scholarly journals Gratitude Expressions Improve Teammates’ Cardiovascular Stress Responses

2020 ◽  
Author(s):  
Yumeng Gu ◽  
Joseph Manuel Andrew Ocampo ◽  
Christopher Oveis ◽  
Sara Algoe
Keyword(s):  
Stress Responses ◽  
Positive Emotions ◽  
Collaborative Work ◽  
Peripheral Resistance ◽  
Individual Performance ◽  
Adaptive Responses ◽  
Social Functions ◽  
Biological Responses ◽  
Stress Responding

Gratitude expressions play a key role in strengthening relationships, suggesting gratitude might promote adaptive responses during teamwork. However, little research has examined gratitude’s impact on loose tie relationships (like coworkers), and similarly little research has examined how gratitude impacts stress responding or biological responses more generally. The present research uses an ecologically valid, dyadic teamwork paradigm to test how gratitude expressions impact in vivo challenge and threat stress responding, assessed via an index of cardiac output and total peripheral resistance. Compared to a control condition, teammates (N = 190) who were randomly assigned to a gratitude expression manipulation showed increased cardiovascular efficiency while jointly completing an acutely stressful collaborative work task (developing a product pitch). These effects persisted later in the session when the teammates completed an individual performance task (pitching the product). The finding that gratitude expressions promote adaptive biological responding at the dyadic level contributes to a growing literature on the social functions of positive emotions and gratitude, specifically. The present results suggest that workplace gratitude interventions can benefit stress responding, promoting resilience in teams

scholarly journals Emotion Regulation Contagion: Stress Reappraisal Promotes Challenge Responses in Teammates

2018 ◽  
Author(s):  
Christopher Oveis ◽  
Yumeng Gu ◽  
Joseph Manuel Ocampo ◽  
Emily J Hangen ◽  
Jeremy Jamieson
Keyword(s):  
Emotion Regulation ◽  
Stress Responses ◽  
Collaborative Work ◽  
Peripheral Resistance ◽  
Individual Performance ◽  
Face To Face ◽  
Individual Work ◽  
The Face ◽  
The Individual

How does emotion regulation impact teammates? We present data from a dyadic experiment(N=266) that assessed in vivo stress responses in teammates during collaborative (a face-to-face product design task) and then individual work (a product pitch to evaluators). Throughout the experiment, one manipulated teammate reappraised their stress arousal (reappraisal), suppressed their emotional displays (suppression), or received no instructions (control). Their non- manipulated teammate received no instructions. Stress reappraisal benefited both teammates, eliciting challenge-like physiological responses (higher cardiac output, lower total peripheral resistance) relative to the suppression and control conditions. These effects were observed during both face-to-face collaborative work and later individual work. A mediation model suggests that the face-to-face social contagion effects of stress reappraisal fed forward to promote non- manipulated teammates’ improved stress responses during the individual performance task. These findings indicate that non-manipulated teammates exhibited improved stress responses simply by interacting with a person who reappraised their stress as functional.

scholarly journals The human hepatocyte TXG-MAPr: WGCNA transcriptomic modules to support mechanism-based risk assessment

2021 ◽  
Author(s):  
Giulia Callegaro ◽  
Steven J. Kunnen ◽  
Panuwat Trairatphisan ◽  
Solene Grosdidier ◽  
Marije Niemeijer ◽  
...  
Keyword(s):  
Risk Assessment ◽  
Stress Responses ◽  
Safety Testing ◽  
Support Mechanism ◽  
Mechanisms Of Toxicity ◽  
Biological Responses ◽  
R Shiny ◽  
Rat Primary Hepatocytes ◽  
Promising Source

