Relevant bibliographies by topics / Mediating Mechanisms

Academic literature on the topic 'Mediating Mechanisms'

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Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Mediating Mechanisms"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Mediating Mechanisms"

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Kopf, Brigitte Sandra. "Neurochemical mechanisms mediating LPS-induced anorexia /." [S.l.] : [s.n.], 2009. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18407.

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Wray, Jonathan. "Hypothalamic mechanisms mediating glucocorticoid-induced metabolic effects." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/hypothalamic-mechanisms-mediating-glucocorticoidinduced-metabolic-effects(6d4314ad-d89d-4d42-b727-d5bbced74073).html.

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Glucocorticoids (GCs) are widely prescribed for inflammatory and autoimmune conditions. However, patients often develop adverse metabolic effects, including hyperphagia, obesity and hyperglycemia. These effects have been recapitulated in a murine model of GC excess, and we hypothesize that they are mediated, in part, through central mechanisms. Therefore, this thesis aimed to identify genes and pathways in the hypothalamic arcuate nucleus (ARC) that are altered with GC treatment, and evaluate their contribution to GC-induced metabolic abnormalities. To better characterize the metabolic phenotype prior to RNA-seq, corticosterone (Cort; 75μg/ml) was administered in the drinking water to male C57Bl/6J mice for 2 days or 4 weeks. Cort treatment produced an early and sustained increase in food intake, with a delayed increase in body weight and adipose tissue mass. Insulin was elevated at 2 days, which progressed to fasting hyperinsulinemia and insulin resistance by 4 weeks. Indirect calorimetry revealed a persistent increase in respiratory exchange ratio, but no change in energy expenditure with 2 weeks GC treatment. However, UCP1 in brown adipose tissue (BAT) was decreased at 4 weeks, suggesting a delayed decrease in energy expenditure. To identify genes and pathways altered in the ARC, RNA-seq was performed on isolated arcuate nuclei from 2 day and 4 week Cort treated mice. RNA-seq revealed a multitude of genes altered at both timepoints, however the wealth of secondary effects at 4 weeks made interpretation of this dataset difficult. Subsequent work focused on genes altered at 2 days that are predicted to contribute to GC-induced hyperphagia and obesity. RNA-seq identified 131 upregulated and 100 downregulated genes after 2 days of Cort treatment. Among the genes altered were known GC-regulated genes, including Cdkn1a, Fkbp5, Mt1, Mt2, as well as some involved in the control of energy balance, such as Agrp, Ghsr, and Nmb. Results were confirmed by qRT-PCR, with a strong correlation between techniques. Thus, RNA-seq has identified candidate genes for investigation. One gene of interest was type-II iodothyronine deiodinase (Dio2), which increases the local availability of triiodothyronine (T3), and in turn increases food intake. With 2 day Cort treatment Dio2 increased (2-fold) in the ARC, which was confirmed by in situ hybridization. To determine the contribution of Dio2 in the development of GC-induced hyperphagia and obesity, AAV-directed CRISPR-Cas9 injections were used to knock down Dio2 in the MBH. Lack of a specific anti-DIO2 antibody meant that it was not possible to quantify DIO2 knockdown. However, the efficiency of CRISPR guide RNAs was pre-validated in vitro and correct targeting of the MBH was determined by immunofluorescence, and by quantification of Cas9 mRNA in MBH micro-punches. Dio2 knockdown mice were then challenged with Cort for 4 weeks, and showed a mild attenuation in BAT weight gain, as well as a 50% reduction in the GC-induced increase in Agrp. However, Dio2 knockdown conferred no protection from GC-induced hyperphagia, obesity, or hyperglycemia. This study has provided further insight into the development of GC side effects, and has identified several hypothalamic genes that may contribute to these effects. Future studies will further investigate the hypothalamic mechanisms driving GC-induced metabolic side effects, thus informing the development of targeted therapies to prevent the GC-induced metabolic sequelae.
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Lu, Jiao. "Central Mechanisms Mediating Ang II-Salt Hypertension." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34811.

