Chronic Stress Hormones May Promote Resistance to EGFR Inhibitors

2017 ◽  
Vol 39 (23) ◽  
pp. 64
Keyword(s):  
Chronic Stress ◽  
Stress Hormones ◽  
Egfr Inhibitors

scholarly journals How stress mediators can cumulatively contribute to Alzheimer’s disease An allostatic load approach

2019 ◽  
Vol 13 (1) ◽  
pp. 11-21 ◽  
Author(s):  
Tatiane Martins Matos ◽  
Juliana Nery De Souza-Talarico
Keyword(s):  
Risk Factors ◽  
Cognitive Decline ◽  
Disease Progression ◽  
Chronic Stress ◽  
Allostatic Load ◽  
Stress Hormones ◽  
Modifiable Risk Factors ◽  
Cognitive Changes ◽  
Stress Mediators ◽  
The Impact

ABSTRACT. Allostatic load is defined as the frequent activation of the neuroendocrine, immunological, metabolic and cardiovascular systems, which makes individuals more susceptible to stress-related health problems. According to this model, physiological dysregulations start to emerge decades before diseases manifest. Consequently, stress research has shifted its attention to anticipating the degree of this dysregulation to better understand the impact of stress hormones and other biomarkers on disease progression. In view of the growing number of studies that demonstrate the influence of modifiable risk factors on cognitive decline, in addition to the effects of chronic stress mediators, the objective of the present review was to present an overview of the development of cognitive changes based on studies on stress and its mediators.

scholarly journals Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Sheela Vyas ◽  
Ana João Rodrigues ◽  
Joana Margarida Silva ◽  
Francois Tronche ◽  
Osborne F. X. Almeida ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Prolonged Exposure ◽  
Stress Hormones ◽  
Behavioral Adaptation ◽  
Mineralocorticoid Receptors ◽  
Cellular Mechanisms ◽  
Ample Evidence ◽  
Synaptic Structure ◽  
Glial Function ◽  
Prolonged Stress

Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer’s (AD) and Parkinson’s (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.

scholarly journals Associations of acute and chronic stress hormones with cognitive functions in autism spectrum disorder

Neuroscience ◽  
2017 ◽  
Vol 343 ◽  
pp. 229-239 ◽  
Author(s):  
Shino Ogawa ◽  
Young-A Lee ◽  
Yoshie Yamaguchi ◽  
Yuka Shibata ◽  
Yukiori Goto
Keyword(s):  
Autism Spectrum Disorder ◽  
Chronic Stress ◽  
Cognitive Functions ◽  
Stress Hormones ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Acute And Chronic Stress

Modification of endothelial biology by acute and chronic stress hormones

2009 ◽  
Vol 78 (3) ◽  
pp. 364-369 ◽  
Author(s):  
T. Nickel ◽  
A. Deutschmann ◽  
H. Hanssen ◽  
C. Summo ◽  
U. Wilbert-Lampen
Keyword(s):  
Chronic Stress ◽  
Stress Hormones ◽  
Acute And Chronic Stress

Unifying mechanisms: nature deficiency, chronic stress, and inflammation

2018 ◽  
pp. 40-48 ◽  
Author(s):  
William Bird ◽  
Elissa Epel ◽  
Jeannette R. Ickovics ◽  
Matilda van den Bosch
Keyword(s):  
Chronic Inflammation ◽  
Chronic Stress ◽  
Stress Hormones ◽  
Accelerated Ageing ◽  
Natural Environments ◽  
Daily Lives ◽  
As Stress ◽  
And Coping ◽  
Prolonged Stress ◽  
Oxidative Species