Mechanism-based risk assessment is urged to advance and fully permeate into current safety assessment practices, possibly at early phases of drug safety testing. Toxicogenomics is a promising source of comprehensive and mechanisms-revealing data, but analysis tools to interpret mechanisms of toxicity and specific for the testing systems (e.g. hepatocytes) are lacking. In this study we present the TXG-MAPr webtool (available at https://txg-mapr.eu/WGCNA_PHH/TGGATEs_PHH/), an R-Shiny-based implementation of weighted gene co-expression networks (WGCNA) obtained from the Primary Human Hepatocytes (PHH) TG-GATEs dataset. Gene co-expression networks (modules) were annotated with functional information (pathway enrichment, transcription factor) to reveal their mechanistic interpretation. Several well-known stress response pathways were captured in the modules, are perturbed by specific stressors and show preserved in rat systems (rat primary hepatocytes and rat in vivo liver), highlighting stress responses that translate across species/testing systems. The TXG-MAPr tool was successfully applied to investigate the mechanism of toxicity of TG-GATEs compounds and using external datasets obtained from different hepatocyte cells and microarray platforms. Additionally, we suggest that module responses can be calculated from targeted RNA-seq data therefore imputing biological responses from a limited gene. By analyzing 50 different PHH donors' responses to a common stressor, tunicamycin, we were able to suggest modules associated with donor's traits, e.g. pre-existing disease state, therefore connected to donors' variability. In conclusion, we demonstrated that gene co-expression analysis coupled to an interactive visualization environment, the TXG-MAPr, is a promising approach to achieve mechanistic relevant, cross-species and cross-platform evaluation of toxicogenomic data.

Kinase Targets for Mycolic Acid Biosynthesis in Mycobacterium tuberculosis

2019 ◽  
Vol 12 (1) ◽  
pp. 27-49 ◽  
Author(s):  
Shahinda S.R. Alsayed ◽  
Chau C. Beh ◽  
Neil R. Foster ◽  
Alan D. Payne ◽  
Yu Yu ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Enzymatic Activity ◽  
Bacterial Pathogen ◽  
Building Blocks ◽  
Mycolic Acid ◽  
Adaptive Responses ◽  
Mycolic Acids ◽  
Hydroxylated Fatty Acids

Background:Mycolic acids (MAs) are the characteristic, integral building blocks for the mycomembrane belonging to the insidious bacterial pathogen Mycobacterium tuberculosis (M.tb). These C60-C90 long α-alkyl-β-hydroxylated fatty acids provide protection to the tubercle bacilli against the outside threats, thus allowing its survival, virulence and resistance to the current antibacterial agents. In the post-genomic era, progress has been made towards understanding the crucial enzymatic machineries involved in the biosynthesis of MAs in M.tb. However, gaps still remain in the exact role of the phosphorylation and dephosphorylation of regulatory mechanisms within these systems. To date, a total of 11 serine-threonine protein kinases (STPKs) are found in M.tb. Most enzymes implicated in the MAs synthesis were found to be phosphorylated in vitro and/or in vivo. For instance, phosphorylation of KasA, KasB, mtFabH, InhA, MabA, and FadD32 downregulated their enzymatic activity, while phosphorylation of VirS increased its enzymatic activity. These observations suggest that the kinases and phosphatases system could play a role in M.tb adaptive responses and survival mechanisms in the human host. As the mycobacterial STPKs do not share a high sequence homology to the human’s, there have been some early drug discovery efforts towards developing potent and selective inhibitors.Objective:Recent updates to the kinases and phosphatases involved in the regulation of MAs biosynthesis will be presented in this mini-review, including their known small molecule inhibitors.Conclusion:Mycobacterial kinases and phosphatases involved in the MAs regulation may serve as a useful avenue for antitubercular therapy.

scholarly journals Increasing Solvent Tolerance to Improve Microbial Production of Alcohols, Terpenoids and Aromatics

2021 ◽  
Vol 9 (2) ◽  
pp. 249
Author(s):  
Thomas Schalck ◽  
Bram Van den Bergh ◽  
Jan Michiels
Keyword(s):  
Stress Responses ◽  
Small Rnas ◽  
Defense Mechanisms ◽  
Industrial Processes ◽  
Solvent Tolerance ◽  
Adaptive Responses ◽  
Environment Friendly ◽  
Pathway Optimization ◽  
Polymer Precursors ◽  
Product Accumulation

Fuels and polymer precursors are widely used in daily life and in many industrial processes. Although these compounds are mainly derived from petrol, bacteria and yeast can produce them in an environment-friendly way. However, these molecules exhibit toxic solvent properties and reduce cell viability of the microbial producer which inevitably impedes high product titers. Hence, studying how product accumulation affects microbes and understanding how microbial adaptive responses counteract these harmful defects helps to maximize yields. Here, we specifically focus on the mode of toxicity of industry-relevant alcohols, terpenoids and aromatics and the associated stress-response mechanisms, encountered in several relevant bacterial and yeast producers. In practice, integrating heterologous defense mechanisms, overexpressing native stress responses or triggering multiple protection pathways by modifying the transcription machinery or small RNAs (sRNAs) are suitable strategies to improve solvent tolerance. Therefore, tolerance engineering, in combination with metabolic pathway optimization, shows high potential in developing superior microbial producers.

scholarly journals Methane and Inflammation - A Review (Fight Fire with Fire)

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Marietta Zita Poles ◽  
László Juhász ◽  
Mihály Boros
Keyword(s):  
Stress Responses ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion ◽  
Signalling Pathways ◽  
Experimental Conditions ◽  
Neuroprotective Effects ◽  
Oxidative And Nitrosative Stress ◽  
Carbohydrate Fermentation ◽  
Insight Into

AbstractMammalian methanogenesis is regarded as an indicator of carbohydrate fermentation by anaerobic gastrointestinal flora. Once generated by microbes or released by a non-bacterial process, methane is generally considered to be biologically inactive. However, recent studies have provided evidence for methane bioactivity in various in vivo settings. The administration of methane either in gas form or solutions has been shown to have anti-inflammatory and neuroprotective effects in an array of experimental conditions, such as ischemia/reperfusion, endotoxemia and sepsis. It has also been demonstrated that exogenous methane influences the key regulatory mechanisms and cellular signalling pathways involved in oxidative and nitrosative stress responses. This review offers an insight into the latest findings on the multi-faceted organ protective activity of exogenous methane treatments with special emphasis on its versatile effects demonstrated in sepsis models.

Increased ACTH response to corticotropin-releasing factor in cold-adapted rats in vivo

1989 ◽  
Vol 257 (3) ◽  
pp. E336-E339 ◽  
Author(s):  
A. Uehara ◽  
Y. Habara ◽  
A. Kuroshima ◽  
C. Sekiya ◽  
Y. Takasugi ◽  
...  
Keyword(s):  
Stress Responses ◽  
Cold Adaptation ◽  
Corticotropin Releasing Factor ◽  
Plasma Acth ◽  
Cold Adapted ◽  
Repeated Restraint Stress ◽  
Cross Adaptation ◽  
Freely Moving ◽  
Increased Activity

We have recently reported that chronically repeated restraint stress results in improved cold tolerance in rats via an increased activity of nonshivering thermogenesis, a characteristic metabolic change observed during cold adaptation, suggesting the presence of cross-adaptation between cold and stress. It is well established that the hypothalamic-pituitary-adrenal (HPA) axis is activated in various stress responses. In the present study, therefore, we examined whether cold adaptation would alter the adrenocorticotropic hormone (ACTH)-releasing state in vivo using freely moving, conscious rats chronically implanted with intra-atrial cannulas. There was no difference in the basal levels of plasma ACTH between warm control and cold-adapted rats. On the other hand, the ACTH response to the intravenous administration of corticotropin-releasing factor (CRF; 2 micrograms/animal) was significantly elevated in cold-adapted rats. However, the injection of 10 micrograms of CRF, which was considered as a dose to elicit the maximal ACTH response, resulted in similar ACTH release patterns between the two groups. These changes in the responsiveness of ACTH secretion have been observed in rats chronically exposed to stressful conditions. The results demonstrated in the present study, therefore, provide further evidence for our hypothesis that there may exist cross-adaptation between cold and nonthermal stress.

scholarly journals RAE-1 ligands for the NKG2D receptor are regulated by E2F transcription factors, which control cell cycle entry

2012 ◽  
Vol 209 (13) ◽  
pp. 2409-2422 ◽  
Author(s):  
Heiyoun Jung ◽  
Benjamin Hsiung ◽  
Kathleen Pestal ◽  
Emily Procyk ◽  
David H. Raulet
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Stress Responses ◽  
Transcriptional Activation ◽  
Posttranscriptional Regulation ◽  
Cellular Proliferation ◽  
Control Cell ◽  
T Cell Subsets ◽  
Cell Cycle Entry

The NKG2D stimulatory receptor expressed by natural killer cells and T cell subsets recognizes cell surface ligands that are induced on transformed and infected cells and facilitate immune rejection of tumor cells. We demonstrate that expression of retinoic acid early inducible gene 1 (RAE-1) family NKG2D ligands in cancer cell lines and proliferating normal cells is coupled directly to cell cycle regulation. Raet1 genes are directly transcriptionally activated by E2F family transcription factors, which play a central role in regulating cell cycle entry. Induction of RAE-1 occurred in primary cell cultures, embryonic brain cells in vivo, and cells in healing skin wounds and, accordingly, wound healing was delayed in mice lacking NKG2D. Transcriptional activation by E2Fs is likely coordinated with posttranscriptional regulation by other stress responses. These findings suggest that cellular proliferation, as occurs in cancer cells but also other pathological conditions, is a key signal tied to immune reactions mediated by NKG2D-bearing lymphocytes.

