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Journal articles on the topic 'Stress response'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Pingitore, Alessandro, Francesca Mastorci, and Giorgio Iervasi. "Heart Failure and Stress Response." Biomed Data Journal 1, no. 3 (2015): 33–35. http://dx.doi.org/10.11610/bmdj.01300.

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2

AV, Valdez. "Plant Mechanism in Response to Stress." Open Access Journal of Agricultural Research 9, no. 4 (2024): 1. https://doi.org/10.23880/oajar-16000374.

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In the advent of plant stress Stress physiology will address Abiotic stress affects plant productivity and yield Biotic stress adds the plant agony in the field Plant response to drought Make the plants continue to sprout

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3

Arsić-Komljenović, Gordana, Dragan Mikić, and Jelena Kenić. "Stress and response to stress." Zdravstvena zastita 39, no. 6 (2010): 9–15. http://dx.doi.org/10.5937/zz1002009a.

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4

Jawwad, Ghazala, Humaira Fayyaz Khan, and Amanat Ali. "STRESS RESPONSE;." Professional Medical Journal 24, no. 09 (2017): 1398–402. http://dx.doi.org/10.29309/tpmj/2017.24.09.822.

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Introduction: Psychological stress activate two axes: Hypothalamic- Pituitary-Adrenal axis and Sympathoadrenal axis leading to production of cortisol and catecholamines.Autonomic disturbances in the body can be evaluated by estimating heart rate variability.Study Design: Cross sectional study. Setting: Islamic International Medical College. Period:June 2014 to December 2014. Materials and Methods: Subjects were labeled as stress andcontrol on basis of DASS questionnaire proforma. Morning Cortisol level of all the subjectswas measured by quantitative ELISA method. Heart rate variability recordi

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5

Rapport, David J. "Stress response." Trends in Ecology & Evolution 13, no. 1 (1998): 36–37. http://dx.doi.org/10.1016/s0169-5347(97)01249-4.

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6

Hameed, Jawad, Amjid Ali, Ayesha Mairaj, Hadiqa Tul Batool, Abid Haleem Khattak, and Mustafa Majeed. "Role of Dexmedetomidine on Post-traumatic Stress Response." Medical Journal of South Punjab 5, no. 2 (2024): 8–15. https://doi.org/10.61581/mjsp.vol05/02/02.

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Objective: to explore the role of dexmedetomidine on the incidence of postoperative post traumatic stress response (PTSD) in trauma patients in the emergency department. Methods: This randomized clinical trial was carried out at Lady Reading Hospital Peshawar from January 2023 to October 2023. Participants were randomly assigned to receive either normal saline or dexmedetomidine. The study medications included 2ml normal saline or dexmedetomidine 200 ?g/2 mL. Results: Postoperative NRS score of normal saline and dexmedetomidine group at day 1 was 4.57±1.79, at day 2 2.66±1.23, and at day was 3

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7

Cummins, Nadia, and Rebecca C. Taylor. "A stress-free stress response." Nature Chemical Biology 16, no. 10 (2020): 1038–39. http://dx.doi.org/10.1038/s41589-020-0616-8.

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8

Motzer, Sandra Adams, and Vicky Hertig. "Stress, stress response, and health." Nursing Clinics of North America 39, no. 1 (2004): 1–17. http://dx.doi.org/10.1016/j.cnur.2003.11.001.

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9

Tarasenko, S.V. Morozova E.A. Zhuravlev A.N. Diachkova E.Yu. "SURGICAL STRESS RESPONSE." INDO AMERICAN JOURNAL OF PHARMACEUTICAL SCIENCES 05, no. 10 (2018): 9812–18. https://doi.org/10.5281/zenodo.1457319.

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<em>The main cause of postoperative complications is considered to be the surgical response, which is a complex of changes in the neuroendocrine, metabolic and inflammatory developing due to the surgical trauma. With the high degree of surgical trauma these changes initially with compensatory-adaptive character become overweight, acquiring, thus, a clearly defined pathological direction. Surgical stress response is a major cause of postoperative dysfunction of various organs and systems (pain syndrome, immune system disorders and hemostasis, dysfunction of the lungs, gastrointestinal tract, ca

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10

Milutinovic, Snezana, Qianli Zhuang, Alain Niveleau, and Moshe Szyf. "Epigenomic Stress Response." Journal of Biological Chemistry 278, no. 17 (2003): 14985–95. http://dx.doi.org/10.1074/jbc.m213219200.

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11

Brown, I. R. "The stress response." Neuropathology and Applied Neurobiology 21, no. 6 (1995): 473–75. http://dx.doi.org/10.1111/j.1365-2990.1995.tb01088.x.

