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Journal articles on the topic 'Stress triggering'

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Author: Grafiati

Published: 10 March 2023

Last updated: 11 March 2023

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1

Gronert, Gerald A., Joseph R. Tobin, and Sheila Muldoon. "Malignant hyperthermia — Human stress triggering." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1813, no. 12 (December 2011): 2191–92. http://dx.doi.org/10.1016/j.bbamcr.2011.08.001.

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2

Wan, Yong-ge, Zhong-liang Wu, Gong-wei Zhou, Jing Huang, and Li-xin Qin. "Research on seismic stress triggering." Acta Seismologica Sinica 15, no. 5 (September 2002): 559–77. http://dx.doi.org/10.1007/s11589-002-0025-y.

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3

Dean, Erin. "Workplace stress triggering unhealthy coping responses." Nursing Standard 37, no. 2 (February 2, 2022): 8–10. http://dx.doi.org/10.7748/ns.37.2.8.s6.

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4

Finsterer, Josef, and Karim Wahbi. "CNS disease triggering Takotsubo stress cardiomyopathy." International Journal of Cardiology 177, no. 2 (December 2014): 322–29. http://dx.doi.org/10.1016/j.ijcard.2014.08.101.

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5

Hardebeck, Jeanne L., and Ruth A. Harris. "Earthquakes in the Shadows: Why Aftershocks Occur at Surprising Locations." Seismic Record 2, no. 3 (July 1, 2022): 207–16. http://dx.doi.org/10.1785/0320220023.

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Abstract For decades there has been a debate about the relative effects of dynamic versus static stress triggering of aftershocks. According to the static Coulomb stress change hypothesis, aftershocks should not occur in stress shadows—regions where static Coulomb stress has been reduced. We show that static stress shadows substantially influence aftershock occurrence following three M ≥ 7 California mainshocks. Within the modeled static Coulomb stress shadows, the aftershock rate is an order of magnitude lower than in the modeled increase regions. However, the earthquake rate in the stress shadows does not decrease below the background rate, as predicted by Coulomb stress change models. Aftershocks in the stress shadows exhibit different spatial–temporal characteristics from aftershocks in the stress increase regions. The aftershock rate in the stress shadows decays as a power law with distance from the mainshock, consistent with a simple model of dynamic stress triggering. These aftershocks begin with a burst of activity during the first few days after the mainshock, also consistent with dynamic stress triggering. Our interpretation is that aftershock sequences are the combined result of static and dynamic stress triggering, with an estimated ∼34% of aftershocks due to dynamic triggering and ∼66% due to static triggering.

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6

Steacy, Sandy, Abigail Jiménez, and Caroline Holden. "Stress triggering and the Canterbury earthquake sequence." Geophysical Journal International 196, no. 1 (October 11, 2013): 473–80. http://dx.doi.org/10.1093/gji/ggt380.

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7

Kilb, Debi, Joan Gomberg, and Paul Bodin. "Aftershock triggering by complete Coulomb stress changes." Journal of Geophysical Research: Solid Earth 107, B4 (April 2002): ESE 2–1—ESE 2–14. http://dx.doi.org/10.1029/2001jb000202.

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8

Strader, Anne, and David D. Jackson. "Near-prospective test of Coulomb stress triggering." Journal of Geophysical Research: Solid Earth 119, no. 4 (April 2014): 3064–75. http://dx.doi.org/10.1002/2013jb010780.

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9

Lei, Dong Ning, Jian Chao Wu, and Yong Jian Cai. "The Stress Triggering of Aftershocks by Badong M5.1 Mainshock from Coulomb Stress Changes." Advanced Materials Research 971-973 (June 2014): 2172–75. http://dx.doi.org/10.4028/www.scientific.net/amr.971-973.2172.

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TheCoulomb stress changes are usually adopted to make analysis on faultinteractions and stress triggering. This paper mainly deals with Coulomb stresschange of mainshock and affect on aftershocks. We preliminarily conclude thatthe mainshock produce Coulomb stress change on aftershocks most behavingpositive and triggered them. By calculating it is obvious that more aftershocksfell into stress increasing area and triggering percentage is up to ninety ofmaximum and seventy-one of minimum.

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10

Bucholc, Magda, and Sandy Steacy. "Tidal stress triggering of earthquakes in Southern California." Geophysical Journal International 205, no. 2 (February 8, 2016): 681–93. http://dx.doi.org/10.1093/gji/ggw045.

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11

Chandra, Joya, Afshin Samali, and Sten Orrenius. "Triggering and modulation of apoptosis by oxidative stress." Free Radical Biology and Medicine 29, no. 3-4 (August 2000): 323–33. http://dx.doi.org/10.1016/s0891-5849(00)00302-6.