Disconnection from nature seems to increase the risk of chronic stress. This is followed by a range of deleterious influences on our bodily systems. Many of these changes are related to chronic inflammation. This chapter evolves around the premise that natural environments are prerequisites for resilience to the various stressors of our daily lives. If our resilience and coping mechanisms are insufficient, we are at risk of entering a vicious circle of negative organ reactions and feedback loops. As stress is prolonged, stress hormones and poor health behaviour are followed by alterations in the gut microbiota and an increase in visceral fat. These reactions lead to damage of the cells’ mitochondria from oxidative stress and release of reactive oxidative species. Finally, the results of oxidative damage and chronic inflammation lead to the shortening of telomeres, the DNA-proteins which protect the chromosomes. Shorter telomeres are associated with accelerated ageing and disease.

scholarly journals Pathophysiology of affective disorders: functional interaction of stress hormones and hippocampal excitation

2017 ◽  
Vol 117 (2) ◽  
pp. 477-479
Author(s):  
M. Adrienne McGinn ◽  
Amanda R. Pahng
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Chronic Stress ◽  
Affective Disorders ◽  
Stress Hormones ◽  
Emotional Behavior ◽  
Hippocampal Function ◽  
Functional Interaction ◽  
Major Depressive ◽  
New Finding

An important new study by Kvarta, Bradbrook, Dantrassy, Bailey, and Thompson ( J Neurophysiol 114: 1713–1724, 2015) examined the effects of persistent stress and excessive glucocorticoid levels on hippocampal function and emotional behavior in rodents. The authors specifically implicate the temporoammonic pathway as being susceptible to reductions in excitatory function in the context of chronic stress. We discuss the importance of this new finding in the broader context of medication development for major depressive disorder.

scholarly journals Evaluation of Health and Social Inequalities in the Occurrence of Different Types of Chronic Stress and Their Effect on Immunoregulation

2021 ◽  
Vol 4 (1) ◽  
pp. 3-16
Author(s):  
Mohamad Reza Vaez Mahdav ◽  
◽  
Leila Nasiri ◽  
Tooba Ghazanfari ◽  
◽  
...  
Keyword(s):  
Chronic Stress ◽  
Animal Studies ◽  
Social Inequalities ◽  
Immune Cell ◽  
Stress Hormones ◽  
Strong Relationship ◽  
Immune Cell Population ◽  
Wide Range ◽  
Inequality In Health ◽  
Stress Influences

Inequality in health and its multiple dimensions is an essential aspect of social injustice. Several studies have shown that mental and physical health in adulthood is not a phenomenon independent of one’s childhood. Those from lower socioeconomic status have higher mortality and shorter life expectancy. Individualism and utilitarianism in social relationships have led to a wide range of social instability, poverty, deprivation, and inequality in societies. In addition to widespread social effects, they have made harmful consequences on the basic vital systems and organs through interference with multiple biological processes. In modern societies, people live in highly stressful situations, and several studies have pointed a strong relationship between the higher prevalence of diseases and social and physiological stresses. Studies of normal and experimental situations also showed their significant effects on the immune response. Accordingly, increased incidence of invasive behaviors has been associated with increased cytokines and immune-cellular activity in animal studies. According to the stimulus type and contact duration, chronic stress influences both innate and acquired immune factors. Stress affects the immune system via activation of the hypothalamus-pituitary-adrenal axis and affects the innate immune agents such as monocytes, macrophages, and proinflammatory cytokines, causing the increase of stress hormones (glucocorticoid-catecholamines). Chronic stress influences the acquired immune components by changing the immune cell population and altering the balance between immune cells and their secreted cytokine levels.

scholarly journals Activation of CRF2 receptor increases gastric vagal afferent mechanosensitivity

2019 ◽  
Vol 122 (6) ◽  
pp. 2636-2642
Author(s):  
Hui Li ◽  
Amanda J. Page
Keyword(s):  
Food Intake ◽  
Glucocorticoid Receptor ◽  
Feeding Behavior ◽  
Chronic Stress ◽  
Hormone Receptors ◽  
Stress Hormones ◽  
Stress Hormone ◽  
Gastric Function ◽  
Crf2 Receptor ◽  
Vagal Afferent