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Abstract Statement of problem Plasma angiotensin II (Ang II) increases blood pressure (BP) through the activation of brain angiotensinergic pathways and the aldosterone-mineralocorticoid receptors (MR)- epithelial Na+ channel (ENaC)-endogenous ouabain (EO) pathway. The response of BP to circulating Ang II is enhanced by high salt intake, but the central mechanisms mediating this elevated response are not known. Methods of investigation Study 1) Male Wistar rats were divided into 4 groups and treated with regular salt diet (0.4% NaCl), high salt diet (2% NaCl), sc Ang II infusion (150 ng/kg/min), or sc Ang II infusion together with 2% salt diet for 14 days; plasma aldosterone and corticosterone levels, CYP11B2 mRNA in adrenal cortex and the mRNA levels of Ang II type 1 receptors (AT1R), CYP11B1 (11-β hydroxylase), CYP11B2 (aldosterone synthase), MR, 11βHSD2, ENaC α, ENaC β and ENaC γ in the subfornical organ (SFO), paraventricular nucleus (PVN), supraoptic nucleus (SON) and rostral ventrolateral medulla (RVLM) were measured. Study 2) MR blockers (eplerenone, spironolactone), ENaC blocker (benzamil), AT1R blocker (losartan) or vehicles were centrally infused in rats treated with Ang II plus high salt, and BP and heart rate (HR) were recorded by telemetry; plasma aldosterone and corticosterone levels and CYP11B2 mRNA expression in adrenal cortex were measured. Major findings Ang II alone caused a small increase in BP. Ang II together with 2% salt diet markedly increased the BP and plasma aldosterone level. Sc Ang II decreased 11βHSD2 and MR mRNA expression in the PVN, increased AT1R and ENaC γ expression in the PVN, and increased AT1R mRNA expression in the RVLM. Other genes tested in the four brain nuclei were not affected by sc Ang II or high salt diet. BP and plasma aldosterone increases in response to Ang II and salt, as well as CYP11B2 mRNA expression in adrenal cortex, were largely prevented by central infusion of eplerenone, spironolactone, benzamil or losartan. Main conclusion BP and plasma aldosterone responses to Ang II-salt are under the control of central mechanisms, and MR-AT1R activation in the brain plays a critical role in Ang II-salt induced hypertension.
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Fox, Daniel Kenneth. "Identification of bovel mechanisms mediating skeletal muscle atrophy." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3086.

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Skeletal muscle atrophy is a common, debilitating consequence of muscle disuse, malnutrition, critical illness, musculoskeletal conditions, neurological disease, cancer, and organ failure. Despite its prevalence, little is known about the molecular pathogenesis of this devastating condition due in large part to an incomplete understanding of the molecular mechanisms that drive the atrophy process. In previous studies, we identified the transcription factor ATF4 as a critical mediator of skeletal muscle atrophy. We found that ATF4 is necessary and sufficient for skeletal muscle atrophy during limb immobilization. However, ATF4 mKO mice were only partially protected from skeletal muscle atrophy during limb immobilization, indicating the existence of another pro-atrophy factor that acts independently of the ATF4 pathway. Using mouse models, we identify p53 as this ATF4-independent factor. We show that skeletal muscle atrophy increases p53 expression in skeletal muscle fibers. In addition, overexpression of p53 causes skeletal muscle atrophy. Further, p53 mKO mice are partially resistant to muscle atrophy during limb immobilization. Taken together, these data indicate that like ATF4, p53 is sufficient and required for skeletal muscle atrophy during limb immobilization. Importantly, overexpression of p53 induces muscle atrophy in the absence of ATF4, whereas ATF4-mediated muscle atrophy does not require p53. Furthermore, overexpression of p53 and ATF4 induces greater muscle atrophy than p53 or ATF4 alone. Moreover, skeletal muscle lacking both p53 and ATF4 is more resistant to skeletal muscle atrophy than muscle lacking either p53 or ATF4 alone. Taken together, these data indicate that p53 and ATF4 mediate distinct and additive mechanisms to skeletal muscle atrophy. However, the precise mechanism by which p53 and ATF4 cause skeletal muscle atrophy remained unclear. Using genome-wide expression arrays, we identify p21 as a skeletal muscle mRNA that is highly induced by p53 and ATF4 during limb immobilization. Further, overexpression of p21 causes skeletal muscle atrophy. In addition, p21 is required for muscle atrophy due to limb immobilization, p53, and ATF4. Collectively, these results identify p53 and ATF4 as critical and complementary mediators of skeletal muscle atrophy during limb immobilization, and discover p21 as an essential downstream mediator of the p53 and ATF4 pathways.
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Nestel, Frederick P. (Frederick Peter). "Macrophage effector mechanisms mediating acute graft-versus-host disease." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41302.

