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Journal articles on the topic 'Stress response'

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Published: 4 June 2021
Last updated: 4 May 2024

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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

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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3

Jawwad, Ghazala, Humaira Fayyaz Khan, and Amanat Ali. "STRESS RESPONSE;." Professional Medical Journal 24, no. 09 (September 8, 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 recording of all the subjectswas done. Results: Low frequency in absolute and normalized unit and low to high frequencyratio was significantly higher in stressed group, compared to control (p≤ .05, p ≤ .001, pp ≤.001 respectively). High frequency in normalized was significantly lower in stressed subjects,compared to control (p ≤ .001). Cortisol level was significantly higher in the stressed group incomparison with control (p ≤ .05). Conclusion: Stress can lead to increase morning cortisollevel and can cause autonomic disturbances which can be evaluated by measuring heart ratevariability.
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4

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

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5

Cummins, Nadia, and Rebecca C. Taylor. "A stress-free stress response." Nature Chemical Biology 16, no. 10 (July 23, 2020): 1038–39. http://dx.doi.org/10.1038/s41589-020-0616-8.

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6

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

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7

Milutinovic, Snezana, Qianli Zhuang, Alain Niveleau, and Moshe Szyf. "Epigenomic Stress Response." Journal of Biological Chemistry 278, no. 17 (February 7, 2003): 14985–95. http://dx.doi.org/10.1074/jbc.m213219200.

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8

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

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9

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

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10

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

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11

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

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12

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

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13

Schroda, Michael, Dorothea Hemme, and Timo Mühlhaus. "TheChlamydomonasheat stress response." Plant Journal 82, no. 3 (March 27, 2015): 466–80. http://dx.doi.org/10.1111/tpj.12816.

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14

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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15

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

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16

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

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17

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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18

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

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19

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 (July 1, 2007): 497–503. http://dx.doi.org/10.15258/sst.2007.35.2.24.

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20

Mammen, Mary, and Sreekumar MR. "Nalbuphine versus Dexmeditomedine Effect on Hemodynamic Stress Response During Intubation." Indian Journal of Anesthesia and Analgesia 8, no. 6 (December 15, 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 population. Methodology: We selected 100 subjects, ASA1 and 2, were randomly grouped into 2 groups of 50 each. All our subjects received 500ml crystalloid solution. Allsubjects were induced on Propofol and intubated on succinylcholine. The stress response was assessed by observing hemodynamic variables SBP, DBP, MAP and HR. Statistical Analysis: Data was digitized and analyzed using SPSS22.0. Independent sample test was used to assess the difference in parameters. Data was stratified on the basis of age and weight of 2 groups. P-value of less than 0.05 was considered statistically significant. Conclusions: Dexmedetomidine influences HR and the effect is more as age advances. In subjects heavier than 80kg, mean HR was higher. The effect of Dexmedetomidine on heart rate was statistically significant at a P value less than 0.05. Nalbuphine, according to studies, increases BP and HR. In our study, this rise in MAP was observed in subjects heavier than 70kg. But this finding was not statistically significant.
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21

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 increase in systolic blood pressure during exercise. This is because different authors have used different criteria for defining abnormal response. An increase in diastolic blood pressure by 10 mm Hg over resting diastolic blood pressure or peak diastolic blood pressure of 110 mm Hg is significant and may be associated with a future risk of hypertension at rest. There is no consensus about the magnitude of the fall in systolic blood pressure during the initial few minutes of recovery. A paradoxical increase rather than a decrease in systolic blood pressure during recovery may be associated with coronary artery disease. Correct auscultatory measurement of blood pressure at peak exercise is difficult. Therefore, some authorities recommend the evaluation of blood pressure at a submaximal workload. This area needs further evaluation.
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22

STERNBERG, ESTHER M. "NEUROENDOCRINE STRESS RESPONSE IN REGULATION OF INFLAMMATORY RESPONSES." Shock 21, Supplement (March 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 (May 18, 2017): 786–87. http://dx.doi.org/10.1080/0142159x.2017.1318586.

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24

Pakos‐Zebrucka, Karolina, Izabela Koryga, Katarzyna Mnich, Mila Ljujic, Afshin Samali, and Adrienne M. Gorman. "The integrated stress response." EMBO reports 17, no. 10 (September 14, 2016): 1374–95. http://dx.doi.org/10.15252/embr.201642195.

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25

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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26

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

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27

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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28

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

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29

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 (December 19, 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 reserves, to retain water and to maintain cardiac output and vascular fluid volume. Objective of the activation observed after trauma is to eventually restore body homeostasis. A primary injury is accompanied by several reactions that may activate stress response.Blood loss, hypotension, acid-base balance disorders, quality of anaesthesia and pain generate impulses that activate the neuro endocrine response. Increased secretion of stress hormones enhances heart rate, heart contractility, blood pressure, oxygen consumption and respiratory rate. Moreover, stress hormones enhance glyconeogenesis, glycogonolysis and lypolysis, whilst they increase insulin resistance and inhibit glucose cell intake, thus leading to hyperglycaemia. Tissue injury is also associated with the release of proinflammatory mediators, such as cytokines. The pro-inflammatory cytokines, released from damaged cells, result in alterations of cell immunity, local and systemic inflammation and pain. The effects of stress response can vary upon the general condition of the animals. Animals in good condition can tolerate it well, although animals in poor condition can show deficiency of energy substrate, cardiovascular collapse, multi-organ failure and, finally, death. Over the years, it has been shown that anaesthesia can modify or limit the stress response. Although anaesthesia cannot eliminate the stress response, it can contribute in decreasing its peri-anaesthetic effects.
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30

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

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31

Mavracordatos, P., J. P. Guinard, and R. Chiolero. "STRESS RESPONSE AFTER THORACOTOMY." Anesthesiology 75, no. 3 (September 1, 1991): A697. http://dx.doi.org/10.1097/00000542-199109001-00696.