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12

Wan, Yong-ge, Zhong-liang Wu, Gong-wei Zhou, Jing Huang, and Li-xin Qin. "Global test of seismic static stress triggering model." Acta Seismologica Sinica 15, no. 3 (May 2002): 318–32. http://dx.doi.org/10.1007/s11589-002-0065-3.

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13

Lei, Dong Ning, Yong Jian Cai, and Heng Li. "Static Stress Changes and Triggering Imposed by Wenchuan Earthquake on Lushan M7 Earthquake." Applied Mechanics and Materials 597 (July 2014): 324–27. http://dx.doi.org/10.4028/www.scientific.net/amm.597.324.

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Some faults rupture the surface followed by coseismic dislocation, which causes space stress changes and transmits or imposes static stress on or to neighboring faults.The static stress triggering leads to the adjacent fault ruptured in advance, which means a Coulomb stress increase and triggers a new earthquake event. In recent two decades, some studies on stress triggering became important field of seismotectonics. The occurrence of both Wenchuan M8.0 earthquake and Japan M9.0 eathquake have arisen interest of many researchers, and obtained much new result and understanding.

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14

Silacci, P., and D. Hayoz. "Oxidative stress as the triggering event for vascular remodelling." Nephrology Dialysis Transplantation 13, no. 6 (June 1, 1998): 1343–46. http://dx.doi.org/10.1093/oxfordjournals.ndt.a027888.

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15

Freed, Andrew M. "EARTHQUAKE TRIGGERING BY STATIC, DYNAMIC, AND POSTSEISMIC STRESS TRANSFER." Annual Review of Earth and Planetary Sciences 33, no. 1 (May 31, 2005): 335–67. http://dx.doi.org/10.1146/annurev.earth.33.092203.122505.

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16

Wan, Y. G., Z. L. Wu, and G. W. Zhou. "Focal mechanism dependence of static stress triggering of earthquakes." Tectonophysics 390, no. 1-4 (October 2004): 235–43. http://dx.doi.org/10.1016/j.tecto.2004.03.028.

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17

Lasley, Samuel J., Russell A. Green, and Adrian Rodriguez-Marek. "New Stress Reduction Coefficient Relationship for Liquefaction Triggering Analyses." Journal of Geotechnical and Geoenvironmental Engineering 142, no. 11 (November 2016): 06016013. http://dx.doi.org/10.1061/(asce)gt.1943-5606.0001530.

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18

Wan, Yong-ge, Zhong-liang Wu, Gong-wei Zhou, and Jing Huang. ""Stress triggering" between different rupture events in several earthquakes." Acta Seismologica Sinica 13, no. 6 (November 2000): 607–15. http://dx.doi.org/10.1007/s11589-000-0062-3.

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19

Wan, Yong-ge, Zheng-kang Shen, Yue-hua Zeng, Shu-zhong Sheng, and Xiao-feng Xu. "Visco-elastic stress triggering model of Tangshan earthquake sequence." Acta Seismologica Sinica 21, no. 6 (November 2008): 585–97. http://dx.doi.org/10.1007/s11589-008-0585-6.

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20

Hainzl, Sebastian, Javad Moradpour, and Jörn Davidsen. "Static stress triggering explains the empirical aftershock distance decay." Geophysical Research Letters 41, no. 24 (December 23, 2014): 8818–24. http://dx.doi.org/10.1002/2014gl061975.

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21

Prasath, R. Arun, Mithila Verma, and Brijesh K. Bansal. "Stress shadow, stress triggering, and recent earthquake activity in the Kashmir Himalaya, India." Journal of Seismology 26, no. 1 (January 31, 2022): 167–79. http://dx.doi.org/10.1007/s10950-021-10067-4.

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22

WU, Xiao-Ping, Hong FU, Bouchon MICHAEL, Jia-Fu HU, Yi-Li HU, Yong HUANG, Xiong-Lin HU, and Chao-Di XIE. "Complete Coulomb Failure Stress Changes and Stress Triggering of Yunnan Longling Earthquake Sequence." Chinese Journal of Geophysics 50, no. 4 (July 2007): 963–74. http://dx.doi.org/10.1002/cjg2.1113.

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23

Angus, D. A., and J. P. Verdon. "Using Microseismicity to Estimate Formation Permeability for Geological Storage of CO2." ISRN Geophysics 2013 (February 26, 2013): 1–7. http://dx.doi.org/10.1155/2013/160758.

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We investigate two approaches for estimating formation permeability based on microseismic data. The two approaches differ in terms of the mechanism that triggers the seismicity: pore-pressure triggering mechanism and the so-called seepage-force (or effective stress) triggering mechanism. Based on microseismic data from a hydraulic fracture experiment using water and supercritical CO2 injection, we estimate permeability using the two different approaches. The microseismic data comes from two hydraulic stimulation treatments that were performed on two formation intervals having similar geological, geomechanical, and in situ stress conditions, yet different injection fluid was used. Both approaches (pore-pressure triggering, and the seepage-force triggering) provide estimates of permeability within the same order of magnitude. However, the seepage-force mechanism (i.e., effective stress perturbation) provides more consistent estimates of permeability between the two different injection fluids. The results show that permeability estimates using microseismic monitoring have strong potential to constrain formation permeability limitations for large-scale CO2 injection.

