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Helga Schultz, Svend Aage Engelholm, Eva Harder, Ulrik Pedersen-Bjergaard, and Peter Lommer Kristensen

Introduction In patients with malignant disease, glucocorticoids are widely used on various indications. High-dose treatment is given as part of chemotherapy regimens and for treating oedema associated with metastatic spinal cord compression

Open access

Yiyan Wang, Yaoyao Dong, Yinghui Fang, Yao Lv, Qiqi Zhu, Xiaoheng Li, Qingquan Lian, and Ren-Shan Ge

DES induced an intrauterine growth restriction of pups in the placentas ( 6 ). However, the mechanism has not been fully elucidated. Figure 1 Chemical structure of cortisol and diethylstilbestrol. Glucocorticoid hormone is an inducing

Open access

Britt J van Keulen, Michelle Romijn, Bibian van der Voorn, Marita de Waard, Michaela F Hartmann, Johannes B van Goudoever, Stefan A Wudy, Joost Rotteveel, and Martijn J J Finken

arterial hypotension ( 13 ). We aimed to examine whether male and female preterm infants differ in cortisol production and metabolism as assessed by glucocorticoid metabolite excretion in urine, as a possible explanation for the sex differences in

Open access

Sarah Zaheer, Kayla Meyer, Rebecca Easly, Omar Bayomy, Janet Leung, Andrew W Koefoed, Mahyar Heydarpour, Roy Freeman, and Gail K Adler

). Glucocorticoids also have a negative impact on the Wnt/β-catenin pathway leading to an imbalance in bone formation and bone resorption, and thereby contributing to glucocorticoid-induced osteoporosis ( 1 , 3 , 10 , 11 , 12 , 13 ). In mice, glucocorticoids

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Masafumi Tetsuka and Misato Tanakadate

, 9 , 10 , 11 , 12 ). Recently, we have demonstrated that the bovine oocyte cumulus complex (COC) undergoing IVM expresses two types of glucocorticoid metabolizing enzymes, namely 11β-hydroxysteroid oxidoreductase type1 (HSD11B1) and type2 (HSD11B

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Sophie Howarth, Luca Giovanelli, Catherine Napier, and Simon H Pearce

insufficient to meet the body’s needs. Overt mineralocorticoid deficiency causes the characteristic presentation of salt craving, postural hypotension, hyponatraemia and hyperkalaemia. Glucocorticoid deficiency causes loss of appetite, early satiety, weight

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Gavin P Vinson and Caroline H Brennan

neural POMC is multifactorial (e.g. (65, 67) , and this is primarily linked to its role in energy balance and nutrition, see text. There is, however, much evidence to show the feedback of glucocorticoids on CRH expression in several brain regions. Mostly

Open access

Legh Wilkinson, Nicolette J D Verhoog, and Ann Louw

pathway of the stress response ( 1 ). This in turn, has many peripheral effects, such as an increase in circulating glucocorticoids (GCs) ( 2 , 3 ). Chronic stress or prolonged exogenous GC treatment also disrupts the central homeostatic nature of GC

Open access

Britt J van Keulen, Conor V Dolan, Bibian van der Voorn, Ruth Andrew, Brian R Walker, Hilleke Hulshoff Pol, Dorret I Boomsma, Joost Rotteveel, and Martijn J J Finken

). Interaction between gonadal steroids and the metabolism of cortisol has been suggested by several studies ( 21 , 22 , 23 , 24 ). However, there is only one cross-sectional study that has investigated glucocorticoid metabolism in children of various ages

Open access

Peter Ergang, Anna Mikulecká, Martin Vodicˇka, Karla Vagnerová, Ivan Mikšík, and Jirˇí Pácha

the sympathetic–adrenal–medullary axis, which subsequently release glucocorticoids and catecholamines, respectively. The HPA and SNS axes are the two major pathways through which stress is able to modulate immune functions depending on the nature