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Journal articles on the topic 'Mediating Mechanisms'

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Published: 4 June 2021
Last updated: 19 February 2022

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1

Rutter, Michael. "Mediating Mechanisms and Emotions." Emotion Review 2, no. 2 (March 31, 2010): 111–12. http://dx.doi.org/10.1177/1754073909356598.

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2

Toomey, Deirdre, H. Paul Redmond, and David Bouchier-Hayes. "Mechanisms mediating cancer cachexia." Cancer 76, no. 12 (December 15, 1995): 2418–26. http://dx.doi.org/10.1002/1097-0142(19951215)76:12<2418::aid-cncr2820761204>3.0.co;2-c.

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3

Artieda, J., J. Muruzabal, R. Larumbe, C. Garc�a de Casasola, and Jos� A. Obeso. "Cortical mechanisms mediating asterixis." Movement Disorders 7, no. 3 (1992): 209–16. http://dx.doi.org/10.1002/mds.870070304.

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4

Sharot, Tali, Alison M. Riccardi, Candace M. Raio, and Elizabeth A. Phelps. "Neural mechanisms mediating optimism bias." Nature 450, no. 7166 (October 24, 2007): 102–5. http://dx.doi.org/10.1038/nature06280.

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5

Wallace, Bruce G. "Signaling mechanisms mediating synapse formation." BioEssays 18, no. 10 (October 1996): 777–80. http://dx.doi.org/10.1002/bies.950181002.

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6

Meroni, Pier Luigi, and Piersandro Riboldi. "Pathogenic mechanisms mediating antiphospholipid syndrome." Current Opinion in Rheumatology 13, no. 5 (September 2001): 377–82. http://dx.doi.org/10.1097/00002281-200109000-00006.

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7

Kangaslampi, Samuli. "Uncovering psychological mechanisms mediating the effects of drugs: some issues and comments using the example of psychedelic drugs." Psychopharmacology 237, no. 12 (November 5, 2020): 3799–802. http://dx.doi.org/10.1007/s00213-020-05703-9.

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AbstractResearchers have begun efforts to uncover the psychological mechanisms by which psychedelic drugs may have beneficial effects on long-term outcomes in some circumstances. The approaches several recent publications on the topic have taken to analyze such mechanisms have some pitfalls and limitations. Based on the rich literature on mechanisms and mediation analysis in psychological science, I comment on five particular issues: (1) Separating mediating and moderating factors, (2) problems inherent in using cross-sectional data, (3) statistical methods in mediation analysis, (4) assumptions and limitations inherent in traditional mediation analysis, and (5) criteria beyond mediation to establish a mechanism. Suggested practices for future research on the psychological mechanisms through which drugs have their effects are presented.
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8

Farina, M. "Mechanisms mediating methylmercury-induced developmental neurotoxicity." Toxicology Letters 259 (October 2016): S51. http://dx.doi.org/10.1016/j.toxlet.2016.07.123.

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9

Johansen, Jorgen, and Kristen M. Johansen. "Molecular Mechanisms Mediating Axon Pathway Formation." Critical Reviews™ in Eukaryotic Gene Expression 7, no. 1-2 (1997): 95–116. http://dx.doi.org/10.1615/critreveukargeneexpr.v7.i1-2.60.

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10

Dakin, Steven C., and Robert F. Hess. "The spatial mechanisms mediating symmetry perception." Vision Research 37, no. 20 (October 1997): 2915–30. http://dx.doi.org/10.1016/s0042-6989(97)00031-x.

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11

PUTS, MARCO J. H., JOEL POKORNY, and VIVIANNE C. SMITH. "Inferred retinal mechanisms mediating illusory distortions." Visual Neuroscience 21, no. 3 (May 2004): 321–25. http://dx.doi.org/10.1017/s0952523804213219.

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The Zoellner illusion is a geometric distortion occurring when nonorthogonal inducing lines appear to tilt veridically parallel bars. The retinal pathways contributing to such illusions are unknown. The goal of this experiment was to investigate the retinal origin of the illusion. This was accomplished by determining the contrast gain for illusion thresholds. The magnocellular (MC-) and parvocellular (PC-) pathways exhibit different contrast gains, and this difference can be used psychophysically to identify the pathway. The stimulus pattern was four vertical bars with a series of inducing lines. The bars were always 5% higher in contrast than the inducing bars. The pattern was presented on a larger pedestal. Two paradigms were used. In the pulsed-pedestal paradigm, the observer adapted to the background and the pedestal and pattern were presented together as a brief pulse. In the steady-pedestal paradigm, the observer adapted to the continuously presented pedestal and the pattern appeared as a brief pulse. The contrast between the pedestal and the pattern was varied to obtain thresholds for two criteria: perceiving the directions of the inner inducing lines, and perceiving the distortion of the bars. The results for both criteria were similar in shape, but displaced in sensitivity. Detection of the directions of the inner inducing lines was 0.16–0.29 log unit more sensitive than perception of the illusion. The data for the pulsed-pedestal paradigm depended on the contrast between the pedestal and the pattern and produced a shallow V-shape. These results were associated with mediation in the PC-pathway. The data for the steady-pedestal paradigm depended on the pedestal luminance in a linear relation and showed similar sensitivity to the data for the pulsed-pedestal paradigm. Perception of the illusion required 10–15% Weber contrast.
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12