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24

Signoretto, Elena, Jens Zierle, Rosi Bissinger, Michela Castagna, Elena Bossi, and Florian Lang. "Triggering of Suicidal Erythrocyte Death by Pazopanib." Cellular Physiology and Biochemistry 38, no. 3 (2016): 926–38. http://dx.doi.org/10.1159/000443045.

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Background/Aims: The multi-targeted kinase inhibitor pazopanib, a drug employed for the treatment of a wide variety of malignancies, has previously been shown to trigger apoptosis. Similar to apoptosis of nucleated cells, erythrocytes may enter suicidal death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Mechanisms involved in the triggering of eryptosis include Ca2+ entry, oxidative stress and ceramide. The present study explored, whether pazopanib induces eryptosis and, if so, whether it is effective by Ca2+ entry, oxidative stress and/or ceramide. Methods: Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, reactive oxygen species (ROS) formation from DCF dependent fluorescence, and ceramide abundance utilizing specific antibodies. Results: A 48 hours exposure of human erythrocytes to pazopanib significantly increased the percentage of annexin-V-binding (≥ 25 µg/ml) and of shrunken erythrocytes (≥ 50 µg/ml). Pazopanib treatment further resulted in significant hemolysis (≥ 25 µg/ml). The effect of pazopanib on annexin-V-binding was significantly blunted but not abolished by removal of extracellular Ca2+. Pazopanib significantly increased DCF fluorescence (50 µg/ml) and ceramide abundance (50 µg/ml). Conclusions: Pazopanib triggers eryptosis, an effect involving Ca2+ entry, oxidative stress and ceramide.

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25

Kachakhidze, M. K., R. Kiladze, N. Kachakhidze, V. Kukhianidze, and G. Ramishvili. "Connection of large earthquakes occurring moment with the movement of the Sun and the Moon and with the Earth crust tectonic stress character." Natural Hazards and Earth System Sciences 10, no. 7 (July 29, 2010): 1629–33. http://dx.doi.org/10.5194/nhess-10-1629-2010.

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Abstract. It is acceptable that earthquakes certain exogenous (cosmic) triggering factors may exist in every seismoactive (s/a) region and in Caucasus among them. They have to correct earthquake occurring moment or play the triggering role in case when the region is at the limit of the critical value of the geological medium of course. Our aim is to reveal some exogenous factors possible to initiate earthquakes, on example of Caucasus s/a region, taking into account that the region is very complex by the point of view of the tectonic stress distribution. The compression stress directed from North to South (and vice versa) and the spread stress directed from East to West (and vice versa) are the main stresses acted in Caucasus region. No doubt that action of the smallest external stress may "work" as earthquakes triggering factor. In the presented work the Moon and the Sun perturbations are revealed as initiative agents of earthquakes when the directions of corresponding exogenous forces coincide with the directions of the compression stress or the spreading tectonic stress in the region.

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26

Al Mamun Bhuyan, Abdulla, Teresa Wagner, Hang Cao, and Florian Lang. "Triggering of Suicidal Erythrocyte Death by Gefitinib." Cellular Physiology and Biochemistry 41, no. 4 (2017): 1697–708. http://dx.doi.org/10.1159/000471823.

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Background/Aims: The epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib is effective against several malignancies and is mainly utilized in the treatment of epidermal growth factor receptor mutation positive non-small cell lung cancer. The anti-cancer effect of the drug involves stimulation of apoptosis. Side effects of gefitinib include anemia. At least in theory, the development of anemia during gefitinib treatment could result from triggering of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i) and generation of oxidative stress. The present study explored, whether gefitinib stimulates eryptosis and, if so, whether its effect involves Ca2+ entry and/or oxidative stress. Methods: Flow cytometry was employed to quantify cell volume from forward scatter, phosphatidylserine exposure at the cell surface from annexin-V-binding, [Ca2+]i from Fluo3-fluorescence, and reactive oxygen species (ROS) abundance from 2’,7’-dichlorodihydrofluorescein diacetate (DCFDA) dependent fluorescence. Results: A 48 hours exposure of human erythrocytes to gefitinib (≥ 2 µg/ml) significantly decreased forward scatter and significantly increased the percentage of annexin-V-binding cells. Gefitinib did not significantly increase Fluo3-fluorescence but the effect of gefitinib on annexin-V-binding was significantly blunted by removal of extracellular Ca2+. Gefitinib further significantly increased DCFDA fluorescence. Conclusions: Gefitinib triggers erythrocyte shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part dependent on extracellular Ca2+ and paralleled by oxidative stress.

