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Published: 4 June 2021
Last updated: 20 February 2023

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1

Wondrak, Georg T., ed. Skin Stress Response Pathways. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43157-4.

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2

Wondrak, Georg T., ed. Stress Response Pathways in Cancer. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9421-3.

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3

Herman, James P. Limbic Pathways to Stress Control. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.

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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.
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4

Wondrak, Georg T. Skin Stress Response Pathways: Environmental Factors and Molecular Opportunities. Springer, 2018.

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5

Wondrak, Georg T. Skin Stress Response Pathways: Environmental Factors and Molecular Opportunities. Springer, 2016.

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6

Wondrak, Georg T. Skin Stress Response Pathways: Environmental Factors and Molecular Opportunities. Springer London, Limited, 2016.

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7

Wondrak, Georg T. Stress Response Pathways in Cancer: From Molecular Targets to Novel Therapeutics. Springer, 2016.

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8

Wondrak, Georg T. Stress Response Pathways in Cancer: From Molecular Targets to Novel Therapeutics. Springer, 2014.

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9

Wondrak, Georg T. Stress Response Pathways in Cancer: From Molecular Targets to Novel Therapeutics. Springer, 2014.

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10

Huang, Ruili, and Menghang Xia, eds. Tox21 Challenge to Build Predictive Models of Nuclear Receptor and Stress Response Pathways as Mediated by Exposure to Environmental Toxicants and Drugs. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-197-5.

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11

Laumbach, Robert, and Michael Gochfeld. Toxicology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0007.

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This chapter describes the basic principles of toxicology and their application to occupational and environmental health. Topics covered include pathways that toxic substances may take from sources in the environment to molecular targets in the cells of the body where toxic effects occur. These pathways include routes of exposure, absorption into the body, distribution to organs and tissues, metabolism, storage, and excretion. The various types of toxicological endpoints are discussed, along with the concepts of dose-response relationships, threshold doses, and the basis of interindividual differences and interspecies differences in response to exposure to toxic substances. The diversity of cellular and molecular mechanisms of toxicity, including enzyme induction and inhibition, oxidative stress, mutagenesis, carcinogenesis, and teratogenesis, are discussed and the chapter concludes with examples of practical applications in clinical evaluation and in toxicity testing.
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12

Barr, Christina S. Gene-by-Environment Interactions in Primates. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.006.

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Because of their complex social structures, behaviors, and genetic similarities to humans, nonhuman primates are useful for studying how genetic factors influence alcohol consumption. The neurobiological systems that influence addiction vulnerability may do so by acting on alcohol response, reward pathways, behavioral dyscontrol, and vulnerability to stress and anxiety. Rhesus macaques show individual differences in alcohol response and temperament, and such differences are influenced by genetic variants that are similar functionally to those present in humans. Genes in which variation moderates these phenotypes provide opportunities for modeling how genetic and environmental factors (i.e., stress exposure, individual’s sex, or alcohol response) interact to influence alcohol consumption. Studies in primates may also reveal selective factors that have driven maintenance or fixation of alleles that increase risk for alcohol use disorders in modern humans.
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13

Heim, Christine, and Charles B. Nemeroff. Neurobiological Pathways Involved in Fear, Stress, and PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0012.

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The symptoms of post-traumatic stress disorder (PTSD) are believed to reflect an inadequate adaptation of neurobiological systems to exposure to severe stressors. A vast number of studies have revealed multiple alterations in neuroendocrine and neurochemical systems in patients with PTSD. It is now evident that certain neurobiological changes in PTSD actually reflect preexisting vulnerability factors that contribute to maladaptive physiological and behavioral responses to traumatic exposure, as well as altered learning and extinction of fear memories. These results suggest the development of novel pathophysiology-driven strategies for intervention that directly target the neurobiological mechanisms that lead to stress sensitization, increased fear memories, and arousal.
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14

Ciano-Oliveira, Caterina Di. Signaling pathways linking osmotic stress to adaptive responses: Roles for Rho family GTPases. 2006.

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15

Rushton, Cynda Hylton. Mapping the Path of Moral Adversity. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190619268.003.0004.

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An alternative path for addressing moral adversity and the resultant moral suffering engages the focal points in a cycle of imperiled integrity in response to moral harms, wrongs, failures, or other forms of moral adversity. Initially moral stress, a neutral state of readiness to respond that will eventually involve an appraisal as positive or negative, may be experienced. Depending on this appraisal and individual capabilities, moral stress may be rebalanced, released, or resolved, engaging our moral resilience to proactively or prospectively respond to moral adversity. Alternatively, when the moral stress of imperiled integrity exceeds our capacities and becomes unmanageable or overwhelming, it can instigate a pathway leading to moral suffering that includes moral distress, outrage, and injury. In some instances moral suffering leads to recalcitrant or persistent forms of moral decline. When moral resilience including a process of moral repair is leveraged, integrity can be restored.
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16

Lau, Hi-Po Bobo, and Cecilia Cheng. The Yin-Yang of Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199348541.003.0020.