Bhakta, Hanisha H., Fares H. Refai, and Matteo A. Avella. "The molecular mechanisms mediating mammalian fertilization." Development 146, no. 15 (August 1, 2019): dev176966. http://dx.doi.org/10.1242/dev.176966.

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13

Braithwaite, Scott R., Edward A. Selby, and Frank D. Fincham. "Forgiveness and relationship satisfaction: Mediating mechanisms." Journal of Family Psychology 25, no. 4 (2011): 551–59. http://dx.doi.org/10.1037/a0024526.

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14

Rainville, S. J. M., and W. L. Makous. "The temporal mechanisms mediating synchrony perception." Journal of Vision 2, no. 7 (March 15, 2010): 225. http://dx.doi.org/10.1167/2.7.225.

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15

Puts, M., J. Pokorny, and V. C. Smith. "Inferred retinal mechanisms mediating illusory distortions." Journal of Vision 3, no. 12 (March 28, 2010): 62. http://dx.doi.org/10.1167/3.12.62.

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16

Hall, W. L., D. J. Millward, P. J. Rogers, and L. M. Morgan. "Physiological mechanisms mediating aspartame-induced satiety." Physiology & Behavior 78, no. 4-5 (April 2003): 557–62. http://dx.doi.org/10.1016/s0031-9384(03)00034-9.

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17

Hudson, Nathan E. "Biophysical Mechanisms Mediating Fibrin Fiber Lysis." BioMed Research International 2017 (2017): 1–17. http://dx.doi.org/10.1155/2017/2748340.

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The formation and dissolution of blood clots is both a biochemical and a biomechanical process. While much of the chemistry has been worked out for both processes, the influence of biophysical properties is less well understood. This review considers the impact of several structural and mechanical parameters on lytic rates of fibrin fibers. The influences of fiber and network architecture, fiber strain, FXIIIa cross-linking, and particle transport phenomena will be assessed. The importance of the mechanical aspects of fibrinolysis is emphasized, and future research avenues are discussed.
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18

Decety, Jean. "Dissecting the Neural Mechanisms Mediating Empathy." Emotion Review 3, no. 1 (January 2011): 92–108. http://dx.doi.org/10.1177/1754073910374662.

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19

Rozeske, Robert R., and Cyril Herry. "Neuronal coding mechanisms mediating fear behavior." Current Opinion in Neurobiology 52 (October 2018): 60–64. http://dx.doi.org/10.1016/j.conb.2018.04.017.

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20

Rudenko, Gloria. "Mechanisms Mediating Antigenic Variation in Trypanosoma brucei." Memórias do Instituto Oswaldo Cruz 94, no. 2 (March 1999): 235–37. http://dx.doi.org/10.1590/s0074-02761999000200021.

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21

Zhuang, Xiaohua, and Steven K. Shevell. "Monocular and binocular mechanisms mediating flicker adaptation." Vision Research 117 (December 2015): 41–48. http://dx.doi.org/10.1016/j.visres.2015.08.020.

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22

COSKUN, T., S. CHU, and M. MONTROSE. "Mechanisms mediating capsaicin-stimulated gastric bicarbonate secretion." Gastroenterology 120, no. 5 (April 2001): A155. http://dx.doi.org/10.1016/s0016-5085(01)80764-2.

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23

Joseph, Elizabeth K., and Jon D. Levine. "Multiple PKCε-dependent mechanisms mediating mechanical hyperalgesia." Pain 150, no. 1 (July 2010): 17–21. http://dx.doi.org/10.1016/j.pain.2010.02.011.

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24

Rodriguez-Ruiz, María E., I. Rodriguez, Olwen Leaman, Fernando López-Campos, Angel Montero, Antonio J. Conde, J. J. Aristu, Pedro Lara, Felipe Manuel Calvo, and Ignacio Melero. "Immune mechanisms mediating abscopal effects in radioimmunotherapy." Pharmacology & Therapeutics 196 (April 2019): 195–203. http://dx.doi.org/10.1016/j.pharmthera.2018.12.002.