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27

Segou, Margarita, and Tom Parsons. "A New Technique to Calculate Earthquake Stress Transfer and to Probe the Physics of Aftershocks." Bulletin of the Seismological Society of America 110, no. 2 (February 11, 2020): 863–73. http://dx.doi.org/10.1785/0120190033.

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ABSTRACT Coseismic stress changes have been the primary physical principle used to explain aftershocks and triggered earthquakes. However, this method does not adequately forecast earthquake rates and diverse rupture populations when subjected to formal testing. We show that earthquake forecasts can be impaired by assumptions made in physics-based models such as the existence of hypothetical optimal faults and regional scale invariability of the stress field. We compare calculations made under these assumptions along with different realizations of a new conceptual triggering model that features a complete assay of all possible ruptures. In this concept, there always exists a set of theoretical planes that has positive failure stress conditions under a combination of background and coseismic static stress change. In the Earth, all of these theoretical planes may not exist, and if they do, they may not be ready to fail. Thus, the actual aftershock plane may not correspond to the plane with the maximum stress change value. This is consistent with observations that mainshocks commonly activate faults with exotic orientations and rakes. Our testing ground is the M 7.2, 2010 El Mayor–Cucapah earthquake sequence that activated multiple diverse fault populations across the United States–Mexico border in California and Baja California. We carry out a retrospective test involving 748 M≥3.0 triggered earthquakes that occurred during a 3 yr period after the mainshock. We find that a probabilistic expression of possible aftershock planes constrained by premainshock rupture patterns is strongly favored (89% of aftershocks consistent with static stress triggering) versus an optimal fault implementation (35% consistent). Results show that coseismic stress change magnitudes do not necessarily control earthquake triggering, instead we find that the summed background stress and coseismic stress change promotes diverse ruptures. Our model can thus explain earthquake triggering in regions where optimal plane mapping shows coseismic stress reduction.

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28

Al Mamun Bhuyan, Abdulla, Rosi Bissinger, Hang Cao, and Florian Lang. "Triggering of Suicidal Erythrocyte Death by Bexarotene." Cellular Physiology and Biochemistry 40, no. 5 (2016): 1239–51. http://dx.doi.org/10.1159/000453178.

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Background/Aims: The retinoid X receptor agonist bexarotene is utilized for the treatment of cutaneous T-cell lymphoma and is effective in several further malignancies. The substance counteracts tumor growth in part by triggering suicidal death or apoptosis of tumor cells. Side effects of bexarotene treatment include anemia. Theoretically, bexarotene induced anemia could be secondary to stimulation of suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i), induction of oxidative stress, increase of ceramide abundance, as well as activation of staurosporine sensitive protein kinase C, SB203580 sensitive p38 kinase, D4476 sensitive casein kinase 1, and zVAD sensitive caspases. The present study explored, whether bexarotene induces eryptosis and, if so, whether its effect involves Ca2+ entry, oxidative stress, ceramide, kinases and/or caspases. Methods: Flow cytometry was employed to quantify phosphatidylserine exposure at the cell surface from annexin-V-binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, reactive oxygen species (ROS) abundance from DCFDA dependent fluorescence, and ceramide abundance utilizing specific antibodies. Hemolysis was estimated from hemoglobin concentration in the supernatant. Results: A 48 hours exposure of human erythrocytes to bexarotene (≥ 0.4 µg/ml) significantly increased the percentage of annexin-V-binding cells without significantly modifying forward scatter. Bexarotene significantly increased Fluo3-fluorescence and DCFDA fluorescence. Bexarotene tended to increase ceramide abundance, an effect, however, not reaching statistical significance. The effect of bexarotene on annexin-V-binding was significantly blunted by removal of extracellular Ca2+ and by addition of D4476 (10 µM), but not by addition of staurosporine (1 µM), SB203580 (2 µM), or zVAD (10 µM). Conclusions: Bexarotene triggers phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca2+ entry, oxidative stress, and activation of D4476 sensitive casein kinase.

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29

Wu, Jianchao, Qing Hu, Weijie Li, and Dongning Lei. "Study on Coulomb Stress Triggering of the April 2015 M7.8 Nepal Earthquake Sequence." International Journal of Geophysics 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7378920.

