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Clinical Applications of Immunoassays
Published in Richard O’Kennedy, Caroline Murphy, Immunoassays, 2017
The adrenal cortex produces a number of important steroids involved in cell metabolism. The secretion of cortisol is dependent on the release of adrenocorticotropic hormone (ACTH) from the pituitary gland, which stimulates cortisol and androgen production in the adrenal cortex and negatively regulates ACTH production. In a hormone disorder known as Cushing’s syndrome, there is sustained over-production of cortisol with loss of the normal cortisol circadian rhythm. Excess cortisol leads to a change in body habitus (weight gain, ‘moon faces’ and ‘buffalo hump’), susceptibility to recurrent infections and a host of other bone, skin and gonadal problems. The most common cause of excess cortisol is the ingestion of prescribed steroids. Other causes of Cushing’s syndrome include an adrenal tumour, hypersecretion of ACTH from a pituitary tumour (Cushing’s disease) or ectopic production of ACTH from a cancer.
Physical Hazards of Space Exploration and the Biological Bases of Behavioral Health and Performance in Extreme Environments
Published in Lauren Blackwell Landon, Kelley J. Slack, Eduardo Salas, Psychology and Human Performance in Space Programs, 2020
Julia M. Schorn, Peter G. Roma
Negative valence systems are responsible for fear, anxiety, threat, and loss, whereas positive valence systems support reward and reinforcement. Fear and anxiety usually manifest in avoidance behaviors and social withdrawal, with physiological markers of increased heart rate; decreased heart rate variability; and elevated cortisol, epinephrine, and norepinephrine. A major component of the negative valence system is stress. The “fight or flight” response is highly complex, with multiple types of stress mediators, like neurotransmitters (noradrenaline, serotonin) and hormones (corticotropin-releasing hormone [CRH], cortisol, and vasopressin). The hypothalamic–pituitary–adrenal (HPA) axis is central to the stress response. In anticipation of a threat, CRH is released from the hypothalamus to the pituitary gland, which releases adrenocorticotrophic hormone (ACTH), which enters the bloodstream and stimulates the release of cortisol and epinephrine from the adrenal gland. Cortisol returns to the hypothalamus to complete a negative feedback loop, diminishing activation (Pariante & Lightman, 2008). Additionally, during a stressful event, levels of inflammatory and immune molecules are also elevated and there are reduced nerve growth factors such as brain-derived neurotrophic factor (BDNF; Berntson et al., 1997; Dowlati et al., 2010; Howren, Lamkin, & Suls, 2009; Jaggar, Fanibunda, Ghosh, Duman, & Vaidya, 2019; Phillips et al., 1998). The limbic system deep in the brain is critical in modulating these processes. Because the limbic system is a functional concept, the strict definition of the anatomical structures within the limbic system is controversial, but it is usually agreed to include the bed nucleus of the stria terminalus, amygdala, and hippocampus (Lebow & Chen, 2016).
Arsenals of Pharmacotherapeutically Active Proteins and Peptides: Old Wine in a New Bottle
Published in Debarshi Kar Mahapatra, Swati Gokul Talele, Tatiana G. Volova, A. K. Haghi, Biologically Active Natural Products, 2020
Adrenocorticotrophic hormone (ACTH) is a hormone regulating the synthesis and release of hormones of adrenal cortex. The ACTH is produced from the precursor pro-opiomelanocortin (POMC) by action of peptidases. POMC also produces opioid peptides and melanocyte-stimulating hormones under the action of enzymes. The receptor for ACTH is a G-linked protein and cAMP is the secondary messenger. Excess synthesis of ACTH results in Cushing’s syndrome [138].
Inflammatory and immunological changes caused by noise exposure: A systematic review
Published in Journal of Environmental Science and Health, Part C, 2022
Amirreza Abouee-Mehrizi, Yahya Rasoulzadeh, Tohid Kazemi, Mehran Mesgari-Abbasi
Destructive effects on the auditory system and inducing hearing loss are some of the most noticeable health effects of noise.25,112,113 Some previous studies showed that noise could increase heart rate,30,114–117 blood pressure,114–116,118,119 and some endocrine hormones such as adrenocorticotropic hormone (ACTH) and cortisol.34,120–122 Previous studies demonstrated that noise could affect the respiratory system by some deteriorating respiratory diseases such as asthma, bronchitis, and wheezing.123–125 Moreover, decreased sexual hormones such as testosterone were reported by exposure to noise.120,122 Noise had also degenerative effects on the brain and its function.126–128
Stress, growth, cytokines and histopathological effects of permethrin in common carp (Cyprinus carpio)
Published in Chemistry and Ecology, 2022
Kenan Erdoğan, Gül Nihal Örün, Nuh Korkmaz, Belda Erkmen, Hüseyin Polat, Arzu Doğru, Mehmet İlker Doğru, İbrahim Örün
In order to maintain homeostasis and survive, fish show various physiological responses regulated by the endocrine system and central nervous system against environmental stress factors such as pesticides [3–6]. Circulating levels of glucocorticoid cortisol, an important component of the stress response in teleost, are controlled and regulated by the hypothalamic-pituitary-interrenal (HPI) axis [7,8]. In response to a stressor in fish, cortisol synthesis and secretion are positively regulated by the corticotropin releasing hormone/adrenocorticotropic hormone (CRH/ACTH) pathway in the brain, and increased CRH and/or ACTH production causes increased plasma cortisol (CORT) levels [6,9]. In many studies, it has been reported that fish cause a temporary increase in plasma CORT levels in order to cope with stress and provide the necessary energy [7,10,11].
Association between ozone air pollution levels and hospitalizations for depression in Taipei: a time-stratified case-crossover study
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Shang-Shyue Tsai, Ya-Wen Chiu, Yi-Hao Weng, Chun-Yuh Yang
Several possible mechanisms were proposed to explain the relationship between O3 exposure and increased risk of hospitalization for depression. (1) O3 exposure may enhance the risk of headache, dizziness, and migraine, and thus subsequently these effects may affect mental status (Walker 2017). (2) O3 exposure was reported to be associated with cardiovascular diseases, asthma, and chronic obstructive pulmonary diseases, which are also important predictors of depression (Chen et al. 2020; Fan et al. 2020; Ng et al. 2008). (3) Exposure to O3 produced an elevation in brain dopamine and tyrosine hydroxylase levels accompanied by a decrease in serotonin and tryptophan hydroxylase levels (Gonzalez-Pina and Paz 1997; Ray et al. 2011; Thomson 2013), suggesting that O3 may interfere with central nervous system functioning, and thus contribute to the pathological processes of mental disorders (Bach-Mizrachi et al. 2008; Pandey 2013). (4) O3 was reported to activate the hypothalamic-pituitary-adrenal (HPA) axis resulting in elevated plasma levels of adrenocorticotropic hormone and corticosterone. Thus, it is conceivable that HPA-axis dysfunction may consequently affect mental states (Jokinen and Nordstrom 2009; Thomson 2013). (5) O3 exposure might provoke inflammatory effects resulting in the production of pro-inflammatory cytokines capable of crossing blood-brain-barrier and thereby affect brain function, suggesting that inflammatory mechanisms may also be involved in the observed depression (Araneda et al., 2008; Holz et al. 2018; Zhao et al. 2018).