Interdependence of emotion: Conceptualization, evidence, and social implications from cultural psychology

People feel a wide range of emotions. In many psychological traditions, emotions are defined as primarily emerging from within the individual, even if influenced by external factors (e.g., approval from other people). This definition is consistent with an independent self-construal. However, in some contexts, emotions are understood to have more interdependent characteristics that can be shared with other people and that arise from social contexts and collective, shared situations. We define the lay theory of interdependence of emotion as the perception that emotional experience or its causes and consequences are shared with other people. Interdependence of emotion can be conceptualized along a spectrum, rather than as categorical. Additionally, the degree to which people understand emotions as interdependent likely varies by cultural context. In this article, we review studies that have investigated this lay theory of emotions across cultures, focusing on function. We suggest that people from non-WEIRD cultures (i.e., cultures that are not Western, Educated, Industrialized, Rich, and Democratic) are more likely than others to experience emotions as interdependent. Next, we highlight examples of this interdependence, focusing on two specific emotions: happiness and awe, which may have both independent and interdependent elements. The mechanisms and functions of the lay theory of interdependence of emotions are discussed using the example of a current collective threat, COVID-19

The effect of voluntary exercise training on LPS-induced TNF-alpha after exhaustive exercise

OBJECTIVES: Acute strenuous exercise attenuates inflammatory cytokine production. The attenuation after strenuous exercise is due to the effect of catecholamine. Voluntary exercise training has many beneficial effects, for example enhanced immune function at rest. However, little is known that the influence of voluntary exercise training on pro-inflammatory cytokine in response to pathogen. In this study, we investigated the effect of voluntary exercise training on production of tumor necrosis factor (TNF)-alpha in response to lipopolysaccharide (LPS) after strenuous exercise. METHODS: Female F344 rats were divided into two groups, voluntary training and sedentary. The voluntary trained rats engaged in wheel running for 10 weeks, while the sedentary rats remained in their cages. After 10 weeks, all rats were treated an exhaustive exercise or a rest for 2 h. The exhaustive exercise was a treadmill running exercise until exhaustion. To measure catecholamine and TNF-alpha concentrations, and TNF-alpha mRNA expression in tissue in response to LPS, the rats received an injection of LPS and were killed 1 h after the LPS injection. RESULTS: Running time until exhaustion in voluntary trained rats was significantly longer than that in sedentary rats (p\u3c0.01). Plasma adrenaline after exhaustive exercise was significantly higher than that in sedentary rats (p\u3c0.01). LPS-induced TNF-alpha concentration in plasma significantly differs by presence or absence of voluntary training and exhaustive exercise (p\u3c0.01, respectively). Although voluntary training significantly reduced the protein content of TNF-alpha in kidney at rest (p\u3c0.05), exhaustive exercise did not affect TNF-alpha in response to LPS in kidney. Also, neither the exhaustive exercise did affect in mRNA expression of TNF-alpha in kidney in trained rats. CONCLUSION: These results suggest that voluntary exercise training may have little effect on the improvement of TNF-alpha response after exhaustive exercise, although voluntary training has a role in reducing LPS-induced TNF-alpha contenet at rest in kidney

Relationship Between Macrophage Differentiation And The Chemotactic Activity Toward Damaged Muscle Cells

Aim: We investigated the effect of macrophage differentiation on the chemotactic activity to invade local damaged muscle using in vitro models of muscle injury. Methods: C2C12 cell myoblasts, and J774 cell macrophages were used. The “killed-C2C12” cells were combined with live C2C12 cells (live:killed C2C12 = 1:0.5) as a partially damaged muscle model. The J774 cells were stimulated with LPS and DEX. The chemotactic activity of J774 cells was examined using TAXIScan device. Results: Although the velocity of J774 cells was little affected by each type of C2C12 cells (live, killed and combination), the directionality of the J774 cells was increased. The highest directionality of J774 cells was observed when the ratio of live-:killed-C2C12 cells was 1:0.5.The TLR4 and CD11c expressions of LPS cells were higher than those in both Ctrl and DEX cells. The LPS cells were strongly stained around the cell membrane by phalloidin, but the F-actin expression in DEX cells was in an orderly line along the long axis of cells. DEX cells showed stretching toward C2C12 cells, and their length/width ratio was higher than that in both Ctrl and LPS cells. Although the chemotactic activity of LPS cells disappeared completely, DEX cells exhibited accelerated chemotactic activity toward damaged muscle cells. The MCP-1 production in live-:killed-C2C12 cells was higher than that in the live-C2C12 cells. The CCR2 expression in DEX cells was higher than that in both Ctrl and LPS cells. Conclusion: Our conclusion is that: 1) the chemotactic activity of macrophages toward areas of damaged muscle induces more live myoblasts than damaged cells, 2) the chemotactic activity of macrophages is not due to velocity, but depends on the directionality toward damaged muscle cells, and 3) macrophage differentiation influences their chemotactic activity toward damaged muscle cells through the expression of CCR2 and/or F-actin