Gastric vagal afferent (GVA) sensing of food-related mechanical stimuli is a crucial mechanism in the control of feeding behavior and gastric function. Stress is an important factor contributing to eating disorders and gastric diseases. Chronic stress has been shown to increase the mechanosensitivity of GVAs in mice and to reduce food intake and body weight. Whether the mechanosensitivity of GVAs is modulated by stress hormones is not known. This study aimed to determine the effect of stress hormones on GVA mechanosensitivity. The expression of stress hormone receptors in GVA cell bodies was determined in 8-wk-old male C57BL/6 mice using quantitative RT-PCR combined with laser capture microdissection. The mechanosensitivity of GVAs was determined in the absence and presence of stress hormones using an in vitro single-fiber recording preparation. NR3C1 and CRHR2 (mRNA isoforms of glucocorticoid receptor and CRF2 receptor, respectively) were expressed in GVA neurons. The glucocorticoid receptor agonist corticosterone had no effect on the mechanosensitivity of either tension or mucosal GVAs. Activation of CRF2 receptor by its specific analog, urocortin 3, significantly increased the mechanosensitivity of both tension and mucosal GVAs, an effect prevented by the CRF2 receptor antagonist astressin 2B. In conclusion, activation of CRF2 receptor increases the mechanosensitivity of GVAs. This may contribute to the stress- and CRF2 receptor-associated changes in feeding behavior and gastric function, possibly contributing to the hypersensitivity of GVAs in chronic stress conditions. NEW & NOTEWORTHY Gastric vagal afferents (GVAs) relay food-related signals to the central nervous system, where they are processed, eventually leading to modulation of food intake and gastric function. GVA signaling can be modulated by an array of hormones. Stress has been shown to induce GVA hypersensitivity. This study demonstrates that GVA neurons express subtypes of stress hormone receptors, specifically CRF2. Furthermore, activation of CRF2 receptor increases GVA mechanosensitivity, which could have implications for food intake and gastric function.

scholarly journals Acupuncture blocks cold stress-induced increases in the hypothalamus–pituitary–adrenal axis in the rat

2013 ◽  
Vol 217 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Ladan Eshkevari ◽  
Eva Permaul ◽  
Susan E Mulroney
Keyword(s):  
Cold Stress ◽  
Chronic Stress ◽  
Stress Hormones ◽  
Control Group ◽  
Adrenal Axis ◽  
Significant Difference ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
The Brain ◽  
Treatment Control Group ◽  
Pituitary Adrenal Axis

Electroacupuncture (EA) is used to treat chronic stress; however, its mechanism(s) of action in allaying stress remains unclear. The interplay of stress hormones of the hypothalamus–pituitary–adrenal axis (HPA) and the sympathetic nervous system (SNS) is critical in the stress response. Our objective was to determine whether EA at acupoint, stomach 36 (EA St36) is effective in preventing chronic cold stress-induced increased hormone levels in the rat by examining four groups of animals, three of which were exposed to cold and one of which was a non-treatment control group. Before exposure to the cold, two groups were treated with either EA St36, or Sham-EA, before 10 days of cold stress. The EA St36 animals demonstrated a significant decrease in peripheral HP hormones (ACTH and CORT) compared with stress animals (P<0.05). These effects were specific; rats receiving Sham-EA had elevation of these hormones, similar to the stress-only animals. These effects were mirrored centrally in the brain; CRH levels were significantly (P<0.05) reduced in EA St36 animals compared with the other animals. Finally, EA effect on peripheral and adrenal SNS hormones (norepinephrine (NE) and neuropeptide Y (NPY) respectively) was examined, with no significant difference noted in adrenal tyrosine hydroxylase or circulating NE in any of the groups. However, EA St36 was effective in preventing stress-induced elevation is adrenal Npy mRNA. These results indicate that EA St36 blocks the chronic stress-induced elevations in the HPA and the sympathetic NPY pathway, which may be a mechanism for its specific stress-allaying effects.

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