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25

Zhuang, Xiaohua, and Steven Shevell. "Monocular and binocular mechanisms mediating flicker adaptation." Journal of Vision 15, no. 12 (September 1, 2015): 395. http://dx.doi.org/10.1167/15.12.395.

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26

Coskun, Tamer, Shaoyou Chu, and Marshall H. Montrose. "Mechanisms mediating capsaicin-stimulated gastric bicarbonate secretion." Gastroenterology 120, no. 5 (April 2001): A155. http://dx.doi.org/10.1016/s0016-5085(08)80764-0.

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27

Yuan, Xin, and Steven P. Balk. "Mechanisms mediating androgen receptor reactivation after castration." Urologic Oncology: Seminars and Original Investigations 27, no. 1 (January 2009): 36–41. http://dx.doi.org/10.1016/j.urolonc.2008.03.021.

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28

Meyer-Lindenberg, Andreas. "NEURAL MECHANISMS MEDIATING URBANICITY AND MIGRATION RISK." Schizophrenia Research 136 (April 2012): S20. http://dx.doi.org/10.1016/s0920-9964(12)70068-3.

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29

Dovidio, John F., Marleen ten Vergert, Tracie L. Stewart, Samuel L. Gaertner, James D. Johnson, Victoria M. Esses, Blake M. Riek, and Adam R. Pearson. "Perspective and Prejudice: Antecedents and Mediating Mechanisms." Personality and Social Psychology Bulletin 30, no. 12 (December 2004): 1537–49. http://dx.doi.org/10.1177/0146167204271177.

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30

Hartwig, J. H. "Mechanisms of actin rearrangements mediating platelet activation." Journal of Cell Biology 118, no. 6 (September 15, 1992): 1421–42. http://dx.doi.org/10.1083/jcb.118.6.1421.

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The detergent-insoluble cytoskeleton of the resting human blood platelet contains approximately 2,000 actin filaments approximately 1 micron in length crosslinked at high angles by actin-binding protein and which bind to a spectrin-rich submembrane lamina (Fox, J., J. Boyles, M. Berndt, P. Steffen, and L. Anderson. 1988. J. Cell Biol. 106:1525-1538; Hartwig, J., and M. DeSisto. 1991. J. Cell Biol. 112:407-425). Activation of the platelets by contact with glass results within 30 s in a doubling of the polymerized actin content of the cytoskeleton and the appearance of two distinct new actin structures: bundles of long filaments within filopodia that end at the filopodial tips (filopodial bundles) and a circumferential zone of orthogonally arrayed short filaments within lamellipodia (lamellipodial network). Neither of these structures appears in cells exposed to glass with cytochalasin B present; instead the cytoskeletons have numerous 0.1-0.3-microns-long actin filament fragments attached to the membrane lamina. With the same time course as the glass-induced morphological changes, cytochalasin-sensitive actin nucleating activity, initially low in cytoskeletons of resting platelets, increases 10-fold in cytoskeletons of thrombin-activated platelets. This activity decays with a time course consistent with depolymerization of 0.1-0.3-microns-long actin filaments, and phalloidin inhibits this decay. Cytochalasin-insensitive and calcium-dependent nucleation activity also increases markedly in platelet extracts after thrombin activation of the cells. Prevention of the rise in cytosolic Ca2+ normally associated with platelet activation with the permeant Ca2+ chelator, Quin-2, inhibits formation of lamellipodial networks but not filopodial bundles after glass contact and reduces the cytochalasin B-sensitive nucleation activity by 60% after thrombin treatment. The filopodial bundles, however, are abnormal in that they do not end at the filopodial tips but form loops and return to the cell body. Addition of calcium to chelated cells restores lamellipodial networks, and calcium plus A23187 results in cytoskeletons with highly fragmented actin filaments within seconds. Immunogold labeling with antibodies against gelsolin reveals gelsolin molecules at the ends of filaments attached to the submembrane lamina of resting cytoskeletons and at the ends of some filaments in the lamellipodial networks and filopodial bundles of activated cytoskeletons. Addition of monomeric actin to myosin subfragment 1-labeled activated cytoskeletons leads to new (undecorated) filament growth off the ends of filaments in the filopodial bundles and the lamellipodial network. The simplest explanation for these findings is that gelsolin caps the barbed ends of the filaments in the resting platelet. Uncapping some of these filaments after activation leads to filopodial bundles.(ABSTRACT TRUNCATED AT 400 WORDS)
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31

Hoggatt, Jonathan, and Louis M. Pelus. "Many mechanisms mediating mobilization: an alliterative review." Current Opinion in Hematology 18, no. 4 (July 2011): 231–38. http://dx.doi.org/10.1097/moh.0b013e3283477962.

