid clinical state and normal serum TSH concentration. It is suggested, therefore, that phenytoin may modify the cellular effects of thyroid hormones.
In order to examine the influence of phenytoin on thyroid hormone action in the pituitary gland we studied its effect on the binding of tri-iodothyronine (T3) to isolated nuclei prepared from rat anterior pituitary tissue. Phenytoin inhibited the nuclear binding of T3 in a dose-dependent fashion. Phenytoin also partially inhibited thyrotrophin-releasing hormone-stimulated TSH release from cultured rat anterior pituitary cells. These studies provide evidence for a direct effect of phenytoin on the thyrotroph mediated via nuclear T3 receptor binding.
J. Endocr. (1985) 104, 201–204
Search for other papers by J. A. Franklyn in
Google Scholar
PubMed
Search for other papers by T. Lynam in
Google Scholar
PubMed
Search for other papers by K. Docherty in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
Search for other papers by M. C. Sheppard in
Google Scholar
PubMed
ABSTRACT
Thyroid hormones may directly regulate gene expression in the anterior pituitary. In order to examine this possibility we have studied the effect of hypothyroidism in the rat on pituitary cytoplasmic concentrations of messenger RNA (mRNA) encoding thyrotrophin (TSH) β and α subunits, prolactin and GH. We demonstrated a marked increase in TSH β and α subunit mRNA, accompanied by a decrease in GH mRNA, in the hypothyroid state, changes largely reversed by thyroid hormone replacement. We have thus shown a direct influence of thyroid status on the pretranslational events occurring in pituitary hormone synthesis. The simultaneous rise in cytoplasmic TSH β and α mRNA levels and fall in GH mRNA in hypothyroidism suggests that thyroid status exerts a differential effect on the expression of these genes.
J. Endocr. (1986) 108, 43–47
Search for other papers by J. A. Franklyn in
Google Scholar
PubMed
Search for other papers by D. F. Wood in
Google Scholar
PubMed
Search for other papers by N. J. Balfour in
Google Scholar
PubMed
Search for other papers by D. B. Ramsden in
Google Scholar
PubMed
Search for other papers by K. Docherty in
Google Scholar
PubMed
Search for other papers by M. C. Sheppard in
Google Scholar
PubMed
ABSTRACT
The role of oestrogen in the regulation of TSH gene expression is unclear. We have examined the effect of administration of oestrogen in the rat on serum TSH, pituitary TSH content and pituitary cytoplasmic concentrations of mRNA encoding the TSH β and α subunits, thus deriving measures of hormone release and synthesis. In addition, we have examined the effect of oestrogen on the binding of tri-iodothyronine (T3) to nuclear receptors in the anterior pituitary.
Administration of oestrogen did not affect serum concentrations of TSH in euthyroid or untreated hypothyroid rats, but did augment the effects of T3 (1 and 2 μg on serum TSH in hypothyroid animals 6 h after injection of T3. No influence of oestrogen or of thyroid status on pituitary content of TSH was seen.
A marked increase in the concentrations of TSH β and α mRNA in pituitary cytoplasm was found in hypothyroidism, compared with those in the euthyroid state. No effect of oestrogen on TSH mRNA was seen in euthyroid animals but concentrations of TSH β and α mRNA were lower in hypothyroid animals than in vehicle-treated controls. A stimulatory influence of T3 on TSH mRNA was seen 6 h after injection of T3; this stimulation was absent in oestrogen-treated rats. No effect of oestrogen on the action of T3 was evident 72 h after beginning treatment with T3. In addition to effects on serum TSH and TSH mRNA, an increase in the number of pituitary nuclear receptors for T3 was seen after oestrogen treatment.
The influences of oestrogen on serum TSH and on TSH mRNA are consistent with augmentation of thyroid hormone effects; this influence may be mediated by an increase in the number of pituitary nuclear receptors for T3.
J. Endocr. (1987) 115, 53–59
Search for other papers by D. B. RAMSDEN in
Google Scholar
PubMed
Search for other papers by T. J. SMITH in
Google Scholar
PubMed
Search for other papers by W. A. BURR in
Google Scholar
PubMed
Search for other papers by E. G. BLACK in
Google Scholar
PubMed
Search for other papers by J. M. LEE in
Google Scholar
PubMed
Search for other papers by R. HOFFENBERG in
Google Scholar
PubMed
The effect of surgical stress and ACTH injection on the peripheral monodeiodination of thyroxine (T4) was studied in the rabbit. These stimuli resulted in a switch from the peripheral formation of tri-iodothyronine (T3) to reverse T3 in normal rabbits and in rabbits whose thyroidal secretion was suppressed by administration of T4. This is analogous to the situation in man. These changes were not due to alterations in the serum binding capacity for thyroid hormones.
