Journal ArticleDOI
The role of adrenocorticoids as modulators of immune function in health and disease: neural, endocrine and immune interactions.
Bruce S. McEwen,Christine A. Biron,Kenneth W. Brunson,Karen Bulloch,William H. Chambers,Firdaus S. Dhabhar,Ronald H. Goldfarb,Richard P. Kitson,Andrew H. Miller,Robert L. Spencer,Jay M. Weiss +10 more
TLDR
This work presents a meta-anatomy of the adrenal gland and its role in the development and management of disease and urges further investigation into the role of “cell reprograming” and “reconcretization” in the course of disease progression.About:
This article is published in Brain Research Reviews.The article was published on 1997-02-01. It has received 822 citations till now. The article focuses on the topics: Endocrine system & Immune system.read more
Citations
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How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.
TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
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Protective and Damaging Effects of Stress Mediators
TL;DR: The long-term effect of the physiologic response to stress is reviewed, which I refer to as allostatic load, which is the ability to achieve stability through change.
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Stress, adaptation, and disease. Allostasis and allostatic load.
TL;DR: The relationship of allostatic load to genetic and developmental predispositions to disease is considered and examples will be given from research pertaining to autonomic, CNS, neuroendocrine, and immune system activity.
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The neurobiology of stress : from serendipity to clinical relevance
TL;DR: In this article, the effects of stress on the immune system and brain are discussed and two new terms, allostasis and allostatic load, are introduced to supplement and clarify the meanings of stress and homeostasis.
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The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders.
TL;DR: It is proposed that a persistent lack of cortisol availability in traumatized or chronically stressed individuals may promote an increased vulnerability for the development of stress-related bodily disorders.
References
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TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties.
Tim R. Mosmann,R L Coffman +1 more
TL;DR: Two types of cloned helper T cells are described, defined primarily by differences in the pattern of lymphokines ynthesized, and the different functions of the two types of cells and their lymphokine synthesis are discussed.
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Précis of The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-Hippocampal System..
TL;DR: It is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system (SHS), the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures.
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Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation
TL;DR: It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
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A Syndrome produced by Diverse Nocuous Agents
TL;DR: If the organism is severely damaged by acute non-specific nocuous agents such as exposure to cold, surgical injury, production of spinal shock, excessive muscular exercise, or intoxications with sublethal doses of diverse drugs, a typical syndrome appears, the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed.
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Stress and the Individual: Mechanisms Leading to Disease
Bruce S. McEwen,Eliot Stellar +1 more
TL;DR: A new formulation of the relationship between stress and the processes leading to disease is presented, emphasizing the cascading relationships between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease.