scholarly journals Neuronal correlates underlying the role of the zinc sensing receptor (GPR39) in passive-coping behaviour

2021 ◽  
pp. 108752
Author(s):  
Anupam Sah ◽  
Maria Kharitonova ◽  
Katarzyna Młyniec
Keyword(s):  
Passive Coping ◽  
Coping Behaviour ◽  
Zinc Sensing

scholarly journals Psychological Correlates of Self-reported Disease Activity in Ankylosing Spondylitis

2010 ◽  
Vol 37 (4) ◽  
pp. 829-834 ◽  
Author(s):  
TAMAR F. BRIONEZ ◽  
SHERVIN ASSASSI ◽  
JOHN D. REVEILLE ◽  
CHARLES GREEN ◽  
THOMAS LEARCH ◽  
...  
Keyword(s):  
New York ◽  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Activity Index ◽  
Disease Activity Index ◽  
Multivariate Regression Analysis ◽  
Passive Coping ◽  
Psychological Variables ◽  
Psychological Measures

Objective.To investigate the role of psychological variables in self-reported disease activity in patients with ankylosing spondylitis (AS), while controlling for demographic and medical variables.Methods.Patients with AS (n = 294) meeting modified New York criteria completed psychological measures evaluating depression, resilience, active and passive coping, internality, and helplessness. Demographic, clinical, and radiologic data were also collected. Univariate and multivariate analyses were completed to determine the strength of the correlation of psychological variables with disease activity, as measured by the Bath AS Disease Activity Index (BASDAI).Results.In the multivariate regression analysis, the psychological variables contributed significantly to the variance in BASDAI scores, adding an additional 33% to the overall R-square beyond that accounted for by demographic and medical variables (combined R-square 18%). Specifically, arthritis helplessness and depression accounted for the most significant portion of the variance in BASDAI scores in the final model.Conclusion.Arthritis helplessness and depression accounted for significant variability in self-reported disease activity beyond clinical and demographic variables in patients with AS. These findings have important clinical implications in the treatment and monitoring of disease activity in AS, and suggest potential avenues of intervention.

scholarly journals Suffering Silence While Exposed to Workplace Bullying: The Role of Psychological Contract Violation, Benevolent Behavior and Positive Psychological Capital

2020 ◽  
Vol 4 (4) ◽  
pp. 15-54
Author(s):  
Namra Jamshaid ◽  
Sadia Arshad
Keyword(s):  
Psychological Contract ◽  
Workplace Bullying ◽  
Psychological Capital ◽  
Turnover Rates ◽  
Passive Coping ◽  
Psychological Contract Violation ◽  
Current Transition ◽  
Free Environment ◽  
Contract Violation

Becoming impediment to organizational functioning in several ways, the prevalence of workplace bullying costs much to organizations. As in the current transition phase of Pakistan, the intentions to leave doesn’t manifest in actual turnover rates.  Hence the current study is conducted to analyze the passive coping strategies of employees in the face of workplace bullying. It is theorized that the relationship is mediated by psychological contract violation. Moreover, it is predicted that the process of mediation is stronger for individuals who report high levels of benevolent behavior and perceives psychological capital to be low. Data is collected from 359 young doctors and nurses of three government administered hospitals. Results indicate a significant bullying-silence relationship where psychological contract violation plays a role of partial mediator. Moreover, benevolence and PsyCap are powerful moderators to alter the already established relationship. Conclusions of the current study are further elaborated in terms of their practical contribution and future directions. Workplace bullying is an organizational reality. Hence efforts to make an entire bullying-free environment is next to impossible.  So, in addition to make an effort in ending up this maltreatment, managers must limit its consequences by understanding its dynamics. Reduce the bullying culture and save precious resources i.e. potential employees.

scholarly journals Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

2004 ◽  
Vol 279 (50) ◽  
pp. 51804-51816 ◽  
Author(s):  
Hagit Azriel-Tamir ◽  
Haleli Sharir ◽  
Betty Schwartz ◽  
Michal Hershfinkel
Keyword(s):  
Cell Proliferation ◽  
Map Kinase ◽  
Ph Homeostasis ◽  
Ht29 Cells ◽  
Intracellular Release ◽  
Map Kinase Pathway ◽  
Zinc Sensing ◽  
Multiple Signaling ◽  
Kinase Pathway

Extracellular zinc promotes cell proliferation and its deficiency leads to impairment of this process, which is particularly important in epithelial cells. We have recently characterized a zinc-sensing receptor (ZnR) linking extracellular zinc to intracellular release of calcium. In the present study, we addressed the role of extracellular zinc, acting via the ZnR, in regulating the MAP kinase pathway and Na+/H+exchange in colonocytes. We demonstrate that Ca2+release, mediated by the ZnR, induces phosphorylation of ERK1/2, which is highly metal-specific, mediated by physiological concentrations of extracellular Zn2+but not by Cd2+, Fe2+, Ni2+, or Mn2+. Desensitization of the ZnR by Zn2+, is followed by ∼90% inhibition of the Zn2+-dependent ERK1/2 phosphorylation, indicating that the ZnR is a principal link between extracellular Zn2+and ERK1/2 activation. Application of both the IP3pathway and PI 3-kinase antagonists largely inhibited Zn2+-dependent ERK1/2 phosphorylation. The physiological significance of the Zn2+-dependent activation of ERK1/2 was addressed by monitoring Na+/H+exchanger activity in HT29 cells and in native colon epithelium. Preincubation of the cells with zinc was followed by robust activation of Na+/H+exchange, which was eliminated by cariporide (0.5 μm); indicating that zinc enhances the activity of NHE1. Activation of NHE1 by zinc was totally blocked by the ERK1/2 inhibitor, U0126. Prolonged acidification, in contrast, stimulates NHE1 by a distinct pathway that is not affected by extracellular Zn2+or inhibitors of the MAP kinase pathway. Desensitization of ZnR activity eliminates the Zn2+-dependent, but not the prolonged acidification-dependent activation of NHE1, indicating that Zn2+-dependent activation of H+extrusion is specifically mediated by the ZnR. Our results support a role for extracellular zinc, acting through the ZnR, in regulating multiple signaling pathways that affect pH homeostasis in colonocytes. Furthermore activation of both, ERK and NHE1, by extracellular zinc may provide the mechanism linking zinc to enhanced cell proliferation.