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32

Sarkar, Sanchoy, Anthony R. Hobson, Paul L. Furlong, Clifford J. Woolf, David G. Thompson, and Qasim Aziz. "Central neural mechanisms mediating human visceral hypersensitivity." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 5 (November 1, 2001): G1196—G1202. http://dx.doi.org/10.1152/ajpgi.2001.281.5.g1196.

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Although visceral hypersensitivity is thought to be important in generating symptoms in functional gastrointestinal disorders, the neural mechanisms involved are poorly understood. We recently showed that central sensitization (hyperexcitability of spinal cord sensory neurones) may play an important role. In this study, we demonstrate that after a 30-min infusion of 0.15 M HCl acid into the healthy human distal esophagus, we see a reduction in the pain threshold to electrical stimulation of the non-acid-exposed proximal esophagus (9.6 ± 2.4 mA) and a concurrent reduction in the latency of the N1 and P2 components of the esophageal evoked potentials (EEP) from this region (10.4 ± 2.3 and 15.8 ± 5.3 ms, respectively). This reduced EEP latency indicates a central increase in afferent pathway velocity and therefore suggests that hyperexcitability within the central visceral pain pathway contributes to the hypersensitivity within the proximal, non-acid-exposed esophagus (secondary hyperalgesia/allodynia). These findings provide the first electrophysiological evidence that central sensitization contributes to human visceral hypersensitivity.
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33

Nagel, Rosemarie, Andrea Brovelli, Frank Heinemann, and Giorgio Coricelli. "Neural mechanisms mediating degrees of strategic uncertainty." Social Cognitive and Affective Neuroscience 13, no. 1 (December 7, 2017): 52–62. http://dx.doi.org/10.1093/scan/nsx131.

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34

Kumar, S. "Mechanisms mediating caspase activation in cell death." Cell Death & Differentiation 6, no. 11 (November 1999): 1060–66. http://dx.doi.org/10.1038/sj.cdd.4400600.

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35

Egashira, Kensuke. "Molecular Mechanisms Mediating Inflammation in Vascular Disease." Hypertension 41, no. 3 (March 2003): 834–41. http://dx.doi.org/10.1161/01.hyp.0000051642.65283.36.

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36

Nippert, Amy R., Kyle R. Biesecker, and Eric A. Newman. "Mechanisms Mediating Functional Hyperemia in the Brain." Neuroscientist 24, no. 1 (April 12, 2017): 73–83. http://dx.doi.org/10.1177/1073858417703033.

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Neuronal activity within the brain evokes local increases in blood flow, a response termed functional hyperemia. This response ensures that active neurons receive sufficient oxygen and nutrients to maintain tissue function and health. In this review, we discuss the functions of functional hyperemia, the types of vessels that generate the response, and the signaling mechanisms that mediate neurovascular coupling, the communication between neurons and blood vessels. Neurovascular coupling signaling is mediated primarily by the vasoactive metabolites of arachidonic acid (AA), by nitric oxide, and by K+. While much is known about these pathways, many contentious issues remain. We highlight two controversies, the role of glial cell Ca2+ signaling in mediating neurovascular coupling and the importance of capillaries in generating functional hyperemia. We propose signaling pathways that resolve these controversies. In this scheme, capillary dilations are generated by Ca2+ increases in astrocyte endfeet, leading to production of AA metabolites. In contrast, arteriole dilations are generated by Ca2+ increases in neurons, resulting in production of nitric oxide and AA metabolites. Arachidonic acid from neurons also diffuses into astrocyte endfeet where it is converted into additional vasoactive metabolites. While this scheme resolves several discrepancies in the field, many unresolved challenges remain and are discussed in the final section of the review.
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37

Mustillo, Pardo. "Binocular mechanisms mediating crossed and uncrossed stereopsis." Psychological Bulletin 97, no. 2 (1985): 187–201. http://dx.doi.org/10.1037/0033-2909.97.2.187.

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38

Goldstein, Robin S., Lisa R. Contardi, Dale A. Pasino, and Jerry B. Hook. "Mechanisms mediating cephaloridine inhibition of renal gluconeogenesis." Toxicology and Applied Pharmacology 87, no. 2 (February 1987): 297–305. http://dx.doi.org/10.1016/0041-008x(87)90291-2.

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39

Dunbar, J. C., D. S. O'Leary, G. Wang, and J. Wright-Richey. "Mechanisms mediating insulin-induced hypotension in rats." Acta Diabetologica 33, no. 4 (December 1996): 263–68. http://dx.doi.org/10.1007/bf00571561.