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In April 2015, a M7.8 earthquake occurred less than one month before a M7.3 earthquake near Kodari, Nepal. The Nepal earthquake sequences also include four larger (M > 6) aftershocks. To reveal the interrelation between the main shock and the aftershocks, we check the role of coseismic coulomb stress triggering on aftershocks that follow the M7.8 main shock. Based on the focal mechanisms of the aftershocks and source models of the main shock, the coulomb failure stress changes on both of the focal mechanism nodal planes are calculated. In addition, the coulomb stress changes on the focal sources of each aftershock are also calculated. A large proportion of the M > 6 aftershocks occurred in positive coulomb stress areas triggered by the M7.8 main shock. The secondary triggering effect of the M7.3 aftershock is also found in this paper. More specifically, the M7.3 aftershock promoted failure on the rupture plane of the M6.3 aftershock. Therefore, we may conclude that the majority of larger aftershocks, which accumulated positive coulomb stress changes during the sequence, were promoted or triggered by the main shock failure. It suggests that coulomb stress triggering contributed to the evolution of the Nepal M7.8 earthquake sequence.

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30

Becker, D., B. Cailleau, T. Dahm, S. Shapiro, and D. Kaiser. "Stress triggering and stress memory observed from acoustic emission records in a salt mine." Geophysical Journal International 182, no. 2 (June 7, 2010): 933–48. http://dx.doi.org/10.1111/j.1365-246x.2010.04642.x.

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31

Mynbaev, Ospan A., Sergei S. Simakov, Antonio Malvasi, and Andrea Tinelli. "Is CO2 Pneumoperitoneum Desufflation Triggering Factor of Postsurgical Oxidative Stress?" Journal of Minimally Invasive Gynecology 23, no. 6 (September 2016): 1013–15. http://dx.doi.org/10.1016/j.jmig.2016.02.023.

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32

Li, Cong, Wei Li, Jian Chen, Yan Jie Ren, Jian Jun He, and Cui Lan Wu. "Investigation of Triggering Stress for Martensitic Transformation in Titanium Alloy." Metal Science and Heat Treatment 59, no. 11-12 (March 2018): 715–20. http://dx.doi.org/10.1007/s11041-018-0216-3.

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33

Zhu, Hang, and Xueze Wen. "Static stress triggering effects related with M s8.0 Wenchuan earthquake." Journal of Earth Science 21, no. 1 (February 2010): 32–41. http://dx.doi.org/10.1007/s12583-010-0001-8.

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34

Ma, Lifeng, Nina Yari, and Marian Wiercigroch. "Shear stress triggering brittle shear fracturing of rock-like materials." International Journal of Mechanical Sciences 146-147 (October 2018): 295–302. http://dx.doi.org/10.1016/j.ijmecsci.2018.07.008.

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35

Mischitelli, Morena, Mohamed Jemaà, Mustafa Almasry, Caterina Faggio, and Florian Lang. "Triggering of Suicidal Erythrocyte Death by Fascaplysin." Cellular Physiology and Biochemistry 39, no. 4 (2016): 1638–47. http://dx.doi.org/10.1159/000447865.

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Background/Aims: The bis-indole alkaloid Fascaplysin is effective against malignancy, an effect at least partially due to stimulation of tumor cell apoptosis. Similar to apoptosis of nucleated cells, erythrocytes could enter suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i), oxidative stress and ceramide. The present study explored, whether Fascaplysin induces eryptosis and, if so, to shed light on the cellular mechanisms involved. Methods: Flow cytometry was employed to estimate phosphatidylserine exposure at the cell surface from annexin-V-binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, ROS formation from DCFDA dependent fluorescence, and ceramide abundance utilizing specific antibodies. Hemolysis was quantified from the hemoglobin concentration in the supernatant. Results: A 48 hours exposure of human erythrocytes to Fascaplysin (≥ 5 µM) significantly increased the percentage of annexin-V-binding cells, significantly decreased forward scatter, and significantly increased Fluo3-fluorescence, DCFDA fluorescence as well as ceramide abundance. The effect of Fascaplysin on annexin-V-binding and forward scatter was significantly blunted but not abolished by removal of extracellular Ca2+. Conclusions: Fascaplysin triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca2+ entry, oxidative stress and ceramide.

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36

Xie, Chaodi, Ye Zhu, Yingfeng Ji, Weiling Zhu, Rui Qu, Yan Xu, and Aitang Li. "Coseismic Stress Change and Viscoelastic Relaxation after the 2008 Great Sichuan Earthquake." Applied Sciences 12, no. 19 (September 24, 2022): 9585. http://dx.doi.org/10.3390/app12199585.

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Long-term stress accumulation influenced by coseismic stress changes and postseismic viscoelastic relaxation is considered critical to triggering giant earthquakes. Nevertheless, how the stress increase is interrupted by aftershocks and how it influences the megaseismic cycle remain enigmatic. In this study, based on the Mohr–Coulomb failure criterion at the nucleated segments of the 2008 great Sichuan earthquake, the stress variation associated with four M > 6 aftershocks was calculated for the period from 2010 to 2017. The results show that (1) the spatial distribution of coseismic stress change is correlated with the rupture pattern of large events and has a fundamental impact on triggering subsequent earthquakes and (2) postseismic viscoelastic relaxation leads to increased Coulomb stress accumulation at the northern and southern edges of the seismogenic Longmenshan fault, which results in enhanced fault instability and the potential for future large events.

