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Dataset results
71 results for “Stress reactivity”
Obesity and acute stress modulate appetite and neural responses in food word reactivity task
<p>Data used in "Carnell S, Benson L, Papantoni A, Chen L, Huo Y, Wang Z, Peterson BS, Geliebter A. Obesity and acute stress modulate appetite and neural responses in food word reactivity task. PloS one"</p>
The Menopause Transition: Estrogen Variability, Stress Reactivity and Mood
ClinicalTrials.gov study NCT03003949. IPD Sharing: YES. Countries: 1. Publications: 1.
The Effects of Suvorexant on Sleep, Stress, and Cue-reactivity in Methamphetamine Use Disorder
ClinicalTrials.gov study NCT05711862. IPD Sharing: NO. Countries: 1. Publications: 0.
Morning Light Treatment for Traumatic Stress: The Role of Amygdala Reactivity
ClinicalTrials.gov study NCT04117347. IPD Sharing: YES. Countries: 1. Publications: 1.
Stress Reactivity Among African American Breast Cancer Survivors
ClinicalTrials.gov study NCT03881085. IPD Sharing: NO. Countries: 1. Publications: 1.
Stress Reactivity in Veterans Receiving Pharmacological Treatment for PTSD and Alcohol Dependence
ClinicalTrials.gov study NCT00923923. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Influence of Dopaminergic Blockade on Stress Responses, Motivation and Emotional Reactivity in Humans.
ClinicalTrials.gov study NCT03863691. IPD Sharing: NO. Countries: 1. Publications: 5.
A Novel Treatment For Chronic Posttraumatic Stress Disorder (PTSD) Using Post-Reactivation Propranolol
ClinicalTrials.gov study NCT01127568. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Reactivation of CMV Infection in Immunocompetent Patients Under Severe Stress
ClinicalTrials.gov study NCT01397058. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Gender, Obesity, C-Reactive Protein, and Oxidative Stress
ClinicalTrials.gov study NCT00079963. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Treatment of Pediatric Post-traumatic Stress Disorder With Memory Reactivation Under the Influence of Propranolol
ClinicalTrials.gov study NCT04985344. IPD Sharing: NO. Countries: 1. Publications: 3.
Effects of Self-Compassion Practice on Stress Reactivity Among Sexual Minority Women
ClinicalTrials.gov study NCT05949060. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Emotional Memory Reactivation in Posttraumatic Stress Disorder
ClinicalTrials.gov study NCT01239173. IPD Sharing: Not stated. Countries: 1. Publications: 20.
FHA: Characterization of Metabolic Status, Brain Circuitry, and Stress-Reactivity
ClinicalTrials.gov study NCT00453219. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Pre- and post-natal effects of experimentally manipulated maternal corticosterone on growth, stress reactivity, and survival of nestling house wrens
1. Corticosterone plays a central role in maintaining homeostasis, promoting energy acquisition, and regulating the stress response in birds. Exposure to elevated levels of corticosterone during development can profoundly alter offspring behaviour and physiology, but the effects of elevated maternal corticosterone on offspring development remain poorly understood. 2. We tested two competing hypotheses concerning the effect of maternally derived corticosterone on growth and development of free-living house wrens: i) elevated maternal corticosterone causes damaging effects on nestling phenotype and fitness (collateral damage hypothesis) and (ii) increased maternal corticosterone enhances offspring fitness by preparing nestlings for the environment experienced by their mother (environmental/maternal-matching hypothesis). 3. We used a non-invasive means to increase maternal corticosterone by providing females with corticosterone-injected mealworms prior to and during egg production in the absence of any overt pre-natal maternal stress. To disentangle pre- and post-natal effects of this elevation in maternal corticosterone, we cross-fostered young in two experiments: i) nestlings of control and experimental females were reared by unmanipulated, natural females in a uniform maternal environment; ii) a split-brood design that enabled us to assess the interaction between the mother's corticosterone treatment and that of the nestlings. 4. There were significant pre-natal effects of increased maternal corticosterone on nestling growth and survival. Offspring of females experiencing experimentally increased corticosterone were heavier and larger than offspring of control females. There also was a significant interaction between maternal corticosterone treatment and the corticosterone treatment to which young were exposed within the egg in their effect on nestling survival while in the nest; experimental young exhibited greater survival than control young, but only when reared by control mothers. There was also a significant effect of maternal corticosterone treatment on nestling stress reactivity and, in both experiments, on the eventual recruitment of offspring as breeding adults in the local population. 5. These patterns are broadly consistent with the environmental/maternal-matching hypothesis, and highlight the importance of disentangling pre- and post-natal effects of manipulations of maternal hormone levels on offspring phenotype.
Data for: Predation risk and the evolution of a vertebrate stress response: parallel evolution of stress reactivity and sexual dimorphism
<p><span><span><span><span><span><span><span><span><span><span><span><span><span>Predation risk is often invoked to explain variation in stress responses. Yet, the answers to several key questions remain elusive, including: 1) how predation risk influences the evolution of stress phenotypes, 2) the relative importance of environmental versus genetic factors in stress reactivity, and 3) sexual dimorphism in stress physiology. To address these questions, we </span></span>explored variation in stress reactivity (ventilation frequency) in a post-Pleistocene radiation of live-bearing fish, where Bahamas mosquitofish (<i>Gambusia hubbsi</i>) inhabit isolated blue holes that differ in predation risk. Individuals of populations coexisting with predators exhibited similar, relatively low stress reactivity as compared to low-predation populations. We suggest that this dampened stress reactivity has evolved to reduce energy expenditure in environments with frequent and intense stressors, such as piscivorous fish. Importantly, the magnitude of stress responses exhibited by fish from high-predation sites in the wild changed very little after two generations of laboratory rearing in the absence of predators. By comparison, low-predation populations exhibited greater among-population variation and larger changes subsequent to laboratory rearing. These low-predation populations appear to have evolved more dampened stress responses in blue holes with lower food availability. Moreover, females showed a lower ventilation frequency, and this sexual dimorphism was stronger in high-predation populations. This may reflect a greater premium placed on energy efficiency in live-bearing females, especially under high predation risk where females show higher fecundities. Altogether, by demonstrating parallel adaptive divergence in stress reactivity, we highlight how energetic trade-offs may mould the evolution of the vertebrate stress response under varying predation risk and resource availability.</span></span></span></span></span></span></span></span></span></span></span></p>
Figure 1 from: Althanoon ZA, Mahmood IH (2021) Effect of lisinopril therapy on serum leptin, oxidative stress and C-reactive protein in hypertensive patients. Pharmacia 68(3): 705-711. https://doi.org/10.3897/pharmacia.68.e73140
Figure 1 The difference in mean of measured parameters (MDA, hsCRP, TAC, and GSH) among the study sampled groups.
Stress-Reactivity and Cannabis Use in Cannabis-Using Older Adults
ClinicalTrials.gov study NCT05072795. IPD Sharing: NO. Countries: 1. Publications: 0.
Effects of Escitalopram on Autonomic Reactivity in Post Traumatic Stress Disorder
ClinicalTrials.gov study NCT01271244. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Impact of Progesterone on Stress Reactivity and Cannabis Use
ClinicalTrials.gov study NCT03729869. IPD Sharing: NO. Countries: 1. Publications: 0.
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