Responses to social evaluative stress in regular cannabis smokers

2021 ◽  
pp. 026988112097233
Author(s):  
Richard J Xia ◽  
Thomas Chao ◽  
Divya Patel ◽  
Gillinder Bedi
Keyword(s):  
Heart Rate ◽  
Stress Responses ◽  
Social Stress ◽  
Physiological Stress ◽  
Negative Mood ◽  
Mood States ◽  
Residual Effects ◽  
Subjective Response ◽  
Negative Mood States ◽  
Stress Responding

Background: Aspects of the canonical stress response differ in stimulant, opioid, and alcohol users relative to controls, and dysregulated responses to stress may contribute to continued use of these drugs. Little prior research has focused on stress responses in regular cannabis smokers. We assessed responses to a standardized laboratory social stress assay (the Trier Social Stress Task; TSST) in regular cannabis smokers (CANs) compared with controls (CONs). Methods: Healthy, non-treatment-seeking adult CANs (⩾4×/week; smoking cannabis as usual) and demographically matched CONs completed the TSST. Outcome measures were subjective mood, heart rate, and salivary cortisol. Results: Nineteen CANs (1 female) and 20 CONs (2 female) participated; groups were matched on trauma exposure, sex, race, and age. CANs smoked cannabis 6.4 ± 1.1 days/week. Eight CANs and one CON smoked tobacco cigarettes daily. Overall, the TSST produced expected increases in anxiety, negative mood states, cortisol, and heart rate. CANs had blunted subjective response to stress relative to CONs, but they did not differ in physiological (cortisol and cardiovascular) stress responding. Conclusion: These results indicate that CANs have blunted mood responses to social stress, but normative physiological stress responding. Observed differences could be due to residual effects of cannabis, reluctance to endorse negative mood states, or to issues related to identifying (i.e., emotional identification) or feeling (i.e., interoception) stress-related affective states. Further research is warranted to characterize the mechanisms of these differences and assess implications for daily functioning and treatment outcomes.

scholarly journals NIK promotes metabolic adaptation of glioblastoma cells to bioenergetic stress

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Michael L. Kamradt ◽  
Ji-Ung Jung ◽  
Kathryn M. Pflug ◽  
Dong W. Lee ◽  
Victor Fanniel ◽  
...  
Keyword(s):  
Stress Responses ◽  
Glucose Deprivation ◽  
Metabolic Adaptation ◽  
Mitochondrial Morphology ◽  
Atp Production ◽  
Tumor Microenvironments ◽  
Iκb Kinase ◽  
Critical Measure

AbstractCancers, including glioblastoma multiforme (GBM), undergo coordinated reprogramming of metabolic pathways that control glycolysis and oxidative phosphorylation (OXPHOS) to promote tumor growth in diverse tumor microenvironments. Adaptation to limited nutrient availability in the microenvironment is associated with remodeling of mitochondrial morphology and bioenergetic capacity. We recently demonstrated that NF-κB-inducing kinase (NIK) regulates mitochondrial morphology to promote GBM cell invasion. Here, we show that NIK is recruited to the outer membrane of dividing mitochondria with the master fission regulator, Dynamin-related protein1 (DRP1). Moreover, glucose deprivation-mediated metabolic shift to OXPHOS increases fission and mitochondrial localization of both NIK and DRP1. NIK deficiency results in decreased mitochondrial respiration, ATP production, and spare respiratory capacity (SRC), a critical measure of mitochondrial fitness. Although IκB kinase α and β (IKKα/β) and NIK are required for OXPHOS in high glucose media, only NIK is required to increase SRC under glucose deprivation. Consistent with an IKK-independent role for NIK in regulating metabolism, we show that NIK phosphorylates DRP1-S616 in vitro and in vivo. Notably, a constitutively active DRP1-S616E mutant rescues oxidative metabolism, invasiveness, and tumorigenic potential in NIK−/− cells without inducing IKK. Thus, we establish that NIK is critical for bioenergetic stress responses to promote GBM cell pathogenesis independently of IKK. Our data suggest that targeting NIK may be used to exploit metabolic vulnerabilities and improve therapeutic strategies for GBM.

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