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The study presented in this thesis is an investigation of M$ phi$ effector mechanisms that mediate the pathogenesis of acute graft-versus-host disease (GVHD). Since the time that the GVH reaction was first described the mechanisms underlying the development of the disease have not been characterized. We have examined the state of M$ phi$ activation in nonirradiated B6AF1 mice injected with either 60 $ times$ 10$ sp6$ (acute GVHD) or 30 $ times$ 10$ sp6$ (nonlethal GVHD) parental B6 lymphoid cells. TNF-$ alpha$ and nitric oxide (NO) generation by M$ phi$ occurs following priming by IFN-$ gamma$ and triggering by LPS. During the early phase of acute GVHD, administration of normally sublethal amounts of LPS triggered release of significant amounts of TNF-$ alpha$ into the serum resulting in death of the animals within 36 hours. The amount of serum TNF-$ alpha$ produced following LPS injection increased during the course of GVHD and was significantly greater in acute GVH reactive mice. Normal animals treated with the same dose of LPS neither died nor produced detectable amounts of serum TNF-$ alpha$. In vitro studies demonstrated that M$ phi$ undergo priming for both TNF-$ alpha$ and NO production during the developing GVH reaction and that priming was greater during acute GVHD than nonlethal GVHD. As a result of M$ phi$ priming during acute GVHD, M$ phi$ mediated the selective release of iron from $ sp{59}$Fe,$ sp{51}$Cr dual-labelled target cells and expressed cytostatic activity when triggered by LPS. NO generation and cytostasis mediated by M$ phi$ from acute GVH-reactive animals were inhibited by NMMA. Endogenous bacterial-derived LPS was detected in the livers and spleens of acute GVH reactive animals and appeared subsequently the serum coincident with the onset of mortality. Immunohistochemical staining for TNF-$ alpha$ during acute GVHD demonstrated TNF-$ alpha$ in the splenic red pulp and liver, however, the hepatic portal infiltrates that characterize acute
Our results demonstrate the entry of bacterial-derived LPS during the acute GVH reaction and that as a result of M$ phi$ priming, LPS in the transplant recipient acts as a trigger for TNF-$ alpha$ and NO production by M$ phi$. The presence of enteric Gram-negative bacteria is a risk factor for development of acute GVHD due to the triggering effect of LPS on M$ phi$ that are primed following bone marrow transplantation. The development of acute GVHD therefore involves the excessive priming of M$ phi$ followed by contact with LPS leading to the activation of NO and TNF-$ alpha$-mediated mechanisms of tissue injury, weight loss, septic shock and death of the transplant recipient.
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Basic, Vladimir. "Molecular mechanisms mediating development of pulmonary cachexia in COPD." Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-36104.

