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Fibroblast-Pneumonocyte Factor
Published in Jason Kelley, Cytokines of the Lung, 2022
Significant quantities of surfactant are not synthesized until close to term. The fine regulation of this quantitative progression in expression of phenotype (e.g., when the fetus is threatened with premature birth) is under multihormonal control (Smith, 1979a, 1984), yet local cell and tissue interactions continue to modulate the endocrine signals. A central role is played by endogenous fetal glucocorticoids. This physiological function has been reviewed (Smith, 1984), and evidence for it has been strengthened by observations that the antiglucocorticoid RU486 delays fetal lung maturation when administered to the dam (Guettari et al., 1989) and by observations that lung maturation is delayed in mice with H-2 (HLA) phenotypes associated with low expression of glucocorticoid receptors (Honig et al., 1984). The use of synthetic steroids antenatally in the prevention of respiratory distress syndrome (Collaborative Group on Antenatal Steroid Therapy, 1981; Liggins and Howie, 1972; Taeusch et al., 1979) represents a pharmacologic attempt to trigger the physiological responses precociously.
Adrenal insufficiency
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Despite the significant rise in cortisol levels, pregnant women do not demonstrate the stigmata classically associated with Cushing’s syndrome, such as ecchymoses, proximal muscle weakness, and dorsocervical adiposity.Prior theories have suggested that the anti-glucocorticoid effects of elevated progesterone levels during pregnancy lead to relatively inert cortisol actions.11,12Similarly, the physiologic cortisol elevation does not affect the developing fetus.11-β-hydroxysteroid dehydrogenase 2 (11β-HSD2) catalyzes the conversion of most of maternal cortisol to inert cortisone, thereby decreasing excess fetal glucocorticoid exposure, which could lead to intrauterine growth restriction and preeclampsia.13
Hormonal Regulation in the Treatment of Fibroids
Published in John C. Petrozza, Uterine Fibroids, 2020
Victoria Fitz, Steven L. Young
At least three factors limit mifepristone's appeal for long-term treatment of fibroids. First, endometrial hyperplasia has been reported with mifepristone use, though the incidence varies widely by study. Additionally, much of the reported “hyperplasia” was actually an unusual endometrial morphology (also seen with ulipristal and asoprisnil) that mimics hyperplasia on ultrasound, but is associated with very low mitotic activity [34]. Another concern with mifepristone is its anti-glucocorticoid effect that could potentially lead to clinically significant adrenal insufficiency [35]. In the United States, mifepristone's abortifacient effects are another potential barrier to wide introduction for fibroid therapy.
Measuring stress: a review of the current cortisol and dehydroepiandrosterone (DHEA) measurement techniques and considerations for the future of mental health monitoring
Published in Stress, 2023
Tashfia Ahmed, Meha Qassem, Panicos A. Kyriacou
Psychological stress is often associated with fluctuations of stress hormones, such as cortisol and adrenaline (Tsigos & Chrousos, 2002). Cortisol is the primary stress hormone that is involved in governing the stress response from the moment of stress elicitation to recovery from stressful events. Alternatively, DHEA is a steroid hormone that has proven to express anti-glucocorticoid properties (Gallagher & Young, 2002). As two steroid hormones with inverse actions, the relationship between cortisol and DHEA is of great interest. The antagonistic relationship between cortisol and DHEA has been discussed at length in regard to their opposing actions on immune function, however, the relationship between cortisol and DHEA in stress management is seldom discussed (Buford & Willoughby, 2008). DHEA is primarily implicated in aging research, whereby an increase in cortisol/DHEA ratio can be a contributing factor of age-related declination in immune function (Buford & Willoughby, 2008). Evidently the biochemical interactions between cortisol and DHEA have proven to be of great importance in the determination of declining functions of biological systems. Therefore, observing the changes in these biomarkers with respect to stress and mental health monitoring could unveil vital details regarding stress management and mental health.
Hearing loss is associated with hippocampal atrophy and high cortisol/dehydroepiandrosterone sulphate ratio in older adults
Published in International Journal of Audiology, 2021
Mitsuhiro Aoki, Hiroshi Okuda, Hiromasa Ishihara, Hisamitsu Hayashi, Toshimitsu Ohashi, Takesumi Nishihori, Bunya Kuze
The DHEA can act as an anti-glucocorticoid with an anti-stress and neuroprotective activity. In serum and the brain, it is present in its sulphated form, DHEAS (Sacco et al. 2002). The production of DHEA and DHEAS is maximal at around 20 years of age and gradually declines with age in humans, whereas the serum cortisol level does not decline with age, resulting in a relative glucocorticoid excess in the elderly (Guazzo et al. 1996; Orgeta et al. 2019). Production of cortisol is usually triggered by stress-induced activation of a hormonal system known as the hypothalamic-pituitary-adrenal (HPA) axis (Starr et al. 2019). Our previous study reported that the C/D ratio is an efficient objective indicator for Meniere’s disease patients suffering from tinnitus and for gauging the response to treatment of cochlear symptoms (Aoki et al. 2011). Cortisol also provides negative feedback to this axis to maintain a physiological concentration. An appropriate balance of the secretion of cortisol and DHEAS is essential for the maintenance of biological function and homeostasis. A high C/D ratio is reportedly associated with mortality, dementia, metabolic syndrome, and reduced immunity following physical stress. The C/D ratio is considered to reflect some significant effects, which are a pro/anti-inflammatory stasis, immune function, glucose metabolism, and memory (Wisniewski et al. 1993; Herman et al. 2009; Phillips et al. 2010; Vuksan-Ćusa et al. 2014; Mocking et al. 2015).
The use of a gene expression signature and connectivity map to repurpose drugs for bipolar disorder
Published in The World Journal of Biological Psychiatry, 2020
Srisaiyini Kidnapillai, Chiara C. Bortolasci, Madhara Udawela, Bruna Panizzutti, Briana Spolding, Timothy Connor, Andrew Sanigorski, Olivia M. Dean, Tamsyn Crowley, Stéphane Jamain, Laura Gray, Elizabeth Scarr, Marion Leboyer, Brian Dean, Michael Berk, Ken Walder
The anti-glucocorticoid agent mifepristone was identified in the CMap analysis. Hypothalamic–pituitary–adrenal (HPA) axis impairment has been associated with the pathophysiology of BD, and can lead to depressive signs and neurocognitive decrement (Young et al. 2004). Glucocorticoids are the final product of the HPA axis and are significant factors in the stress response (Daban et al. 2005). Hypercortisolism can lead to impaired neurogenesis and dendritic atrophy (Young et al. 2004), which are characteristics seen in people with BD (Maletic and Raison 2014). There is evidence for HPA dysregulation and changes in glucocorticoid responsivity in BD, such as hyperactivity of the HPA axis and its variable activity during different phases of BD (Belvederi Murri et al. 2016). This raises the possibility that anti-glucocorticoids have the potential for therapeutic efficacy in BD. Mifepristone has been proposed to improve neurocognition and act as an antidepressant in people with BD, and has been recommended for treating BD (Young et al. 2004). Therefore, this drug is one of the more promising drugs that could be repurposed for BD, further demonstrating the validity of this method.