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12

Boerner, T. F., R. R. Bartkowski, M. Torjman, E. Frank, and H. Schieren. "SYMPATHOADRENAL STRESS RESPONSE." Anesthesiology 77, Supplement (1992): A888. http://dx.doi.org/10.1097/00000542-199209001-00888.

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13

Seelye, Edward E. "Stress Response Syndromes." American Journal of Psychotherapy 41, no. 2 (1987): 310–11. http://dx.doi.org/10.1176/appi.psychotherapy.1987.41.2.310.

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14

Dmitrieva, Natalia I., and Maurice B. Burg. "Hypertonic stress response." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 569, no. 1-2 (2005): 65–74. http://dx.doi.org/10.1016/j.mrfmmm.2004.06.053.

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15

Hobbs, Mike. "Stress Response Syndromes." Journal of Psychosomatic Research 49, no. 1 (2000): 101–2. http://dx.doi.org/10.1016/s0022-3999(99)00003-3.

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16

Schroda, Michael, Dorothea Hemme, and Timo Mühlhaus. "TheChlamydomonasheat stress response." Plant Journal 82, no. 3 (2015): 466–80. http://dx.doi.org/10.1111/tpj.12816.

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17

Giannoudis, Peter V., Haralambos Dinopoulos, Byron Chalidis, and George M. Hall. "Surgical stress response." Injury 37 (December 2006): S3—S9. http://dx.doi.org/10.1016/s0020-1383(07)70005-0.

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18

Sanders, Brenda M., and Scott D. Dyer. "Cellular stress response." Environmental Toxicology and Chemistry 13, no. 8 (1994): 1209–10. http://dx.doi.org/10.1002/etc.5620130801.

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19

Yoshida, Hiderou. "ER stress response, peroxisome proliferation, mitochondrial unfolded protein response and Golgi stress response." IUBMB Life 61, no. 9 (2009): 871–79. http://dx.doi.org/10.1002/iub.229.

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20

Campbell, Jana, and Ulrike Ehlert. "Acute psychosocial stress: Does the emotional stress response correspond with physiological responses?" Psychoneuroendocrinology 37, no. 8 (2012): 1111–34. http://dx.doi.org/10.1016/j.psyneuen.2011.12.010.

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21

OGAWA, Kazuhiro. "Proteins in Response to Environmental Stress. Heme Metabolism in Stress Response." Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 56, no. 4 (2002): 615–21. http://dx.doi.org/10.1265/jjh.56.615.

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22

STERNBERG, ESTHER M. "NEUROENDOCRINE STRESS RESPONSE IN REGULATION OF INFLAMMATORY RESPONSES." Shock 21, Supplement (2004): 76. http://dx.doi.org/10.1097/00024382-200403001-00302.

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23

Baker, B. G., and J. P. Williams. "Response to: Inadequate stress responses in clinical situations." Medical Teacher 39, no. 7 (2017): 786–87. http://dx.doi.org/10.1080/0142159x.2017.1318586.

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24

Hughes, Ariel M., H. Tucker Hallmark, Lenka Plačková, Ondrej Novák, and Aaron M. Rashotte. "Clade III cytokinin response factors share common roles in response to oxidative stress responses linked to cytokinin synthesis." Journal of Experimental Botany 72, no. 8 (2021): 3294–306. http://dx.doi.org/10.1093/jxb/erab076.

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Abstract Cytokinin response factors (CRFs) are transcription factors that are involved in cytokinin (CK) response, as well as being linked to abiotic stress tolerance. In particular, oxidative stress responses are activated by Clade III CRF members, such as AtCRF6. Here we explored the relationships between Clade III CRFs and oxidative stress. Transcriptomic responses to oxidative stress were determined in two Clade III transcription factors, Arabidopsis AtCRF5 and tomato SlCRF5. AtCRF5 was required for regulated expression of &gt;240 genes that are involved in oxidative stress response. S

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25

Reichard, John F., Timothy P. Dalton, Howard G. Shertzer, and Alvaro Puga. "Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor." Dose-Response 3, no. 3 (2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.03.003.

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TCDD and other polyhalogenated aromatic hydrocarbon ligands of the aryl hydrocarbon receptor (AHR) have been classically considered as non-genotoxic compounds because they fail to be directly mutagenic in either bacteria or most in vitro assay systems. They do so in spite of having repeatedly been linked to oxidative stress and to mutagenic and carcinogenic outcomes. Oxidative stress, on the other hand, has been used as a marker for the toxicity of dioxin and its congeners. We have focused this review on the connection between oxidative stress induction and the toxic effects of fetal and adult

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26

Jalil Hafeez Ahmad, Sanaullah. "Response of Sunflower under Charcoal Rot (Macrophomina phaseolina) Stress Conditions." International Journal of Scientific Engineering and Research 1, no. 3 (2013): 89–92. https://doi.org/10.70729/j201338.