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Cigarette smoking (CS) represents the main causative agent underlying development and progress of COPD. Recently, involvement of CS in the pathogenesis of COPDassociated muscle abnormalities is becoming increasingly evident. Nevertheless, involved triggers and underlying mechanisms remain largely unknown. This study was conceived in order to examine effects of cigarette smoke exposure on skeletal muscle morphology, vascular supply and function. For this purpose, we have specifically designed murine COPD/emphysema model and gastrocnemius muscle was examined, while in vitro experiments were conducted using murine C2C12 skeletal muscle myocytes. In addition to the mild emphysematous changes present in the lungs of CS-exposed mice, our results demonstrated evident signs of muscle atrophy reflected by decreased fiber cross-sectional area, profound fiber size variation and reduced body mass. Furthermore, we have observed impairment in terminal myogenesis and lower number of myonuclei in skeletal muscles of CS-exposed animals despite evident activation of muscle repair process. Additionally, our results demonstrate capillary rarefaction in skeletal muscles of CS-exposed animals which was associated with deregulation of hypoxia-angiogenesis signaling, reduced levels of angiogenic factors such as HIF1-α and VEGF and enhanced expression of VHL and its partner proteins PHD2 and Ube2D1. The results of our in-vitro experiments demonstrated that VHL and its ubiquitination machinery can be synergistically regulated by TNF and hypoxia consequentially impairing angiogenic potential of skeletal muscle myocytes. Finally, we have shown that CS elicits chronic ER stress in murine skeletal muscles which is associated with activation of ERAD and apoptotic pathways as mirrored by elevated expression of Usp19, caspase 12 and caspase 3 in skeletal muscles of CSexposed animals. Moreover, molecular and morphological alterations in CS-exposed mice resulted in impairment of muscle function as reflected by their impaired exercise capacity. Taken together, from our results it is evident that cigarette smoke exposure elicits set of morphological, vascular and functional changes highly resembling those observed in COPD. Additionally, CS induces wide range of molecular alterations and signaling pathway deregulations suggesting profound effects of cigarette smoke exposure on skeletal muscle cell homeostasis.
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Booth, Paul James. "Physiological mechanisms mediating nutrition-reproduction interactions in the gilt." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254056.

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Christiansen, Anne M. "Neural mechanisms mediating persistent stress relief by comfort food." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275921773.

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Crosswhite-Gamble, Jennifer Marie. "Mediating mechanisms understanding the link between parenting and adolescent deviance /." Auburn, Ala., 2005. http://repo.lib.auburn.edu/2005%20Fall/Dissertation/CROSSWHITE_JENNIFER_46.pdf.

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Sharma, Abhishek. "The psychological and physiological mechanisms mediating human oesophageal pain hypersensitivity." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489007.

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Books on the topic "Mediating Mechanisms"

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Ramkumar, Vickram, and Leonard P. Rybak, eds. Inflammatory Mechanisms in Mediating Hearing Loss. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3.

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Hillier, Andrew. Mediating Empire. GB Folkestone: Amsterdam University Press, 2020. http://dx.doi.org/10.5117/9781912961023.

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As part of the growing scholarship on family and empire, this study examines Britain’s presence in China through the lens of one family, arguing that, as the physical embodiment of the imperial project, it provided a social and cultural mechanism for mediating Britain’s imperial power, authority and presence, and forging connections and networks throughout the expanding British world. Drawing on public and private papers, it breaks significant new ground in its development of those themes.
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Winn, Louise Mary. Oxidative damage as a potential molecular mechanism mediating phenytoin teratogenesis. Ottawa: National Library of Canada, 1994.

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Dahlem Workshop on What Are the Mechanisms Mediating the Genetic and Environmental Determinants of Behavior? Twins as a Tool of Behavioral Genetics (1992 Berlin, Germany). Twins as a tool of behavioral genetics: Report of the Dahlem Workshop on What Are the Mechanisms Mediating the Genetic and Environmental Determinants of Behavior? Twins as a Tool of Behavioral Genetics, Berlin 1992, May 17-22. Chichester: J. Wiley, 1993.

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Acharya, N. K. Alternate dispute settlement mechanisms: Arbitration, settlement, conciliation, pre-arbitral proceedings in civil works, international law governing commercial arbitration & lok adalat. Hyderabad: N.K. Acharya, 1999.

