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Nanoparticle-Stabilized Liposomes as an Effective Bio-Active Drug Molecule Delivery for Acne Treatment
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Catherine Wilkinson, Marco N. De Canha, Namrita Lall
Corticotropin-releasing hormone (CRH) regulates the body’s behavioral and neuroendocrine stress responses. Sebocytes bind CRH via the presence of CRH receptors, thus linking the influence of stress to the development of acne. The essential fatty acid content in acne-afflicted patients is different when compared to patients without the skin disorder. Linoleic acid, in particular, regulates the secretion of Interleukin-8 (IL-8), a pro-inflammatory cytokine (Van De Kerkhof et al., 2006). Deficiencies of linoleic acid can be linked to comedone formation. This occurs when the infundibula and pilosebaceous cells are stimulated by the cytokine interleukin 1 alpha (IL-1α), which affects toll-like receptor (TLR) activity (Selway et al., 2013). Linoleic acid deficiencies have been correlated with increased sebaceous liquids in the pilosebaceous ducts, as well as with weakened integrity of the follicular epithelium barrier. An unstable follicular epithelium allows substances such as fatty acids to cross the barrier, thereby affecting the fatty acid composition of the follicle and leaving it vulnerable to the negative effects of reactive oxygen species (ROS). These ROS promote lysis and aid invading microorganisms (Garg, 2016; Ottaviani et al., 2010; Van De Kerkhof et al., 2006).
Cushing's syndrome
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Corticotropin-releasing hormone (CRH) physiologyCRH is normally synthesized in the hypothalamus. The placenta also synthesizes and releases biologically active CRH. There is an exponential rise in CRH secretion from the placenta by 1000-fold beginning at 8 weeks gestation. This production peaks at 40 weeks, preceding onset of labor.5–7The CRH level later normalizes to nonpregnant levels within 24 hours of delivery. Placental CRH assists with development and maturation of the fetal HPA axis and fetal adrenal glands resulting in fetal adrenal steroidogenesis.4–7 The placental CRH acts on the maternal HPA axis as well and triggers increased maternal cortisol production.
Post-Traumatic Stress Disorder and Deception
Published in Harold V. Hall, Joseph G. Poirier, Detecting Malingering and Deception, 2020
Harold V. Hall, Joseph G. Poirier
In a study by Baker et al. (1999), male combat veterans were tested by a technique of continuous sampling of cerebrospinal fluid for corticotropin-releasing hormone concentrations. The corticotropin-releasing hormone concentration is intimately related to adrenocortical activity, which directly influences emotional responsiveness, and specifically depression. Urinary-free cortisol excretion was also measured. The mean cerebrospinal fluid/corticotropin-releasing hormone levels were significantly greater in the PTSD patients compared with normal subjects. Urinary-free cortisol excretion levels were negatively and significantly correlated with PTSD symptoms.
Diabetes and mood disorders: shared mechanisms and therapeutic opportunities
Published in International Journal of Psychiatry in Clinical Practice, 2022
Laís Bhering Martins, Jenneffer Rayane Braga Tibães, Michael Berk, Antonio Lucio Teixeira
The HPA axis can be activated during acute and chronic stress responses (Steensberg et al. 2003). This activation generates the release of corticotropin-releasing hormone by the hypothalamus, which increases the synthesis and release of adrenocorticotropic hormone (ACTH) by the pituitary. ACTH, in turn, leads to increased production of adrenal cortisol (Joseph and Golden 2017). Although several factors can influence the activity of the HPA axis in MDD (e.g., severity of depressive symptoms, age, hospitalisation, and medication use), patients with MDD tend to have higher levels of cortisol and ACTH than non-depressive subjects (Stetler and Miller 2011; Joseph and Golden 2017; Jia et al. 2019). Cortisol causes an increase in the visceral adiposity and insulin resistance, which can favour the development of DM2 (Joseph and Golden 2017; Stalder et al. 2017; Nandam et al. 2019). Furthermore, patients with DM2 show variation in serum cortisol concentration and prolonged stress response (Geer et al. 2014), and HPA axis dysregulation by impaired CNS insulin signalling can favour the development of mood disorders (Lyra e Silva et al. 2019).
Efficacy and safety of proactive treatment with twice-weekly topical Cal/BD foam in patients with plaque psoriasis undergoing HPA-axis testing: a PSO-LONG subgroup analysis
Published in Journal of Dermatological Treatment, 2022
Kim Papp, Zygmunt Adamski, Lyn Guenther, Monika Liljedahl, Agnieszka Miasik-Pogodzinska, Anna Szponar-Bojda, Charles Lynde, Terri Nutt, Marie Holst Mørch, Stephen Tyring, William Werschler, Adam Reich, Neil Sadick, Irina Turchin, Jean-Philippe Lacour
Beyond any local adverse effects, a systemic, albeit rare, concern with topical steroid use is suppression of the hypothalamic-pituitary-adrenal (HPA) axis (6). Corticosteroids can decrease corticotrophin-releasing hormone (CRH) synthesis and secretion, thus blocking the trophic and adrenocorticotropic hormone (ACTH)-releasing actions of CRH on the anterior pituitary. As a result, the adrenal cortex loses the ability to produce cortisol leading to adrenal insufficiency. Long-term use of systemic corticosteroids has been associated with reductions in calcium absorption from the intestine and calcium reabsorption in the kidney, leading to parathyroid hormone-induced bone loss and an increased risk of fractures (7); this association is relevant for patients with psoriasis using topical treatment (8).
The role of neuropeptide Y, orexin-A, and ghrelin in differentiating unipolar and bipolar depression: a preliminary study
Published in Nordic Journal of Psychiatry, 2022
Mehmet Ünler, İrem Ekmekçi Ertek, Nigar Afandiyeva, Mustafa Kavutçu, Nevzat Yüksel
Stress response appears to be associated with both a rapid corticotropin-releasing hormone (CRH) activation and a slow release of NPY. NPY release may represent a compensatory mechanism, and it has been suggested that NPY can act as a functional antagonist of CRH [36]. In depression, due to chronic stress, this balance changes in favor of CRH and causes HPA activation and a decrease in NPY levels. It is known that there is hyperactivity in the HPA axis in both UP and BP. HPA axis impairment is not specific to any psychiatric disease, but it is associated with the severity of depression. In a study, 422 UP and 65 BP patients in depressive episodes were investigated by performing 1 mg dexamethasone suppression test, and it was shown that non-suppression was observed at a rate of 43% in the BP group and 25% in the UP group [37]. Therefore, the lower NPY levels in BP patients in our study may be related to the greater impairment in the HPA axis compared to UP patients. Furthermore, it has been reported that the interaction between childhood adverse life events and the NPY genotype is associated with depressive symptoms and trait anxiety [38]. The difference between the BP and UP groups in terms of NPY levels may also be associated with early adverse life events, but it is not evaluated in our study.