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37

Dutta, P. K., and O. P. Mishra. "Identification of Collision Mechanism at Seismogenic Fault Interface Using Finite Element Analysis Involving Plate Bending Applications Using Ant Colony Optimization." Journal of Applied Engineering Sciences 7, no. 1 (May 1, 2017): 15–22. http://dx.doi.org/10.1515/jaes-2017-0002.

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AbstractUnderstanding space-time correlation in equilibrium matrix when force of collision involving earthquake stress strain interaction. The proposed study shows that non-linear dynamics of earthquake behaviour simulated with ant colony optimization in short timescale deformation by analysis of the stiffness matrix and the stress strain interaction process of the rock pattern. An improved ant colony optimization combined with local search is proposed for solving this complex optimization problem of finding trigger zones for earthquake occurrences. The disturbances at trigger basins for any system cause the collapse of a subsystem leading to stress evolution and slip due to strain nucleation. The stress strain network based on redistribution of stress accumulation are discretized into four states of low stress and strain and a finite element model is established to identify vertices for the stress-strain component and edges for global coupling effects have been constructed for dynamic monitoring of stress and strain behaviour at triggering zones. In this paper, an efficient algorithm is developed for the formation of null basis of triangular and rectangular plate bending finite element models, corresponding to highly sparse flexibility matrices. Triggering basins serve as harbingers of large earthquake where stress-strain interactions have been analyzed by the quasi-static mechanics of seismic precursory stress-strain propagation in the crustal lithosphere. The simulation framework shows that with time, spatial triggering points as stress varies from one point to another to identify the external influences for the body forces and the surface forces for geodynamic frameworks.

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38

Bellet, Benjamin W., Payton J. Jones, and Richard J. McNally. "Self-Triggering? An Exploration of Individuals Who Seek Reminders of Trauma." Clinical Psychological Science 8, no. 4 (June 1, 2020): 739–55. http://dx.doi.org/10.1177/2167702620917459.

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Trauma survivors who self-trigger, or seek reminders of their traumatic events, have been noted in the clinical literature but have not yet been the subject of a systematic empirical inquiry. This article presents the results of two exploratory studies of self-triggering. In Study 1 ( N = 545), we estimated the behavior’s clinical relevance among trauma survivors. In Study 2 ( N = 360), we examined descriptive characteristics of self-triggering as well as potential motivations for the behavior. We found that self-triggering is uniquely associated with more severe symptoms of posttraumatic stress disorder. Self-triggering takes place via a wide variety of methods and can become compulsive for many individuals. Reasons endorsed for self-triggering comprised several broad motives, but the desire to make meaning of one’s trauma was most predictive of self-triggering frequency. Limitations, clinical implications, and directions for further research are discussed.

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39

Prasath, R. Arun, Mithila Verma, and Brijesh K. Bansal. "Correction to: Stress shadow, stress triggering, and recent earthquake activity in the Kashmir Himalaya, India." Journal of Seismology 26, no. 2 (March 2, 2022): 415. http://dx.doi.org/10.1007/s10950-022-10081-0.

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40

Maleki Asayesh, Behnam, Hamid Zafarani, and Mohammad Tatar. "Coulomb stress changes and secondary stress triggering during the 2003 (Mw 6.6) Bam (Iran) earthquake." Tectonophysics 775 (January 2020): 228304. http://dx.doi.org/10.1016/j.tecto.2019.228304.

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Huang, Chi-Wei, Shang-Wei Li, and Vivian Hsiu-Chuan Liao. "Long-term sediment exposure to ZnO nanoparticles induces oxidative stress in Caenorhabditis elegans." Environmental Science: Nano 6, no. 8 (2019): 2602–14. http://dx.doi.org/10.1039/c9en00039a.

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Barthwal, Himanshu, and Mirko van der Baan. "Role of fracture opening in triggering microseismicity observed during hydraulic fracturing." GEOPHYSICS 84, no. 3 (May 1, 2019): KS105—KS118. http://dx.doi.org/10.1190/geo2018-0425.1.

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Hydraulic fracturing in low-permeability hydrocarbon reservoirs creates/reactivates a fracture network leading to microseismic events. We have developed a simplified model of the evolution of the microseismic cloud based on the opening of a planar fracture cavity and its effect on elastic stresses and pore pressure diffusion during fluid injection in hydraulic fracturing treatments. Using a material balance equation, we compute the crack tip propagation over time assuming that the hydraulic fracture is shaped as a single penny-shaped cavity. Results indicate that in low-permeability formations, the crack tip propagates much faster than the pore pressure diffusion front thereby triggering the microseismic events farthest from the injection domain at any given time during fluid injection. We use the crack tip propagation to explain the triggering front observed in distance versus time plots of published microseismic data examples from hydraulic fracturing treatments of low-permeability hydrocarbon reservoirs. We conclude that attributing the location of the microseismic triggering front purely to pore pressure diffusion from the injection point may lead to incorrect estimates of the hydraulic diffusivity by multiple orders of magnitude for low-permeability formations. Moreover, the opening of the fracture cavity creates stress shadow zones perpendicular to the principal fracture walls in which microseismic triggering due to the elastic stress perturbations is suppressed. Microseismic triggering in this stress shadow region may be attributed mainly to pore pressure diffusion. We use the width, instead of the longest size, of the microseismic cloud to obtain an enhanced diffusivity measure, which may be useful for subsequent production simulations.