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Haroutyunian, Sona, and Dario Miccoli. Orienti migranti: tra letteratura e traduzione. Venice: Fondazione Università Ca’ Foscari, 2020. http://dx.doi.org/10.30687/978-88-6969-499-8.

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The book series, edited by Nicoletta Pesaro and sponsored by the Department of Asian and North African Studies, aims to give voice to a time-honoured branch of theoretical and practical research across the disciplines and research domains within the Department. The series aims to establish a platform for scholarly discussion and a space for international dialogue on the translation of Asian and North African languages. In doing so, the project aims to observe and verify the translingual and transcultural dynamics triggered by translation from and into said ‘languages-cultures’, as well as to identify and explore the deep cultural mechanisms and structures involved in interethnic behaviours and relationships. Translation is also a major research tool in the humanities. As a matter of fact, a hermeneutic potential in terms of cultural mediation is inherent in translation activities and in the reflection on translation: it is precisely this potential that allows scholars, in both their research and dissemination work, to bring to the surface the interethnic and intercultural dynamics regulating the relationships between civilisations, both diachronically and synchronically. The project is a continuation and a development of the research carried out in recent years by the former Department of East Asian Studies – now Department of Asian and North African Studies – of Ca’ Foscari University of Venice through a series of initiatives organised by the research group on the translation of Asian languages “Laboratorio sulla Traduzione delle Lingue orientali” (Laboratori sulle lingue orientali). Such activities involved periodical meetings on translation, whose objective was to introduce and discuss specific issues in translation from and into Asian languages, as well as several international events (workshops, conferences, and symposia).
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Ramkumar, Vickram, and Leonard P. Rybak. Inflammatory Mechanisms in Mediating Hearing Loss. Springer, 2019.

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Ramkumar, Vickram, and Leonard P. Rybak. Inflammatory Mechanisms in Mediating Hearing Loss. Springer, 2018.

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Sung, Michael T. Design of multivalent, peptide-based drug delivery vehicles and investigation into mechanisms mediating their cellular uptake. 2006.

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Brondolo, Elizabeth, Irene V. Blair, and Amandeep Kaur. Biopsychosocial Mechanisms Linking Discrimination to Health: A Focus on Social Cognition. Edited by Brenda Major, John F. Dovidio, and Bruce G. Link. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190243470.013.8.

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This chapter presents a theoretical framework that highlights the role of social cognition in mediating the effects of discrimination on health. This framework suggests that through alterations in schemas and appraisal processes, long-term discrimination increases the experienced frequency, intensity, and duration of threat exposure and concomitant distress. At the same time, the ability to recover from threat exposure may be impaired by the effects of discrimination on cognitive control processes that are necessary for modulating stress responses. Together, these processes may influence the ability to initiate and sustain health-promoting behavior, avoid health-impairing behavior, attenuate stress reactivity, and facilitate stress recovery. Through effects on social cognition, persistent exposure to discrimination may potentiate sustained dysregulation of psychophysiological systems responsible for maintaining health.
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Book chapters on the topic "Mediating Mechanisms"

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Hyyppä, Markku T. "Proposed Biological Mediating Mechanisms." In Healthy Ties, 125–29. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9606-7_13.

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Bao, Wan-Ning. "Mediating Mechanisms of Strain and Delinquency." In Delinquent Youth in a Transforming China, 113–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-63727-3_4.

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Gholamnezhad, Zahra, Bruno Mégarbane, and Ramin Rezaee. "Molecular Mechanisms Mediating Adaptation to Exercise." In Physical Exercise for Human Health, 45–61. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1792-1_3.

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Rybak, Leonard P. "The Cochlea." In Inflammatory Mechanisms in Mediating Hearing Loss, 1–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_1.