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27

Sidari, M., A. Muscolo, U. Anastasi, G. Preiti, and C. Santonoceto. "Response of four genotypes of lentil to salt stress conditions." Seed Science and Technology 35, no. 2 (2007): 497–503. http://dx.doi.org/10.15258/sst.2007.35.2.24.

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28

Mammen, Mary, and Sreekumar MR. "Nalbuphine versus Dexmeditomedine Effect on Hemodynamic Stress Response During Intubation." Indian Journal of Anesthesia and Analgesia 8, no. 6 (2021): 577–82. http://dx.doi.org/10.21088/ijaa.2349.8471.8621.84.

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Aims: Sympathetic system gets stimulated ondirect laryngoscopy and intubationand catecholamines are released. This response though of short duration, is hazardous to compromised subjects with brain and cardiac dysfunction. Vagus nerve also can be stimulated during laryngoscopy and intubation. Ourstudy is to find out the effects of Nalbuphine Hcl 5mgm and Dexmedetomidine 25mgm on hemodynamic variables SBP, DBP, MAP and HR at the time of laryngoscopy and intubation. Study was carried out in Pushpagiri Institute of Medical Sciences. Consecutive sampling technique was used to select study populati

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29

SR, Mittal. "Blood Pressure Response to Treadmill Stress TestingInterpretation and Critical Appraisal." Open Access Journal of Cardiology 7, no. 1 (2023): 1–18. http://dx.doi.org/10.23880/oajc-16000182.

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A progressive and sustained decrease in systolic blood pressure on the continuation of exercise suggests severe left ventricular dysfunction irrespective of the cause. A transient decrease in systolic blood pressure followed by a normal increase in the continuation of exercise does not have any clinical significance. Failure of systolic blood pressure to increase commensurate to an increase in workload suggests the failure of adequate increase in left ventricular stroke volume with increasing workload. At present there is no consensus about the definition and significance of the exaggerated in

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30

Morshed, Syed A., and Terry F. Davies. "Understanding Thyroid Cell Stress." Journal of Clinical Endocrinology & Metabolism 105, no. 3 (2019): e66-e69. http://dx.doi.org/10.1210/clinem/dgz193.

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Abstract Understanding the regulatory mechanisms that control intracellular stress has fundamental importance since its failure results in cell death. Evidence has emerged indicating that the intracellular signals that are induced in response to diverse stresses include the deoxyribonucleic acid damage response, the unfolded protein response, the mitochondrial and/or endoplasmic reticulum stress responses, and the autophagy signals to degrade dangerous protein aggregates. These signals bring changes to the stressed cells that may support systemic homeostasis or contribute to disease pathology.

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31

Rattan, Suresh I. S. "Hormetic Modulation of Aging and Longevity by Mild Heat Stress." Dose-Response 3, no. 4 (2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.04.008.

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Aging is characterized by a stochastic accumulation of molecular damage, progressive failure of maintenance and repair, and consequent onset of age-related diseases. Applying hormesis in aging research and therapy is based on the principle of stimulation of maintenance and repair pathways by repeated exposure to mild stress. In a series of experimental studies we have shown that repetitive mild heat stress has anti-aging hormetic effects on growth and various other cellular and biochemical characteristics of human skin fibroblasts undergoing aging in vitro. These effects include the maintenanc

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32

Pakos‐Zebrucka, Karolina, Izabela Koryga, Katarzyna Mnich, Mila Ljujic, Afshin Samali, and Adrienne M. Gorman. "The integrated stress response." EMBO reports 17, no. 10 (2016): 1374–95. http://dx.doi.org/10.15252/embr.201642195.

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33

HIRAI, HISASHI. "Psychological stress and response." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 13, no. 2 (1993): 105–14. http://dx.doi.org/10.2199/jjsca.13.105.

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34

Saito, Haruo, and Francesc Posas. "Response to Hyperosmotic Stress." Genetics 192, no. 2 (2012): 289–318. http://dx.doi.org/10.1534/genetics.112.140863.

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35

Dief, Abeer E., Elena V. Sivukhina, and Gustav F. Jirikowski. "Oxytocin and Stress Response." Open Journal of Endocrine and Metabolic Diseases 08, no. 03 (2018): 93–104. http://dx.doi.org/10.4236/ojemd.2018.83010.

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36

H. Tønnesen, L. Puggaard, J. Braaga. "Stress Response to Endoscopy." Scandinavian Journal of Gastroenterology 34, no. 6 (1999): 629–31. http://dx.doi.org/10.1080/003655299750026119.