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32

Ljungman, Mats. "The Transcription Stress Response." Cell Cycle 6, no. 18 (September 15, 2007): 2252–57. http://dx.doi.org/10.4161/cc.6.18.4751.

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33

Rodrigues-Pousada, Claudina, Tracy Nevitt, and Regina Menezes. "The yeast stress response." FEBS Journal 272, no. 11 (May 13, 2005): 2639–47. http://dx.doi.org/10.1111/j.1742-4658.2005.04695.x.

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34

Ray, L. B. "Coordinating Response to Stress." Science Signaling 2, no. 74 (June 9, 2009): ec191-ec191. http://dx.doi.org/10.1126/scisignal.274ec191.

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35

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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36

Leiser, Scott, Christopher Choi, Ajay Bhat, and Charles Evans. "A Metabolic Stress Response." Innovation in Aging 4, Supplement_1 (December 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 response, the pentose phosphate pathway, and the dietary restriction pathway. Based on the commonalities of these pathways, we hypothesized that fmo-2, a classically annotated xenobiotic enzyme, might play a key endogenous role in responding to metabolic stress. Our resulting data, using metabolic profiling and further epistatic analysis, both support this hypothesis and link fmo-2’s mechanism to modifications to one-carbon metabolism (OCM), a key intermediate pathway between the nucleotide metabolism, methylation, and transsulfuration pathways. Using mathematical modeling and a novel metabolomics approach, we were able to further identify the likely mechanism of fmo-2-mediated metabolic effects, and connect them to both OCM and downstream components. We propose a model whereby nematode fmo-2 represents a class of enzymes that are able to modify large aspects of metabolism, similar to how transcription factors modify gene expression, and that fmo-2 is a key member of a conserved metabolic stress response.
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37

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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38

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

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39

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

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40

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

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41

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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42

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

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43

Russell, Georgina, and Stafford Lightman. "The human stress response." Nature Reviews Endocrinology 15, no. 9 (June 27, 2019): 525–34. http://dx.doi.org/10.1038/s41574-019-0228-0.

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44

Mager, W. H., and P. M. Ferreira. "Stress response of yeast." Biochemical Journal 290, no. 1 (February 15, 1993): 1–13. http://dx.doi.org/10.1042/bj2900001.

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45

Segawa, Hajime, and Kenjiro Mori. "Anesthesia and Stress Response." PAIN RESEARCH 8, no. 1 (1993): 1–8. http://dx.doi.org/10.11154/pain.8.1.

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46

Herd, J. A. "Cardiovascular response to stress." Physiological Reviews 71, no. 1 (January 1, 1991): 305–30. http://dx.doi.org/10.1152/physrev.1991.71.1.305.

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The behavioral characteristics of psychological stressors have been operationally defined. A psychological stressor is one that causes a stress response in a predictable percentage of index subjects. However, it may not always produce a stress response, and the probability of producing such a response depends on interactions between the behavioral situation and the individual involved. Thus there is a danger that a psychological stressor will be defined according to the stress response it causes rather than its structural characteristics. The characteristics that enhance the likelihood that a psychological stressor will cause a stress response are its novel, challenging, or threatening aspects that engage a subject in continuous active mental effort. The intensity of the stress response depends on the intensity of mental effort exerted to meet a challenging situation, whether or not that situation is perceived as threatening. The behavioral response to a psychological stressor also has been defined. It includes somatomotor, neuroendocrine, and cardiovascular components. The somatomotor response to stressful psychological events includes purposeful active coping to counter the challenge or threat posed by the stressor. The neuroendocrine response includes a combination of pituitary-adrenal cortical and hypothalamic-sympathetic-adrenal medullary secretions. The cardiovascular response includes a combination of increased rate and force of cardiac contraction, skeletal muscle vasodilation, venoconstriction, splanchnic vasoconstriction, renal vasoconstriction, and decreased renal excretion of sodium. Of all the modifiers that influence the stress response to a psychological stressor, family history is the one most likely to have an effect. A family history of essential hypertension increases the likelihood that a subject will respond to a psychological stressor with a cardiovascular stress response pattern. Other predisposing characteristics that increase the likelihood of a stress response include behavioral patterns of response to challenge or threat but may also include anatomic or biochemical characteristics that increase susceptibility to neurogenic activation of central aminergic mechanisms.
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47

Lithgow, Gordon J. "Stress response and aging." Drug Discovery Today: Disease Mechanisms 3, no. 1 (March 2006): 27–31. http://dx.doi.org/10.1016/j.ddmec.2006.03.008.

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48

Catalan, Jose. "Stress and sexual response." Stress Medicine 2, no. 1 (January 1986): 45–53. http://dx.doi.org/10.1002/smi.2460020109.

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49

Haigis, Marcia. "Sirtuins in Stress Response." Free Radical Biology and Medicine 87 (October 2015): S7. http://dx.doi.org/10.1016/j.freeradbiomed.2015.10.012.

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50

Rattan, Suresh I. S. "Hormetic Modulation of Aging and Longevity by Mild Heat Stress." Dose-Response 3, no. 4 (October 1, 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 maintenance of stress protein profiles, reduction in the accumulation of oxidatively and glycoxidatively damaged proteins, stimulation of the proteasomal activities for the degradation of abnormal proteins, improved cellular resistance to ethanol, hydrogenperoxide and ultraviolet-B rays, and enhanced levels of various antioxidant enzymes. Anti-aging hormetic effects of mild heat shock appear to be facilitated by reducing protein damage and protein aggregation by activating internal antioxidant, repair and degradation processes.
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