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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).
Adrenal Gland
Published in Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod
The hypothalamus secretes corticotrophin-releasing hormone (CRH), which stimulates release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. ACTH stimulates cortisol secretion from the zona fasciculata of the adrenal cortex. Cortisol exerts negative feedback on both CRH and ACTH release.
A Biopsychosocial Approach to Anxiety
Published in Stephen M. Stahl, Bret A. Moore, Anxiety Disorders: A Guide for Integrating Psychopharmacology and Psychotherapy, 2013
Allison M. Greene, Christopher R. Bailey, Alexander Neumeister
Corticotropin-releasing hormone (CRH) is a polypeptide hormone secreted by the hypothalamus that is traditionally implicated as a cardinal neurochemical in an individual's physiological and behavioral responses to stress. CRH mediates stress activation of the hypothalamic-pituitary-adrenal (HPA) axis, a neuroendocrine system involved in stress, by stimulating the synthesis of adrenocorticotropic hormone (ACTH) in the pituitary gland, which ultimately leads to corticotropin and glucocorticoid release (Bonfiglio et al., 2011). CRH neurons are distributed throughout the brain; however, with regard to stress, a particular CRH circuit has been theorized. This circuit originates in the lateral hypothalamus, dorsal raphe, and the central nucleus of the amygdala (CeA) (Lee & Davis, 1997), which then projects to the bed nucleus of stria terminalis (BNST), which then in turn signals the paraventricular nucleus of the hypothalamus (PVN), activating the HPA axis. In response to stressful stimuli, CRH levels increase and exert their effect by activating CRHj and CRH2, G-coupled protein receptors throughout the brain, to mediate an adaptive physiological and behavioral response (Bonfiglio et al., 2011).
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).
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.
Advances in the pharmacotherapeutic management of post-traumatic stress disorder
Published in Expert Opinion on Pharmacotherapy, 2021
Ansab Akhtar, Sangeeta Pilkhwal Sah
Stress and trauma that leads to PTSD affect brain regions like PFC, amygdala, hypothalamus, hippocampus and alter the neurocircuitry of fear memory processing in such a way that top-down control of PFC on amygdala is lost making the amygdala hyperactive which gives output to the hypothalamus, releasing corticotropin-releasing hormone (CRH). CRH further promotes adrenocorticotrophin (ACTH) to get released which then stimulates the adrenal gland to produce the major stress hormone cortisol to combat elevated stress. But due to the fast-negative feedback mechanism observed in PTSD, cortisol levels markedly decrease, leading to unopposed elevated stress and increased cytokine levels. The high CRH continues to activate the sympathetic nervous system via brain stem locus coeruleus and also causes norepinephrine release from the anterior cingulate cortex. The resulting catecholamines are responsible for several symptoms evident in PTSD patients like changes in heart rate, blood pressure, hyperarousal, and anxiety. CRF is thus central to the neurocircuit of fear-related behaviors.