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Books on the topic 'Stress modulation'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and their Modulation. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2032-9.

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2

Chakraborti, Sajal, Naranjan S. Dhalla, Madhu Dikshit, and Nirmal K. Ganguly, eds. Modulation of Oxidative Stress in Heart Disease. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7.

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3

OHOLO Conference (40th 1996 Zikhron Ya'akov, Israel). New frontiers in stress research: Modulation of brain function. Australia: Harwood Academic Publishers, 1998.

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4

Bezaire, Jake. Lead stress and modulation of TCA cycle enzymes in "Pseudomonas fluorescens". Sudbury, Ont: Laurentian University, 2001.

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5

Singh, Ranji. The modulation of NADPH, NADH, and a-ketoglutarate in Pseudomonas fluorescens exposed to oxidative stress. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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6

Rainville, Nathalie-Sylvie. Modulation des voies métaboliques impliquant glutamate déhydrogénase chez Pseudomonas fluorescens stressé par l'aluminium. Sudbury, Ont: Université Laurentienne, 2005.

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7

Saso, Luciano, Alessandro Giuffrè, Giuseppe Valacchi, and Mauro Maccarrone. Pharmacological Modulation of Oxidative Stress. Elsevier Science & Technology Books, 2023.

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8

Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer (India) Private Limited, 2014.

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9

Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2014.

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10

Bansal, Mohinder, and Naveen Kaushal. Oxidative Stress Mechanisms and Their Modulation. Springer, 2016.

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11

Stress et immunologie : Neuro-immuno-modulation. Presses Universitaires de France - PUF, 1989.

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12

Dhalla, Naranjan S., Nirmal K. Ganguly, Sajal Chakraborti, and Madhu Dikshit. Modulation of Oxidative Stress in Heart Disease. Springer Singapore Pte. Limited, 2021.

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13

Dhalla, Naranjan S., Nirmal K. Ganguly, Sajal Chakraborti, and Madhu Dikshit. Modulation of Oxidative Stress in Heart Disease. Springer, 2019.

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14

New Frontiers in Stress Research: Modulation of Brain Function. Informa Healthcare, 1998.

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15

(Editor), Young-Joon Surh, Zigang Dong (Editor), Enrique Cadenas (Editor), and Lester Packer (Editor), eds. Dietary Modulation of Cell Signaling Pathways (Oxidative Stress and Disease). CRC, 2008.

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16

O’Flaherty, Brendan M., Chia-Chun Hsu, M. Anzar Abbas, and Donald G. Rainnie. Cellular Physiology of the Basolateral Complex of the Amygdala and Its Modulation by Stress. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0003.

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Fear is a critical emotional response that allows an organism to safely navigate through dangerous environments. The neural systems underlying the fear response have been well characterized, and include the amygdala, hippocampus, prefrontal cortex, bed nucleus of stria terminalis, nucleus accumbens, and others. While normally these brain regions coordinate to produce an appropriate fear response, the fear network in humans can become dysregulated after a traumatic event. The resulting phenotype of hyperarousal, avoidance, and re-experiencing of fear known as post-traumatic stress disorder (PTSD) is a growing problem in the United States. This chapter focuses on the role of the basolateral complex (BLC) of the amygdala, which has been implicated in the neuropathology of PTSD, particularly the hyperarousal, fear generalization, and fear extinction deficits characteristic of the disorder, as well as aspects of the microcircuitry, network connectivity, and neuromodulation of the BLC that may be involved in the pathophysiology of PTSD.
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17

Phan, Nam. Stress induced modulation of mitochondrial protein import in differentiated PC12 cells: The role of Tom20. 2006.

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18

R, Wunderlich Glen. Effects of chronic amphetamine and chronic restraint stress on cholecystokinin modulation of mesolimbic dopamine-mediated behaviour in the rat. 2003.

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19

Luyten, Patrick, and Peter Fonagy. The Neurobiology of Attachment and Mentalizing. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0006.

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This chapter addresses the neurobiology of attachment and mentalizing from a developmental psychopathology perspective. It defines attachment, considers its key role in the modulation of the stress response, and describes the general neurobiological process by which this occurs. The chapter then considers the neurobiology of attachment and proceeds to discuss the neurobiological underpinning of mentalizing in relation to attachment and stress regulation. It also focuses on the early development of both capacities in relation to stress regulation and discusses the relationship to the development of psychopathology and personality disorder in particular across the lifespan, with a focus on early childhood and adolescence.
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20

Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.
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21

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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22

Razzoli, Maria, Alessandro Bartolomucci, and Valeria Carola. Gene-by-Environment Mouse Models for Mood Disorders. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.013.

