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`12th'JOINT
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`_
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`.
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`‘ OF ‘
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`- BRITISH
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`SOCIETIES
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`29 Min-ch - 1 April 1993
`Liverpool
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`These abstracts are published in good faith exactly as received from the submitting
`authors. The opinions and views within are those of the submitting authors and
`have not been verified by the Societies, who accept no scientific responsibility for
`the statements made or for their content.
`It is not possible to guarantee that the
`abstracts printed in this Supplement will be presented at the Meeting.
`
`© 1993 Mutual of Endocrinology Ltd
`
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`InnoPharma Licensing LLC V. AstraZeneca AB IPR2017-00905
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`BRITISH ENDOCRINE SOCIETIES
`
`Benefactors
`
`Clinical Endocrinology Trust
`Farmitalia Carlo Erba
`
`Ferring Pharmaceuticals
`Kabi Pharmacia
`Novo Nordisk
`Sandoz Pharmaceuticals
`Serono Laboratories
`ZENECA Pharma
`
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`CONTENTS
`
`PLENARY LECTURERS’ BIOGRAPHICAL NOTES
`
`PLENARY LECTURES
`
`Society for Endocrinology Medal Lecture
`Society for Endocrinology Dale Medal Lecture
`Society for Endocrinology Transatlantic Medal Lecture
`Thyroid Club Pitt-Rivers Lecture
`Clinical Endocrinology Trust Lecture
`Royal Society of Medicine Lecture
`
`SYMPOSIA
`
`Steroids and the brain
`
`Paracrinology of early pregnancy
`Angiogenesis as an endocrine response
`Aetiology of endocrine tumours
`Renin-angiotensin-aldosterone axis
`Endocrine autoimmunity
`
`CLINICAL MANAGEMENT WORKSHOPS
`
`Endocrine management of breast cancer
`Thyroid eye disease
`Secondary osteoporosis
`
`METHODS UPDATES
`
`Non-isotopic in—situ hybridization
`Gonadotrophin bioassay versus immunoassay
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`RESEARCH COLLOQUIA
`Steroid action
`
`Intracellular signalling
`
`ORAL COMMUNICATIONS
`Growth
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`Reproduction
`Endocrine pathology
`Thyroid
`Neuroendocrinology
`Steroidogenesis
`
`POSTER PRESENTATIONS
`Adrenal
`Bone and calcium
`Diabetes
`
`Endocrine pathology
`Growth
`
`Methodology
`
`SI
`
`82
`S3
`S4
`SS
`86
`
`87-810
`31 1-814
`SIS-$18
`819-522
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`823-826
`527-831
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`832-833
`834-835
`836-838
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`839-840
`S4 1
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`S42, RCl-RC4
`S43, RCS—RCS
`
`0C 1-OCS
`OC6-OC1 1
`OC12-OC17
`OC18—OC28
`OC29—OC33
`
`OC34-OC38
`
`P1-P26
`P27—P4O
`P41-P50
`P51-P67
`P68-P89
`P90-P98
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`Neuroendocrinology
`Pituitary
`Regulatory peptides
`Reproduction
`Thyroid
`
`INDEX OF FIRST AUTHORS
`
`P99-P121
`P122-P152
`P15 3-P165
`P166—P207
`P208-P237
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`A PURE ANTI-OESTROGEN,
`182,780,
`lCI
`P183 THE EFFECTS OF
`ENDOCRINOLOGY IN NORMAL PRE-MENOPAUSAL WOMEN
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`0N REPRODUCTIVE
`
`E.J. Thomas‘, N.M. Thomas‘, P.L. Walton2 and M. Dowsett3
`‘Obstetrics
`and Gynaecology, Southampton,
`ZICI Pharmaceuticals, Alderley Edge
`3Biochemistry, Royal Marsden Hospital
`
`and
`
`ICI 182,780 has been found in vitro and in animal models to exert a pure anti-oestrogenic action
`with no agonist activity. 19 pro-menopausal women were prescribed 182,780, 12 mg
`intramuscularly, daily for 7 seven days prior to hysterectomy starting between day 5 to day 9 of
`the menstrual cyclé, for benign gynaecological disease. 11 controls were also recruited. No
`significant adverse events were reported in either group. 3 women in the treatment group were
`withdrawn because of endocrine abnormalities or because they were in the luteal phase at the
`beginning of treatment. 12 of the 16 remaining treated women showed a consistent response to
`ICI 182,780 characterised by no increase in the plasma concentration of LH and FSH, no LH surge,
`continuing follicular growth ultrasonically, increasing plasma oestradiol concentrations, no increase
`in endometrial thickness and no ultrasonic evidence of ovarian hyperstimulation. The remaining 4
`women showed an increase in endometrial thickness in parallel with an increase in plasma
`oestradiol concentration. Overall plasma oestradiol concentrations were significantly higher in the
`treated group compared with control group over the sampling interval. Pharmacodynamic data are
`being analyzed. Overall
`the results suggest
`that
`in a majority of ore-menopausal women
`ICl 182,780, 12 mg daily for 7 days does not stimulate gonadotrophin secretion and will suppress
`endometrial growth in spite of continuing oestradiol stimulation. The absence of adverse events
`or of evidence of ovarian hyperstimulation suggests that this compound may be able to be used
`for the treatment of oestrogen dependent diseases in pre-menopausal women.
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`P184 COMPARISONS OF THE BIOACTIVITY OF FEMALE RAT PITUITARY AND PLASMA LH
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`A.J. Leigh, T. Shakil", S.A. Fickling+ and C.A. Wilson. Departments
`obstetrics & Gynaecology, Physiology” and Cellular & Molecular Science+,
`St. George’s Hospital Medical School, London SW17 ORE.
`
`physico—chemical
`different
`possess
`LH
`plasma
`and
`Pituitary
`We have now compared their bioactives “in vitro",
`characteristics (1).
`investigating their ability to stimulate the production of testosterone,
`progesterone and tissue plasminogen activator (tPA).
`the
`Pituitaries (n=9) and plasma (n=7) were collected on proestrus,
`former were homogenised in buffer and the supernatant diluted 1:500. All
`samples were assayed by radioimmunoassay (RIA;NIH—RP3 standard) and the
`mouse Leydig cell bioassay.
`Samples were incubated for 48 hours with
`cultured granulosa cells isolated from rat ovarian follicles (2400 en
`diameter) and then the culture medium was assayed for progesterone by
`RIA.
`Samples were also incubated for 48 hours with SV4O transected
`human umbilical vein endothelial cells (SGHEC7) and the incubate assayed
`for total tPA by Elisa.
`Results standardised to the concentration of steroid or tPA produced
`per ng of immunogenic LH showed that the ratio of plasma to pituitary
`activity was 4.1:1 for testosterone production;
`3.821 for progesterone
`production, while for tPA, plasma LH produced 107i16.5 ng/ml/ng LH (n=7)
`but pituitary LH applied to the cells at 4.9:0.2 ng (n=9) was inactive.
`These findings indicate that on release of LH from the pituitary gland
`into the circulation,
`there is a 4-fold increase in steroidogenic
`activity of LH, and also an increase in it’s ability to produce tPA
`1. Leigh, A.J., Chapman, A.J. & Wilson, C.A. J. Reprod. Fertil. Abstract
`Series 3. No 115 (1989).
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