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Hawthorne, M. Symmetry and dynamics of molecular rotors in amphidynamic molecular crystals. ScienceDaily, 9 August University of California - Los Angeles. Brain pathways linking social stress and inflammation identified. Retrieved July 3, from www. The results suggest that family history should be This study Although a complex phenomenon encompassing food availability, affordability, utilization, and even the social norms that define Below are relevant articles that may interest you.
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Stress-mediated inflammation is a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. Depressive disorders are often accompanied by profound changes in immunity. Clinical observations in depression disorders showed that immune dysfunction is the main cause of increased risks in other oncological, inflammatory, and infectious diseases.
Immunological reactions in psychoemotional stress play an important role. Studying Antidepressant-Sensitive Catalepsy ASC in mice showed a decrease in IgM immune responses and sensitivity to the administration of antidepressants. Stress-induced inflammation is a key pathogenic factor in inherited diseases and autoinflammatory syndromes.
The stress contributes severity of the symptoms in these diseases. A study showed the correlation among basal stress, disease severity, and antioxidant response in two different cryopyrin-associated periodic syndrome CAPS patients sharing same nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 NLRP3 mutation [ 5 ]. Hence, similar stress-related mechanisms may operate in other genetic diseases, where inflammation causes disease progression and mutant protein present in monocytes.
Improving the responses to stress represents a promising therapeutic opportunity for this kind of serious diseases, while considering the genetic factor individual tolerance levels may play a major role. Identification of mechanisms underlying a dysregulation of major components of the stress response system is a very challenging task as it involves complex cellular interactions at the level of different organs and systems. One of the main features of the stress response is the activation of the hypothalamic-pituitary-adrenal axis HPA [ 6 ].
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The main regions of the brain that shows stress response are hippocampus, amygdala, and prefrontal cortex. Decreased activity and neuronal atrophy in the hippocampus and in the prefrontal cortex, as well as increased activity and neuronal growth in the amygdala, are involved in post-traumatic stress disorder PTSD [ 6 ]. The changes that stress induces mainly affect the levels of cortisol and catecholamines epinephrine, norepinephrine, dopamine. Catecholamines are released shortly after stress onset and go back to normal levels upon stress termination.
Glucocorticoids act by binding to two types of receptors—mineralocorticoid receptors MR and glucocorticoid receptors GR.
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Molecular mechanisms involving this stress response are genetic, epigenetic, and immunological nature. The primary hormonal end product of the HPA axis is cortisol.
The results showed that depressive symptoms were positively associated with violent outcomes when CAR levels are low [ 7 ]. Mental and physical stress can suppress the immune system in both humans and animals. Chronic stress-induced alterations in immune responses could result from increased cell death and apoptosis or decreased cell proliferation. It is well known that exhausting physical activity and mental stress lead to immunosuppression of the immune system by steroid hormone regulation.
Chronic stress significantly enhances corticosterone production and induces lymphocyte apoptosis [ 8 , 9 ]. Stress hormones like cortisol play a fundamental role in regulating immune responses and the balance of T helper Th 1 and Th2 cytokines, thereby modulating the susceptibility of various immune-related disorders. Toll-like receptors TLRs play a key role in modulating immune responses, cell apoptosis, and cell survival. Among 11 known TLRs in mammals, TLR9 plays a major role in chronic stress-induced immune suppression by modulating corticosteroid levels [ 10 ].
Psychosocial stressors increase peripheral cytokine production, a potentially important factor in the development of depression or anxiety [ 11 , 12 ]. Subsets of patients with the major depressive disorder MDD and post-traumatic stress disorder have higher levels of multiple inflammatory markers, including the cytokine interleukin 6 IL-6 [ 11 , 13 ]. Molecular studies of the stress phenomenon have found some genes which are differentially expressed in stressed individuals and control subjects. Studies involving effect at individual genes as well as genome-wide studies at cellular, tissue, and individual levels are reported.
A study of DNA microarray from circulating leucocytes showed that the stress causes some genes upregulated and some other genes downregulated. The downregulated genes are mainly related to apoptosis, cell cycle inhibitors, NF-KB inhibitor Apo J , and antiproliferative cytokines. The upregulated genes are involved in cell cycle activation, and enzymes involved in nucleic acid biosynthesis and proteins.
Other upregulated genes are transcription factors that control chromatin structure and cell growth [ 15 ].
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The transcription factor that controls many of these genes is NF-KB. Hence, NF-KB plays a key role in the cellular stress response.
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