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Much of the impact of genes on mood disorders likely depends on interactions between genes and the environment. Recent studies demonstrating an interaction between specific genes and life stressful events (early and/or adult) in the modulation of several mood disorders (e.g., serotonin transporter and brain-derived neurotrophic factor genes) have compelled researchers to incorporate information about adverse environmental experiences into the study of genetic risk factors; these same gene-by-environment (G×E) interactions have been identified in mouse models. Notably, G×E not yet described in humans (e.g., serotonin 1A receptor gene) have been uncovered, providing helpful indications to discover similar interactions in humans. Accurate knowledge of the modality of expression of gene-by-stress interaction may help design prevention protocols aimed at identifying susceptibility to mood disorders on the basis of genetic predisposition and exposure to environmental stressful conditions, thus providing patients with appropriate pharmacological and psychological support.
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23

Hernandez-Ledesma, Blanca, and Cristina Martinez-Villaluenga. Current Advances for Development of Functional Foods Modulating Inflammation and Oxidative Stress. Academic Press, 2021.

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24

Current Advances for Development of Functional Foods Modulating Inflammation and Oxidative Stress. Elsevier, 2022. http://dx.doi.org/10.1016/c2019-0-05479-9.

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25

Hernandez-Ledesma, Blanca, and Cristina Martinez-Villaluenga. Current Advances for Development of Functional Foods Modulating Inflammation and Oxidative Stress. Elsevier Science & Technology Books, 2021.

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26

Brondolo, Elizabeth, Irene V. Blair, and Amandeep Kaur. Biopsychosocial Mechanisms Linking Discrimination to Health: A Focus on Social Cognition. Edited by Brenda Major, John F. Dovidio, and Bruce G. Link. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.013.8.

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This chapter presents a theoretical framework that highlights the role of social cognition in mediating the effects of discrimination on health. This framework suggests that through alterations in schemas and appraisal processes, long-term discrimination increases the experienced frequency, intensity, and duration of threat exposure and concomitant distress. At the same time, the ability to recover from threat exposure may be impaired by the effects of discrimination on cognitive control processes that are necessary for modulating stress responses. Together, these processes may influence the ability to initiate and sustain health-promoting behavior, avoid health-impairing behavior, attenuate stress reactivity, and facilitate stress recovery. Through effects on social cognition, persistent exposure to discrimination may potentiate sustained dysregulation of psychophysiological systems responsible for maintaining health.
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27

Todder, Doron, Keren Avirame, and Hagit Cohen. Neuromodulation Methods in PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0039.

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This chapter discusses the rationale and methodology for applying techniques of active and passive neuromodulation for treatment-refractory post-traumatic stress disorder (PTSD). Neuromodulation derives from the concept of neuroplasticity, which signifies long-term changes in the effectiveness of connections between distinct parts of the central nervous system. These changes are reflected across multiple levels of the nervous system, going from the cellular level to circuits and large-scale brain networks. It has been long suggested that altered neuroplasticity is a biomarker of neuropsychiatric diseases. With recent advances in neuroscience, research is emerging on evaluating the potential of modulating neural circuits by using innovative technologies, including noninvasive and invasive brain stimulation, EEG-neurofeedback, and fMRI neurofeedback.
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28

DelCarmen-Wiggins, Rebecca, and Alice S. Carter, eds. The Oxford Handbook of Infant, Toddler, and Preschool Mental Health Assessment. Oxford University Press, 2019. http://dx.doi.org/10.1093/oxfordhb/9780199837182.001.0001.