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Windsor, Alanna M., and Michael J. Ruckenstein. "Anti-inflammatory Therapies for Sensorineural Hearing Loss." In Inflammatory Mechanisms in Mediating Hearing Loss, 189–210. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_10.

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Vambutas, Andrea, and Martin L. Lesser. "Implementation and Outcomes of Clinical Trials in Immune-Mediated Hearing Loss and Other Rare Diseases." In Inflammatory Mechanisms in Mediating Hearing Loss, 211–23. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_11.

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Jamesdaniel, Samson. "Oxidative Stress and Hearing Loss." In Inflammatory Mechanisms in Mediating Hearing Loss, 15–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_2.

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Vetter, Douglas E., and Kathleen T. Yee. "Corticotropin Releasing Factor Signaling in the Mammalian Cochlea: An Integrative Niche for Cochlear Homeostatic Balance Against Noise." In Inflammatory Mechanisms in Mediating Hearing Loss, 31–60. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_3.

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Shi, Xiaorui. "Cochlear Vascular Pathology and Hearing Loss." In Inflammatory Mechanisms in Mediating Hearing Loss, 61–90. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_4.

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Keithley, Elizabeth M. "Cochlear Inflammation Associated with Noise-Exposure." In Inflammatory Mechanisms in Mediating Hearing Loss, 91–114. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_5.

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Conference papers on the topic "Mediating Mechanisms"

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"The Mediating Mechanisms of the Relationship between HR Systems and Organizational Performance." In 2018 2nd International Conference on e-Education, e-Business and Information Management. Clausius Scientific Press, 2018. http://dx.doi.org/10.23977/eeim.2018.047.

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Azoulay, Rina, and Esther David. "Ad Exchange: Intention Driven Auction Mechanisms for Mediating Between Publishers and Advertisers." In 2015 IEEE / WIC / ACM International Conference on Web Intelligence and Intelligent Agent Technology (WI-IAT). IEEE, 2015. http://dx.doi.org/10.1109/wi-iat.2015.35.

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Chen, Chao. "Metabolic mechanisms mediating the miserable months: Metabolomics of periodic arousal in insect diapause." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.112887.

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Vishnoi, Kanchan, Rong Ke, Randhir Kumar, Navin Viswakarma, Ajay Rana, and Basabi Rana. "Abstract 2614: Elucidation of the molecular mechanisms mediating sorafenib-resistance in Hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2614.

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Kocak, A., D. Harmancı, M. Birlik, and G. Guner. "AB0182 Molecular mechanisms mediating antioxidant effect of epigallocatechin-3-gallate in experimental scleroderma model." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6677.

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Ye, Xiaobing, Dongmei Song, and Shu F. Liu. "Mechanisms Mediating The Vascular Protective Effect Of Endothelial NF-ºB Blockade In Endotoxemic Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6349.

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Kirchner, Stephen J., James T. Bartram, D. Christian Ellis, Daniel S. Wechsler, and Michael B. Armstrong. "Abstract B32: The role of Exon 0 in mediating Mxi0 activity in neuroblastoma." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-b32.

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Doan, Stacey N., Thomas E. Fuller-Rowell, Daniel B. Schmolze, and Victoria Seewaldt. "Abstract C078: Relations between sleep and inflammation in African American and White young adults: Testing mediating and moderating mechanisms." In Abstracts: Eleventh AACR Conference on The Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 2-5, 2018; New Orleans, LA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp18-c078.

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Akl, Mohamed R., Belnaser A. Busnena, Mohamed M. Mohyeldin, and Khalid El Sayed. "Abstract C259: Olive phenolics as c-Met inhibitors: Molecular mechanisms mediating the anticancer effects of oleocanthal in breast cancer cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c259.

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Tang, Karen, Elijah Otis, Alexandra Loverock, Cameron Wild, and Igor Yakovenko. "The Role of Motives in Understanding the Link Between Personality and Cannabis Misuse." In 2020 Virtual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2021. http://dx.doi.org/10.26828/cannabis.2021.01.000.19.