Exhaustive Exercise Enhances Immune Response To Flagellin Via Adrenaline-Mediated Up-Regulation of TLR5 Expression

Objective: We already reported that lipopolysacchride (LPS)-induced tumor necrosis factor (TNF)-α production as a bacterial infection model to induce immune response, was inhibited by exhaustive exercise. However, it remains unclear whether or not the immune response to flagellin (FG), which binds to toll like receptor 5(TLR5) and induces pro-inflammatory cytokine production, is also inhibited by this severe exercise. The aim of this study was to determine whether or not exhaustive exercise affects TNF-α productions after FG injection in mice. Methods: Both exhaustive-exercised (EX; n=12) and non-exercised (N-EX; n=12) male C3H/HeN mice were injected with FG (1 mg/kg, i.v), and blood samples were collected. In addition, to clarify the effect of catecholamine on immune response macrophage and intestinal cells after FG stimulation, RAW264 cells and Caco2 cells were cultured 30min after propranolol (Prop; β-adrenergic receptors blocker) or Ly294002 (Ly; PI3K inhibitor) treatments, and were then stimulated with adrenaline (AD; 1 μM) and FG (5 μg/ml). Moreover, the effect of Prop (10 mg/kg, n=12) on FG-induced TNF-α production in EX mice was also examined. Results: TNF-α in EX group was significantly higher than that in N-EX group after FG injection. In epithelium cells, more intensity of TLR5 localization was observed on the plasma membrane area than in the cytosol area in EX mice, but not N-EX mice. Caco2 cells, but not RAW264 cells, significantly increased the FG-induced TNF-α production using AD treatment. Moreover, Prop treatment attenuated the AD-induced TNF-α production in response to FG in Caco2 cells. Although TLR5 expression on RAW264 cells was significantly decreased after AD treatment, the expression on Caco2 cells was rapidly increased. In fact, we observed the AD-dependent TLR5 translocation from cytoplasm to cell membrane in Caco2 cells, and the membrane translocation was inhibited by Prop and Ly treatment. Moreover, the pretreatment with Prop attenuated the exercise-induced plasma TNF-α response to FG in vivo. Conclusion: Our results suggest that immune response to FG via TLR5 might be enhanced by exhaustive exercise in mice

Oncostatin M suppresses IL31RA expression in dorsal root ganglia and interleukin-31-induced itching

BackgroundAtopic dermatitis (AD) is a chronic inflammatory skin disease characterized by intermittent itchy rash. Type 2 inflammatory cytokines such as interleukin (IL)-4, IL-13, and IL-31 are strongly implicated in AD pathogenesis. Stimulation of IL-31 cognate receptors on C-fiber nerve endings is believed to activate neurons in the dorsal root ganglion (DRG), causing itch. The IL-31 receptor is a heterodimer of OSMRβ and IL31RA subunits, and OSMRβ can also bind oncostatin M (OSM), a pro-inflammatory cytokine released by monocytes/macrophages, dendritic cells, and T lymphocytes. Further, OSM expression is enhanced in the skin lesions of AD and psoriasis vulgaris patients.ObjectiveThe current study aimed to examine the contributions of OSM to AD pathogenesis and symptom expression.MethodsThe expression levels of the OSM gene (OSM) and various cytokine receptor genes were measured in human patient skin samples, isolated human monocytes, mouse skin samples, and mouse DRG by RT-qPCR. Itching responses to various pruritogens were measured in mice by counting scratching episodes.ResultsWe confirmed overexpression of OSM in skin lesions of patients with AD and psoriasis vulgaris. Monocytes isolated from the blood of healthy subjects overexpressed OSM upon stimulation with IL-4 or GM-CSF. Systemic administration of OSM suppressed IL31RA expression in the mouse DRG and IL-31-stimulated scratching behavior. In contrast, systemic administration of OSM increased the expression of IL-4- and IL-13-related receptors in the DRG.ConclusionThese results suggest that OSM is an important cytokine in the regulation of skin monocytes, promoting the actions of IL-4 and IL-13 in the DRG and suppressing the action of IL-31. It is speculated that OSM released from monocytes in skin modulates the sensitivity of DRG neurons to type 2 inflammatory cytokines and thereby the severity of AD-associated skin itch

Cerebral air embolism as a complication of peptic ulcer in the gastric tube: case report

<p>Abstract</p> <p>Background</p> <p>The reported incidence of ulcer formation in the gastric tube in esophageal replacement is rare.</p> <p>Case Presentation</p> <p>This is the first report of a case of cerebral air embolism as a result of spontaneous perforation of an ulcer in the constructed gastric tube into the pulmonary vein during post-operative follow-up in a patient with esophageal cancer.</p> <p>Conclusions</p> <p>Cerebral air embolism is a rare complication of penetrating gastric ulcer, but should be considered in patients with a history of esophagectomy with gastric conduit that present with acute neurologic findings.</p