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The fully revised and updated Handbook of Infant, Toddler, and Preschool Mental Health Assessment remains the first clinically-informative, research-based reference for those seeking to understand and assess mental health in infants and young children. It describes the latest empirical research on measures and methods of infant and young child assessment and provides clinically applicable information for those seeking to stay apprised of the latest empirical research on measures and procedures in early assessment. Through authoritative examination by leading developmental and clinical scholars, this handbook takes a closer look at current developmentally based conceptualizations of mental health function and dysfunction in infants and young children as well as current and new diagnostic criteria in such as specific disorders as sensory modulation dysfunction, autism spectrum disorders, affective disorders, and post-traumatic stress disorder. Translation and application to a variety of settings is also discussed. The chapters are presented in four sections corresponding to four broad themes: (1) contextual factors in early assessment; (2) temperament and regulation in assessment of young children; (3) early problems and disorders; and (4) translation and varied applied settings for assessment. Each chapter presents state of the science information on valid, developmentally based clinical assessment and makes recommendations based on developmental theory, empirical findings, and clinical experience. Chapters have been revised and updated, and new chapters have been added to cover family assessment, early care and educational environments, new approaches to distinguish temperament from psychopathology, assess language, and implement second stage screening and referral. The volume recognizes and highlights the important role of developmental, social, and cultural contexts in approaching the challenge of assessing early problems and disorders. This new, updated volume will be an ideal resource for teachers, researchers, and wide variety of clinicians and trainees including child psychologists and psychologists, early interventionists, and early special educators.
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29

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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30

Waldmann, Carl, Neil Soni, and Andrew Rhodes. Renal disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0019.

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Prevention of acute renal failure 312Diagnosis of acute renal failure 314Acute kidney injury (AKI) often complicates the course of critical illness and was previously considered as a marker rather than a cause of adverse outcomes, it is independently associated with an increase in both morbidity and mortality. The major causes of AKI in the ICU include hypoperfusion, sepsis and direct nephrotoxicity, with the common aetiology believed to be a change in intrarenal haemodynamics with resultant acute tubular dysfunction and oxidant stress. Treatment of established acute renal failure in the ICU entails the use of RRT by means of various modalities, although this therapy itself carries an inherent morbidity and risk. Therefore, preventing or minimizing renal injury should confer a benefit to patients. Consequently, several pharmacological interventions have been tried to treat AKI. These interventions can be separated into measures influencing renal perfusion and measures modulating intrarenal pathophysiology....
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31

Hamilton, Matthew Lloyd. COMT genotypes in pain responses. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0080.

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The landmark study discussed in this chapter is ‘COMT val158met genotype affects μ‎-opioid neurotransmitter responses to a pain stressor’, published by Zubieta et al. in 2003. Catechol-O-methyl-transferase (COMT) is a key modulator of dopaminergic and noradrenergic neurotransmission. This study focused on a single nucleotide polymorphism of the COMT gene encoding the substitution of valine (val) by methionine (met) at Codon 158 (val158met), resulting in a three- to fourfold reduction in its activity. Individuals with the val/val genotype have the highest activity of COMT, val/met genotypes have intermediate activity, and met/met genotypes have the lowest activity of COMT. Using a mixture of PET imaging of the binding of μ‎-opioid receptors and correlation with clinical outcomes, this groundbreaking study provided evidence that confirmed their hypothesis and established the COMT val158met SNP as one of the first gene modifications with direct ramifications on human pain.
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32

MacLean, Allan B. Vulval pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749547.003.0009.

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Vulval pain or pain involving the vulval tissue is discussed in Chapter 9. It becomes chronic when lasting for at least three months. Vulvodynia is a subset of chronic vulval pain, once known causes (infective, inflammatory, neoplastic, neurological, traumatic, iatrogenic and hormone deficiencies) are excluded. It reportedly affects one in six women at some stage of their lives. Uncertain terminology has hampered understanding. Even the latest classification from the International Society for the Study of Vulvovaginal Disease has deficiencies but it allows the discarding of previously used unhelpful terms. Differentiating features between provoked (entry dyspareunia), and unprovoked, localised and generalised, overlap, both in diagnosis and management. Older theories on causation included infection, irritation and inflammation but laboratory-based research has not supported these. Hormonal and neural mechanisms seem more likely to cause the pain, while the interplay of biological, psychological, and social factors has recently gained credence. Publications on successful management demonstrate a powerful placebo effect. The role of specially designated vulval pain clinics, multidisciplinary approaches, and team working is emphasised. General measures in vulval care, such as wearing clothes made of natural fibre, using emollients or carrying out pelvic floor exercises besides reducing stress, can minimise the pain. Topical anaesthetic creams or systemic treatments with antidepressants or anti-epileptics have advocates. Treatment is most effective when careful selection, adequate counselling, and ongoing psychosomatic evaluation address all the interactive factors that initiate, and maintain vulval pain besides modulating patient response. Case scenarios illustrate the complexities of diagnosis and management.
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