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Williams, Scott, and Jonathan Williams. "Traumatic stress sufferers: work as therapy or trigger?" Management Research Review 44, no. 7 (January 18, 2021): 991–1011. http://dx.doi.org/10.1108/mrr-01-2020-0050.

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Purpose While a return to work following trauma exposure can be therapeutic, this is not always so. As with many topics related to traumatic stress in organizations, several contingency factors complicate the effort to draw an overarching conclusion about whether returning to work is therapeutic. The purpose of this paper is to present important determinants of whether work is therapeutic or triggering for those with traumatic stress conditions. The need for contingency approaches in the study of traumatic stress in organizations is illustrated. Design/methodology/approach Literature on traumatic stress in organizations is reviewed. Findings Three of the key determinants of whether a return to work is therapeutic or triggering for traumatic stress sufferers are trauma-type contingencies, condition-type contingencies and work-setting contingencies. For instance, human-caused and task-related traumas are more likely than natural disasters to make a return-to-work triggering. Additionally, the time since developing a traumatic stress condition is inversely related to the degree of improvement in that condition through the experience of working. Moreover, managerial actions can affect how therapeutic an employee’s return to work is. Practical implications These findings suggest the challenges of reintegrating a traumatized employee to the workplace can be highly situation-specific. Careful consideration of the traumatic event suffered by each traumatic stress victim, their traumatic stress condition, and the work setting to which they would return are recommended. Social implications Promoting mental health in organizations can contribute to employers’ social performance. Originality/value Examination of the factors that complicate predicting whether work is therapeutic posttrauma demonstrates how contingency approaches can advance research on trauma in organizations.

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Peng, Wei, and Shinji Toda. "Tests of Remote Dynamic Aftershock Triggering by Small Mainshocks Using Taiwan’s Earthquake Catalog." Seismological Research Letters 92, no. 4 (February 24, 2021): 2464–76. http://dx.doi.org/10.1785/0220200384.

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Abstract To understand earthquake interaction and forecast time-dependent seismic hazard, it is essential to determine which static or dynamic stress change due to a mainshock plays a major role in triggering its aftershocks and subsequent mainshocks. Using small mainshocks (2≤M<3) and their aftershocks, Felzer and Brodsky (2006) argued that mainshock induced dynamic stress change is responsible for earthquake triggering in a form of power-law decay within 50 km. Richards-Dinger et al. (2010), however, studied the foreshock decay and claimed that mainshock had no effect at distances outside its static stress triggering range, which required an alternative explanation. We tested these hypotheses using Taiwan’s earthquake catalog by taking advantage of its lack of large events and the absence of active volcano and associated significant seismic swarm. In examining earthquakes occurring in 1994–2010, following Felzer and Brodsky’s method, we found a linear aftershock density with a power-law decay of −1.12±0.38 that is very similar to the one seen in Felzer and Brodsky (2006). None of the mainshock–aftershock pairs were associated with an M 7 rupture event or M 6 event. We further demonstrated that the density decay in a short time period is more likely a randomized behavior than mainshock–aftershock triggering. These pairs were located mostly in high geothermal gradient areas, which are probably triggered by a small-scale aseismic process.

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Sousa, Kayo Henrique Jardel Feitosa, Jaqueline Carvalho e. Silva Sales, Samantha Alves Fernandes, Maryane Francisca de Araujo Freitas, Patrícia Maria Gomes de Carvalho, and Dennise Alves Costa. "Triggering factors of work-related stress in nursing: evidenced in literature." Revista de Pesquisa Cuidado é Fundamental Online 5, no. 6 (February 20, 2014): 372–81. http://dx.doi.org/10.9789/2175-5361.2013.v5i6.372-381.