scholarly journals The role of proneness to self-forgiveness in coping behaviour

2018 ◽  
Vol VI(163) (67) ◽  
pp. 74-77
Author(s):  
A. V. Sokur ◽  
E. L. Nosenko
Keyword(s):  
Coping Behaviour ◽  
Self Forgiveness

scholarly journals Stressor Appraisal on a Pathway to Health: The Role of the Sense of Coherence

2022 ◽  
pp. 69-78
Author(s):  
Maurice B. Mittelmark
Keyword(s):  
Sense Of Coherence ◽  
Central Place ◽  
Black Box ◽  
Coping Behaviour ◽  
Key Questions

AbstractIn this chapter, the focus is on how the sense of coherence (SOC) influences stressor appraisal, positively as well as negatively. The processes of stimulus appraisal have a central place in salutogenic theory, even if they have received relatively little theoretical and empirical attention since Aaron Antonovsky’s extensive treatment of stimulus appraisal in Unraveling the mystery of health: How people manage stress and stay well. The chapter aims to elevate researchers’ appreciation of stimulus appraisal as Antonovsky’s little-tested answer to three key questions: How does the SOC concept link to coping behaviour, what is the mechanism that makes the connection and what is the black box in between?

scholarly journals Infralimbic cortical glutamate output is necessary for the neural and behavioral consequences of chronic stress

2020 ◽  
Author(s):  
Sebastian A. Pace ◽  
Connor Christensen ◽  
Morgan K. Schackmuth ◽  
Tyler Wallace ◽  
Jessica M. McKlveen ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Forced Swim Test ◽  
Glutamate Release ◽  
Cortical Cell ◽  
Early Gene ◽  
Male Rats ◽  
Infralimbic Cortex ◽  
Passive Coping ◽  
Avoidance Behaviors

AbstractExposure to prolonged stress is a major risk-factor for psychiatric disorders such as generalized anxiety and major depressive disorder (MDD). Human imaging studies have identified structural and functional abnormalities in the prefrontal cortex of MDD patients, particularly Brodmann’s area 25 (BA25). Further, deep brain stimulation of BA25 reduces symptoms of treatment-resistant depression. The rat homolog of BA25 is the infralimbic cortex (IL), which is critical for cognitive appraisal, executive function, and physiological stress reactivity. Previous studies indicate that the IL undergoes stress-induced changes in excitatory/inhibitory balance culminating in reduced activity of glutamate output neurons. However, the regulatory role of IL glutamate output in mood-related behaviors after chronic variable stress (CVS) is unknown. Here, we utilized a lentiviral-packaged small-interfering RNA to reduce translation of vesicular glutamate transporter 1 (vGluT1 siRNA), thereby constraining IL glutamate output. This viral-mediated gene transfer was used in conjunction with a quantitative anatomical analysis of cells expressing the stable immediate-early gene product ΔFosB, which accumulates in response to repeated neural activation. Through assessment of ΔFosB-expressing neurons across the frontal lobe in adult male rats, we mapped regions altered by chronic stress and determined the coordinating role of the IL in frontal cortical plasticity. Specifically, CVS-exposed rats had increased density of ΔFosB-expressing cells in the IL and decreased density in the anterior insula. The latter effect was dependent on IL glutamate output. Next, we examined the interaction of CVS and reduced IL glutamate output in behavioral assays examining coping, anxiety-like behavior, associative learning, and nociception. IL glutamate knockdown decreased immobility during the forced swim test compared to GFP controls, both in rats exposed to CVS as well as rats without previous stress exposure. Further, vGluT1 siRNA prevented CVS-induced avoidance behaviors, while also reducing risk aversion and passive coping. Ultimately, this study identifies the necessity of IL glutamatergic output for regulating frontal cortical neural activity and behavior following chronic stress. These findings also highlight how disruption of excitatory/inhibitory balance within specific frontal cortical cell populations may impact neurobehavioral adaptation and lead to stress-related disorders.HighlightsChronic stress increased ΔFosB in the infralimbic cortex and decreased insular ΔFosBDecreased insular ΔFosB was dependent on infralimbic glutamate outputKnockdown of infralimbic glutamate release reduced passive copingAvoidance behaviors after chronic stress were dependent on infralimbic glutamateInfralimbic projections innervated excitatory and inhibitory neurons in the insula

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