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Dialectical thinking refers to the (primarily East Asian) tendency to tolerate contradiction, expect change, and perceive interconnections. Drawing upon a process-oriented approach to coping, in this chapter, two pathways through which dialectical thinking may influence East Asians’ ways of coping are proposed. First, dialectical (and holistic) thinking may enable East Asians to attribute events to both situational and dispositional factors. This breadth in attribution may lead to the perception of less personal control, as well as a weaker association between perceived personal control and coping outcomes among East Asians than among Westerners. In addition, dialectical thinking may facilitate complex cognitive processes such as differentiation and integration, and a reduced need for closure. In turn, this facilitates flexibility in appraising the controllability of stressful events and deployment of situation-appropriate coping responses (i.e., coping flexibility). Areas for future research are also discussed in the chapter.
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17

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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18

Miu, Andrei C., Judith R. Homberg, and Klaus-Peter Lesch, eds. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.

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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.
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19

Carpenter, Gregory, and Meenal Patil. Gender Differences in Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0005.

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Epidemiologic and clinical findings demonstrate that women are at increased risk for chronic pain, experience greater pain-related distress, and show heightened sensitivity for pain compared to men. There are differences in analgesic responses to pain and to both opioid and non-opioid medications as well as for endogenous analgesic processes. Many stress-related disorders, such as fibromyalgia and chronic pain, are more prevalent in women. Studies of experimentally induced pain show that women exhibit greater pain sensitivity, enhanced pain facilitation, and reduced pain inhibition compared to men. Mechanisms that implicated in the underlying sex differences include biological involvement of estrogen and progesterone versus testosterone. Sex-related differences in pain may also reflect differences in the endogenous opioid system. Other mechanisms include steroid action differences in adulthood, modulation of various biological systems such as the cardiovascular and inflammatory pathways, and sociocultural differences
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20

Major, Brenda, John F. Dovidio, Bruce G. Link, and Sarah K. Calabrese. Stigma and Its Implications for Health: Introduction and Overview. Edited by Brenda Major, John F. Dovidio, and Bruce G. Link. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.013.1.

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There is growing recognition that stigma plays an important role in producing health disparities between members of socially advantaged and disadvantaged (marginalized) groups. This chapter defines stigma, describes differences among stigmatized marks, and discusses the functions that stigma may serve for individuals, groups, and societies. It also provides a conceptual model of the pathways by which stigma relates to health. This model posits that socially conferred marks that are devalued in society are the basis for four key stigma processes: enacted stigma, felt stigma, internalized stigma, and anticipated stigma. These stigma processes lead to stress and accompanying individual-level affective, cognitive, behavioral, and physiological responses, as well as to social and community-level exclusion from important domains of life that collectively have downstream negative consequences for health. This chapter provides an integrative overview of the chapters in the current volume and concludes with suggestions for future research on stigma and health.
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21

Neuberg, Steven L., and Andreana C. Kenrick. Discriminating Ecologies: A Life History Approach to Stigma and Health. Edited by Brenda Major, John F. Dovidio, and Bruce G. Link. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.013.5.

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How does being discriminated against affect one’s health, and through what mechanisms? Most research has focused on two causal pathways, highlighting how discrimination increases psychological stress and exposure to neighborhood hazards. This chapter advances an alternative, complementary set of mechanisms through which stigma and discrimination may shape health. Grounded in evolutionary biology’s life history theory, the framework holds that discrimination alters aspects of the physical and social ecologies in which people live (e.g., sex ratio, unpredictable extrinsic causes of mortality). These discriminating ecologies pull for specific behaviors and physiological responses (e.g., risk-taking, sexual activity, offspring care, fat storage) that are active, strategic, and rational given the threats and opportunities afforded by these ecologies but that also have downstream implications for health. This framework generates a wide range of nuanced insights and unique hypotheses about the discrimination-health relationship, and suggests specific approaches to intervention while pointing to complex ethical issues.
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22

Major, Brenda, John F. Dovidio, and Bruce G. Link, eds. The Oxford Handbook of Stigma, Discrimination, and Health. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.001.0001.

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Throughout the world, groups that are socially disadvantaged have poorer health compared to groups that are more advantaged. This book examines the role that stigma and discrimination play in creating and sustaining these group health disparities. Stigma is a social construction in which people who are distinguished by a “mark” are viewed as deviant, socially excluded, and devalued. Stigma and the discrimination it engenders negatively affect health through multiple mechanisms operating at several different levels of influence. Collectively, these shape both the orientations of people toward members of stigmatized groups and the experiences, and often the self-concepts, of members of groups targeted by stigma. Stigma affects individual-level affective, cognitive, behavioral, and physiological responses that increase stress in the lives of stigmatized groups. Stigma also restricts access to social and community-level resources relevant to good health and exposes individuals to more toxic environments. All act to erode the health of people who are stigmatized. This volume provides a cutting edge, multidisciplinary, multilevel analysis of health and health disparities through the integrative lens of stigma. It brings together the research of leading social and health psychologists, sociologists, public health scholars, and medical ethicists who study stigma and health. It integrates independent literatures on the health-related outcomes of stigma and discrimination and the diverse pathways and processes by which stigma and discrimination affect multiple health outcomes. The book is also forward-looking: It discusses the implications of these themes for policy, interventions, and health care, as well as identifies the most important directions for future research.
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23

Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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