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37

FLOURAKI (Ε. Σ. ΦΛΟΥΡΑΚΗ), E. S., G. M. KAZAKOS (Γ.Μ. ΚΑΖΑΚΟΣ), and L. G. PAPAZOGLOU (Λ.Γ. ΠΑΠΑΖΟΓΛΟΥ). "Stress response to trauma." Journal of the Hellenic Veterinary Medical Society 64, no. 3 (2017): 213. http://dx.doi.org/10.12681/jhvms.15501.

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Trauma generates a series of alterations in the body, which are termed ‘stress response’. Injury triggers a reaction proportional to the intensity and duration of the stimuli imposed. Stress response reaction is mainly attributed to the sympathoadrenal axis and the hypothalamic-pituitary-adrenal axis. Activation of these two axes elicits secretion of several hormones, such catecholamines and cortisol from the adrenal glands or various other hormones from the hypothalamus and the pituitary gland. That affects body metabolism and the cardiovascular system, in order to ensure adequate energy rese

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38

Plunkett, J. J., J. D. Reeves, and J. G. Ramsay. "POSTOPERATIVE RESPONSE TO STRESS." Anesthesiology 81, SUPPLEMENT (1994): A144. http://dx.doi.org/10.1097/00000542-199409001-00143.

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39

Mavracordatos, P., J. P. Guinard, and R. Chiolero. "STRESS RESPONSE AFTER THORACOTOMY." Anesthesiology 75, no. 3 (1991): A697. http://dx.doi.org/10.1097/00000542-199109001-00696.

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40

Ljungman, Mats. "The Transcription Stress Response." Cell Cycle 6, no. 18 (2007): 2252–57. http://dx.doi.org/10.4161/cc.6.18.4751.

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41

Rodrigues-Pousada, Claudina, Tracy Nevitt, and Regina Menezes. "The yeast stress response." FEBS Journal 272, no. 11 (2005): 2639–47. http://dx.doi.org/10.1111/j.1742-4658.2005.04695.x.

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42

Ray, L. B. "Coordinating Response to Stress." Science Signaling 2, no. 74 (2009): ec191-ec191. http://dx.doi.org/10.1126/scisignal.274ec191.

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43

Kanba, S., F. Shintani, E. Suzuki, H. Manki, M. Asai, and T. Nakaki. "Cytokines in Stress Response." Japanese Journal of Pharmacology 71 (1996): 39. http://dx.doi.org/10.1016/s0021-5198(19)36410-8.

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44

Leiser, Scott, Christopher Choi, Ajay Bhat, and Charles Evans. "A Metabolic Stress Response." Innovation in Aging 4, Supplement_1 (2020): 123. http://dx.doi.org/10.1093/geroni/igaa057.404.

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Abstract An organism’s ability to respond to stress is crucial for long-term survival. These stress responses are coordinated by distinct but overlapping pathways, many of which have been found to also regulate longevity in multiple organisms across species. Despite extensive effort, our understanding of these pathways and how they affect aging remains incomplete and thus is a key area of study in Geroscience. Our previous work identified flavin-containing monooxygenase-2 (fmo-2) as a key longevity-promoting gene downstream of at least three longevity promoting pathways, including the hypoxic

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45

Hermesz, E., J. Nemcsók, and M. Ábrahám. "Stress response in fish." Pathophysiology 5 (June 1998): 96. http://dx.doi.org/10.1016/s0928-4680(98)80657-3.

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46

Haigis, Marcia C., and Bruce A. Yankner. "The Aging Stress Response." Molecular Cell 40, no. 2 (2010): 333–44. http://dx.doi.org/10.1016/j.molcel.2010.10.002.

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47

Ciavarra, Richard P., and Alan Simeone. "T lymphocyte stress response." Cellular Immunology 131, no. 1 (1990): 11–26. http://dx.doi.org/10.1016/0008-8749(90)90231-f.

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48

Ciavarra, Richard P., and Alan Simeone. "T lymphocyte stress response." Cellular Immunology 129, no. 2 (1990): 363–76. http://dx.doi.org/10.1016/0008-8749(90)90212-a.

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49

Freeman, M. L., E. L. Saunders, and M. J. Meredith. "Stress response and glutathione." Free Radical Biology and Medicine 9 (January 1990): 3. http://dx.doi.org/10.1016/0891-5849(90)90179-m.

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50

Cotgreave, I. A. "Session 3: Stress Response." Toxicology in Vitro 12, no. 5 (1998): 569–73. http://dx.doi.org/10.1016/s0887-2333(98)00038-1.

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