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Objetivo: Analisar a produção científica quanto aos fatores desencadeadores de estresse em profissionais de enfermagem no ambiente hospitalar. Metodologia: Trata-se de estudo de cunho qualitativo, do tipo revisão da literatura, nas bases de dados BVS, em suas sub-bases LILACS e BDENF, e na base de dados SCOPUS. Foram investigados artigos na íntegra, em português, publicados entre os anos de 2009 e 2013. Resultados: Revelou-se que os estressores mais prevalentes no ambiente hospitalar para os profissionais da enfermagem são a falta de profissionalismo, descontentamento com a profissão, falta de condições de trabalho, falta de materiais, recursos humanos escassos e pessoais não treinados, a divisão do trabalho, o conteúdo da tarefa, as relações de poder, a hierarquia, e as questões de responsabilidade. Conclusão: Conhecer e analisar os fatores desencadeadores de estresse é de grande valia para os profissionais e para as instituições sendo essenciais para a promoção da saúde dos trabalhadores e para a melhoria da assistência prestada por estes.

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Hou, Shaozhi, Yang Song, Di Sun, Shujun Zhu, and Zhenhua Wang. "Xanthohumol-Induced Rat Glioma C6 Cells Death by Triggering Mitochondrial Stress." International Journal of Molecular Sciences 22, no. 9 (April 26, 2021): 4506. http://dx.doi.org/10.3390/ijms22094506.

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AIM: To investigate the underlying mechanisms of xanthohumol (XN) on the proliferation inhibition and death of C6 glioma cells. METHODS: To determine the effects of XN on C6 cells, cell proliferation and mortality after XN treatment were assessed by SRB assay and trypan blue assay respectively. Apoptotic rates were evaluated by flowcytometry after Annexin V-FITC/PI double staining. The influence of XN on the activity of caspase-3 was determined by Western blot (WB); and nuclear transposition of apoptosis-inducing factor (AIF) was tested by immunocytochemistry and WB. By MitoSOXTM staining, the mitochondrial ROS were detected. Mitochondrial function was also tested by MTT assay (content of succinic dehydrogenase), flow cytometry (mitochondrial membrane potential (MMP)—JC-1 staining; mitochondrial abundance—mito-Tracker green), immunofluorescence (MMP—JC-1 staining; mitochondrial morphology—mito-Tracker green), WB (mitochondrial fusion-fission protein—OPA1, mfn2, and DRP1; mitophagy-related proteins—Pink1, Parkin, LC3B, and P62), and high-performance liquid chromatography (HPLC) (energy charge). Finally, mitochondrial protein homeostasis of C6 cells after XN treatment with and without LONP1 inhibitor bortezomib was investigated by trypan blue assay (proliferative activity and mortality) and WB (mitochondrial protease LONP1). All cell morphology images were taken by a Leica Microsystems microscope. RESULTS: XN could lead to proliferation inhibition and death of C6 cells in a time- and dose-dependent manner and induce apoptosis of C6 cells through the AIF pathway. After long incubation of XN, mitochondria of C6 cells were seriously impaired, and mitochondria had a diffuse morphology and mitochondrial ROS were increased. The content of succinic dehydrogenase per cell was significantly decreased after XN insults of 24, 48, and 72 h. The energy charge was weakened after XN insult of 24 h. Furthermore, the MMP and mitochondrial abundance were significantly decreased; the protein expression levels of OPA1, mfn2, and DRP1 were down-regulated; and the protein expression levels of Pink1, Parkin, LC3B-II/LC3B-I, and p62 were up-regulated in long XN incubation times (24, 48, and 72 h). XN incubation with bortezomib for 48 h resulted in lower proliferative activity and higher mortality of C6 cells and caused the cell to have visible vacuoles. Moreover, the protein expression levels of LONP1 was up-regulated gradually as XN treatment time increased. CONCLUSION: These data supported that XN could induce AIF pathway apoptosis of the rat glioma C6 cells by affecting the mitochondria.

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Cabaniss, Haley E., Patricia M. Gregg, and Eric B. Grosfils. "The Role of Tectonic Stress in Triggering Large Silicic Caldera Eruptions." Geophysical Research Letters 45, no. 9 (May 4, 2018): 3889–95. http://dx.doi.org/10.1029/2018gl077393.

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Yerasi, Charan, Edward Koifman, Gaby Weissman, Zuyue Wang, Rebecca Torguson, Jiaxiang Gai, Joseph Lindsay, et al. "Impact of triggering event in outcomes of stress-induced (Takotsubo) cardiomyopathy." European Heart Journal: Acute Cardiovascular Care 6, no. 3 (February 17, 2016): 280–86. http://dx.doi.org/10.1177/2048872616633881.

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Felzer, K. R., and E. E. Brodsky. "Decay of aftershock density with distance indicates triggering by dynamic stress." Nature 441, no. 7094 (June 2006): 735–38. http://dx.doi.org/10.1038/nature04799.

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Nieddu, P., M. Massidda, V. Farina, M. Cuccu, A. Manca, and M. P. Dore. "P.17.16 STRESS TRIGGERING A CRONKHITE-CANADA SYNDROME: A CASE REPORT." Digestive and Liver Disease 44 (March 2012): S202—S203. http://dx.doi.org/10.1016/s1590-8658(12)60574-x.

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