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Background and aim: A robust association exists between substance use and personality, with personality risk factors representing phenotypes of vulnerability to substance misuse. As such, personality risk factors may be valuable constructs for understanding specific motivations for substance misuse. Given the loosening of restrictions on cannabis worldwide, research focusing on understanding cannabis use in young adults, a particularly at-risk population, remains a vital area of research. The existing data provides extensive support for the mediating role of coping motives on personality risk factors and problematic cannabis use; however, the role of other types of motives has remained largely unexplored. Our study examined the mediating role of cannabis use motives between personality and cannabis misuse among university students. We also explored the predictive value of personality phenotypes for cannabis use problems. Research question and hypothesis: Do motivations for cannabis use mediate or explain the relationship between personality type and cannabis use problem severity? Hypothesis 1: sensation-seeking (SS) and impulsivity (IMP), but not anxiety sensitivity and hopelessness, will be associated with greater cannabis use problem severity. Hypothesis 2: motives for use (i.e., coping, conformity, social, enhancement, expansion) will mediate the association between personality risk and cannabis use problem severity. Method: A survey was administered to 1073 undergraduate students. We examined whether motivations for use (mediator variable) explained the relationship between personality (predictor variable) and cannabis use disorder severity (outcome variable) using an ordinary least-squares (OLS) based mediation analysis. Results: As hypothesized, SS and IMP predicted greater cannabis use problems. A noteworthy finding was that conformity motives were a significant mediator between SS and IMP and cannabis use, whereby higher levels of SS/IMP led to greater endorsement of conformity motives, which in turn led to lower cannabis misuse. Enhancement motives were also a significant mediator between IMP and cannabis use. Expansion motives were a significant mediator between SS and cannabis use. Conclusion: Understanding reasons for use (i.e., motives) allows us to identify those at greatest risk for cannabis misuse. Findings from this study may help explain the underlying mechanisms by which personality risk factors lead to cannabis use disorder in young adults. A greater understanding of these personality phenotypes may have implications for the development of personality-specific interventions for cannabis use.
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Reports on the topic "Mediating Mechanisms"

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Warren, Richard M. Mechanisms Mediating the Perception of Complex Acoustic Patterns. Fort Belvoir, VA: Defense Technical Information Center, September 1988. http://dx.doi.org/10.21236/ada200530.

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Burlacu, Gabriela. Supervisor-Subordinate Directional Age Differences and Employee Reactions to Formal Performance Feedback: Examining Mediating and Moderating Mechanisms in a Chinese Sample. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.662.

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Bonilla-Mejía, Leonardo, and Erika Londoño-Ortega. Geographic Isolation and Learning in Rural Schools. Banco de la República, August 2021. http://dx.doi.org/10.32468/be.1169.

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Rural schools are usually behind in terms of learning, and part of this could be related to geographical isolation. We explore this hypothesis, assessing the effect of distance between rural schools and local governments on learning in Colombia. We use spatial discontinuous regression models based on detailed administrative records from the education system and granular geographic information. Results indicate that distance to towns and Secretary of Education has significant negative effects on students’ standardized test scores. We evaluated alternative mechanisms, finding that the effect of distance is partly explained by differences in critical educational inputs, such as teachers’ education attainment and contract stability. Finally, we assess the mediating role of a program providing monetary incentives to teachers and principals in remote areas.
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Pearl, Judea. The Causal Mediation Formula - A Guide to the Assessment of Pathways and Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada557663.

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Carraway, Robert E. Prostate Cancer Cell Growth: Role of Neurotensin in Mediating Effect of Dietary Fat and Mechanism of Action. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada431644.

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Carraway, Robert E. Prostate Cancer Cell Growth: Role of Neurotensin in Mediating Effect of Dietary Fat and Mechanism of Action. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada413288.

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Carraway, Robert E. Prostate Cancer Cell Growth: Role of Neurotensin in Mediating Effect of Dietary Fat and Mechanism of Action. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada419819.

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