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40

Dunbar, J. C., D. S. O'Leary, G. Wang, and J. Wright-Richey. "Mechanisms mediating insulin-induced hypotension in rats." Acta Diabetologica 33, no. 4 (December 1, 1996): 263–68. http://dx.doi.org/10.1007/s005920050048.

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41

Thuan, Le Cong, and Bui Thi Thanh. "Mediating mechanisms linking developmental feedback with employee creativity." Journal of Workplace Learning 32, no. 2 (November 3, 2019): 108–21. http://dx.doi.org/10.1108/jwl-06-2019-0070.

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Purpose The purpose of this paper is to investigate mediating mechanisms linking leaders’ developmental feedback with employee creativity and the moderating role of intrinsic motivation in the effects of employees’ skills on employee creativity. Design/methodology/approach Using data collected from 326 employees at information technology organizations in Vietnam, this study tested the hypotheses by using structural equation modeling. Findings The results show that leaders’ developmental feedback has a positive indirect relationship with employee creativity via creativity-relevant skills, domain-relevant skills and intrinsic motivation. There are no significant differences in the effects of developmental feedback on employee creativity through proposed mediators. Further, intrinsic motivation positively moderates the impact of domain-relevant skills on employee creativity. However, intrinsic motivation does not moderate the effect of creativity-relevant skills on employee creativity. Originality/value This research is one of the first efforts to investigate intrinsic motivation as a motivational mechanism as well as creativity-relevant skills and domain-relevant skills as cognitive mechanisms for understanding the relationship between leaders’ developmental feedback and employee creativity. This research also examines how intrinsic motivation moderates the effects of employees’ skills on employee creativity.
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42

Stavrou, Brigitte. "Diadenosine Polyphosphates: Postulated Mechanisms Mediating the Cardiac Effects." Current Medicinal Chemistry-Cardiovascular & Hematological Agents 1, no. 2 (June 1, 2003): 151–69. http://dx.doi.org/10.2174/1568016033477513.

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43

Higuchi, Masataka, Hitomi Kuranaga, Hiromi Fukada, and Yoshino Teruya. "Mediating mechanisms of embarrassment in non-negative situations." JAPANESE JOURNAL OF RESEARCH ON EMOTIONS 19, no. 3 (2012): 90–97. http://dx.doi.org/10.4092/jsre.19.90.

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44

R. Schleiss, Mark. "Congenital Cytomegalovirus Infection: Molecular Mechanisms Mediating Viral Pathogenesis." Infectious Disorders - Drug Targets 11, no. 5 (October 1, 2011): 449–65. http://dx.doi.org/10.2174/187152611797636721.

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45

Duprez, Daniel A. "Aldosterone and the Vasculature: Mechanisms Mediating Resistant Hypertension." Journal of Clinical Hypertension 9 (January 2007): 13–18. http://dx.doi.org/10.1111/j.1524-6175.2007.06367.x.

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46

Watkins, Susanne, Polly Dalton, Nilli Lavie, and Geraint Rees. "Brain Mechanisms Mediating Auditory Attentional Capture in Humans." Cerebral Cortex 17, no. 7 (September 21, 2006): 1694–700. http://dx.doi.org/10.1093/cercor/bhl080.

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47

Monnier, P. "The bandwidth of chromatic mechanisms mediating visual search." Journal of Vision 7, no. 9 (March 23, 2010): 680. http://dx.doi.org/10.1167/7.9.680.

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48

LaMarca, Babbette, Denise C. Cornelius, Ashlyn C. Harmon, Lorena M. Amaral, Mark W. Cunningham, Jessica L. Faulkner, and Kedra Wallace. "Identifying immune mechanisms mediating the hypertension during preeclampsia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 1 (July 1, 2016): R1—R9. http://dx.doi.org/10.1152/ajpregu.00052.2016.

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Preeclampsia (PE) is a pregnancy-associated disorder that affects 5–8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role
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49

Bonet, Ivan J. M., Dionéia Araldi, Eugen V. Khomula, Oliver Bogen, Paul G. Green, and Jon D. Levine. "Mechanisms Mediating High-Molecular-Weight Hyaluronan-Induced Antihyperalgesia." Journal of Neuroscience 40, no. 34 (July 14, 2020): 6477–88. http://dx.doi.org/10.1523/jneurosci.0166-20.2020.

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50

Premen, Andre J. "Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration." FASEB Journal 2, no. 2 (February 1988): 131–37. http://dx.doi.org/10.1096/fasebj.2.2.3277887.

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