Searchable abstracts of presentations at key conferences in endocrinology

ea0031s5.4 | Sex in the brain (Supported by <emphasis role="italic">Endocrine Connections</emphasis>) | SFEBES2013

Hormone-dependent chromatin modifications regulating sexually differentiated animal behaviour

Pfaff Donald

Among all brain functions, the most strongly sexually differentiated are those which are directly related to reproduction. In addition to neuroendocrine controls of pituitary hormone release, we consider reproductive behaviors whose expression depends on steroid hormones. The hormone-dependent transcriptional activations in hypothalamic neurones long known to be required for female-specific reproductive behaviour, lordosis (Drive, MIT Press, 1999) involve binding to specific D...

ea0034p251 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2014

Metformin and acute kidney injury: is it the culprit?

Lee Phey Shen , Mackay Jonathan Donald

Three people (two males), with mean age (range) 65 (49–75) years, presented as emergencies with acute renal failure (AKI). They had type 2 diabetes mellitus, with mean duration 7 (2–12) years. All three were taking anti-hypertensive therapy: two were on ramipril and one on losartan and indapamide. All three were taking metformin with mean daily dose 2.6 (1.7–3.0) g. All three patients had mild renal impairment (CKD stage 3), but renal function was stable 2–...

ea0081p45 | Calcium and Bone | ECE2022

Phosphate-mediated inhibition of calcium-sensing receptor expressed endogenously in the thyroidal TT cell-line

Alghamdi Khaleda , Mun Hee-Chang , Conigrave Arthur , Ward Donald

The calcium-sensing receptor (CaR) is the key controller of parathyroid hormone (PTH) secretion and extracellular calcium homeostasis. Hyperphosphataemia increases PTH secretion and is associated with secondary hyperparathyroidism (SHPT). We reported recently that inorganic phosphate (Pi), and sulphate, can attenuate CaR activity directly (in CaR-transfected HEK-293 cells) and Pi can increase PTH secretion rapidly from human and murine parathyroid cells. To investigate this fu...

ea0089b14 | Basic Science | NANETS2022

Pancreatic Mixed Acinar-Neuroendocrine Carcinoma: a Single Institutional Genomic Characterization Report

Amin Manik , Castellano Juliana , Green Donald , Tsongalis Gregory

Background: Pancreatic mixed acinar-neuroendocrine carcinomas are a rare distinctive entity with histologic and immunohistochemical features of pancreatic acinar cell carcinoma and pancreatic neuroendocrine tumor and pose diagnostic challenges. Very few cases have been described in the literature. Genomic information about these tumors remains unknown. We identified two cases of mixed acinar- neuroendocrine carcinoma from our database since January 2020 who had full genomic in...

ea0049gp63 | Developmental &amp; Protein Endocrinology | ECE2017

Does the loss of RAD52 in PC contribute to resistance to antiandrogen therapy?

Alfaqih Mahmoud A. , Chang Ching yi , Norris John , McDonnell Donald P.

Recent statistics indicate that prostate cancer (PC) is the most frequent cancer in men worldwide and is the leading cause of cancer death in men above 50 years of age. The Androgen receptor (AR), a member of the superfamily of nuclear hormone receptors, plays a well-established role in the development and progression of the disease. PC localized to the prostate is commonly treated with surgical removal of the gland and is often associated with a favorable outcome. However, me...

ea0044ep21 | (1) | SFEBES2016

Severe hypercalcaemia following Vitamin D replacement therapy in patient found to have co-existing sarcoidosis and primary hyperparathyroidism

Sabin Jodie , Scannell Jack , Donald Jane , Evans Alison

Current guidance recommends replacing vitamin D in patients with mild primary hyperparathyroidism although there are reports of worsening hypercalcaemia in some patients. Vitamin D replacement has also been known to cause hypercalcaemia in patients with sarcoidosis. We present a case of a patient with co-existent sarcoidosis and primary hyperparathyroidism, who developed severe hypercalcaemia following treatment with high dose Vitamin D.A 63 year old lad...

ea0022s12.2 | Thyroid hormone metabolism and action: new developments | ECE2010

Life without T4 to T3 conversion

Galton Valerie Anne , St Germain Donald , Hernandez Arturo

Abundant evidence indicates that the three deiodinases (D1, D2 and D3) function at the pre-receptor level to influence both extracellular and intracellular thyroid hormone levels and hence thyroid hormone action. Indirect evidence supports the concept that a major function of the D1 is to generate T3 for export to plasma whereas the D2 generates T3 primarily for local use. To obtain direct evidence concerning their individual physiological roles we have g...

ea0013p191 | Diabetes, metabolism and cardiovascular | SFEBES2007

Renal effects of ACTH: functional and microarray studies in the mouse

Kenyon Christopher , Mullins Linda , Dunbar Donald , Mullins John , Bailey Matthew

We investigated ACTH-induced hypertension in mice by studying renal function in vivo and by analysing renal gene expression by microarray and RT PCR methods. During two weeks sc infusion with Synacthen, mean blood pressure in adult male mice increased (89±5 vs 110±2 mmHg), and plasma corticosterone, adrenal weights and drinking rate increased by 5, 2 and 2.5-fold respectively (P<0.01); renal mass was unaffected. Greater mineralocorticoid activity wa...

ea0008p37 | Diabetes, metabolism and cardiovascular | SFE2004

Increasing oestrogen dose reduces intima media thickness in women with Turner Syndrome

Ostberg JE , Storry C , Donald AE , Halcox JP , Conway GS

Cardiovascular disease is the major cause of mortality in women with Turner Syndrome(TS), and may be congenital or acquired. There is a high prevalence of risk factors for ischaemic heart disease(IHD) including hypertension, dyslipidaemia, diabetes and obesity. This oestrogen dose-ranging vascular physiology study compared women with TS (n=14) and 46,XX gonadal dysgenesis(GD) (n=11) to determine the relative contributions of oestrogen deficiency and genetics, and to assess the...

ea0008dp17 | Diabetes, metabolism and cardiovascular | SFE2004

Increasing oestrogen dose reduces intima media thickness in women with Turner Syndrome

Ostberg JE , Storry C , Donald AE , Halcox JP , Conway GS

Cardiovascular disease is the major cause of mortality in women with Turner Syndrome(TS), and may be congenital or acquired. There is a high prevalence of risk factors for ischaemic heart disease(IHD) including hypertension, dyslipidaemia, diabetes and obesity. This oestrogen dose-ranging vascular physiology study compared women with TS (n=14) and 46,XX gonadal dysgenesis(GD) (n=11) to determine the relative contributions of oestrogen deficiency and genetics, and to assess the...