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Experiments prompting people to engage in more prosocial behavior (e.g., acts of kindness) or simple social interactions (e.g., acting extraverted) have both shown promise in boosting well-being. However, little is known about how much the impact on well-being depends on the type of interpersonal interaction (i.e., social vs. prosocial) or on other proximal features (e.g., whether the interaction takes place online vs. in-person, the closeness of the relationship, or amount of social connection associated with a given interaction). We randomly assigned a sample of full-time employees recruited via a special employed mTurk sample (N = 754) to perform weekly acts of kindness online versus in-person, to engage in weekly social interactions online versus in-person, or to list their daily activities (control) over the course of 4 weeks. First, on average, all conditions reported improvements in well-being (i.e., increases in positive affect and life satisfaction, decreases in negative affect) across the 4-week intervention period. Second, relative to controls, the four experimental groups reported increases in general social connectedness over time. Finally, according to auxiliary analyses collapsed across the experimental condition, closer relationship with target and non-digital medium of delivery predicted episode-level social connection, which, in turn, was associated with general social connectedness and positive affect. We conclude that the "who" and the "how" of a behavior (i.e., its target, its delivery method, and the feelings of social connection generated) are important for well-being, but not the "what" (i.e., whether the behavior is social or prosocial). (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Experiments prompting people to engage in more prosocial behavior (e.g., acts of kindness) or simple social interactions (e.g., acting extraverted) have both shown promise in boosting well-being. However, little is known about how much the impact on well-being depends on the type of interpersonal interaction (i.e., social versus prosocial) or on other proximal features (e.g., whether the interaction takes place online versus in-person, the closeness of the relationship, or in-the-moment social connection). We randomly assigned a sample of full-time employees recruited via mTurk (N = 754) to perform weekly acts of kindness online vs. in person, to engage in weekly social interactions online vs. in person, or to list their daily activities (control) over the course of 4 weeks. First, on average, all conditions reported improvements in well-being (i.e., increases in positive affect and life satisfaction, decreases in negative affect) across the 4-week intervention period. Second, relative to controls, the four experimental groups reported increases in general social connectedness over time. Finally, according to auxiliary analyses collapsed across experimental condition, closer relationship with target and non-digital medium of delivery predicted in-the-moment (or episode-level) social connection, which, in turn, was associated with general social connectedness and positive affect. We conclude that the “who” and the “how” of a behavior (i.e., its target, its delivery method, and the feelings of social connection generated) may be as important for well-being as the “what” (i.e., whether the behavior is social or prosocial).

The adenosine 5′-triphosphate-gated P2X4 receptor channel is a promising target in neuroinflammatory disorders, but the ability to effectively target these receptors in models of neuroinflammation has presented a constant challenge. As such, the exact role of P2X4 receptors and their cell signalling mechanisms in human physiology and pathophysiology still requires further elucidation. To this end, research into the molecular mechanisms of P2X4 receptor activation, modulation, and inhibition has continued to gain momentum in an attempt to further describe the role of P2X4 receptors in neuroinflammation and other disease settings. Here we provide an overview of the current understanding of the P2X4 receptor, including its expression and function in cells involved in neuroinflammatory signalling. We discuss the pharmacology of P2X4 receptors and provide an overview of P2X4-targeting molecules, including agonists, positive allosteric modulators, and antagonists. Finally, we discuss the use of P2X4 receptor modulators and antagonists in models of neuroinflammatory cell signalling and disease.

Purinergic receptors of the P2 subclass are commonly found in human and rodent macrophages where they can be activated by adenosine 5′-triphosphate (ATP) or uridine 5′-triphosphate (UTP) to mediate Ca2+ mobilization, resulting in downstream signalling to promote inflammation and pain. However, little is understood regarding these receptors in canine macrophages. To establish a macrophage model of canine P2 receptor signalling, the expression of these receptors in the DH82 canine macrophage cell line was determined by reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemistry. P2 receptor function in DH82 cells was pharmacologically characterised using nucleotide-induced measurements of Fura-2 AM-bound intracellular Ca2+. RT-PCR revealed predominant expression of P2X4 receptors, while immunocytochemistry confirmed predominant expression of P2Y2 receptors, with low levels of P2X4 receptor expression. ATP and UTP induced robust Ca2+ responses in the absence or presence of extracellular Ca2+. ATP-induced responses were only partially inhibited by the P2X4 receptor antagonists, 2′,3′-O-(2,4,6-trinitrophenyl)-ATP (TNP-ATP), paroxetine and 5-BDBD, but were strongly potentiated by ivermectin. UTP-induced responses were near completely inhibited by the P2Y2 receptor antagonists, suramin and AR-C118925. P2Y2 receptor-mediated Ca2+ mobilization was inhibited by U-73122 and 2-aminoethoxydiphenyl borate (2-APB), indicating P2Y2 receptor coupling to the phospholipase C and inositol triphosphate signal transduction pathway. Together this data demonstrates, for the first time, the expression of functional P2 receptors in DH82 canine macrophage cells and identifies a potential cell model for studying macrophage-mediated purinergic signalling in inflammation and pain in dogs.

The current study investigates whether perceived time has an effect on blood glucose level in people with type 2 diabetes. The hypothesis is that perceived time will have a greater influence over blood glucose level than actual time. Changes in blood glucose levels were measured in 46 participants with diabetes while they completed simple tasks during a 90-min period. Participants' perception of time was manipulated by having them refer to clocks that were either accurate or altered to run fast or slow. Blood glucose levels changed in accordance with how much time they believed had passed instead of how much time had actually passed. These results are an example of the influence psychological processes can directly exert on the body. [ABSTRACT FROM AUTHOR]

Purinergic receptors of the P2 subclass are commonly found in human and rodent macrophages where they can be activated by adenosine 5′-triphosphate (ATP) or uridine 5′-triphosphate (UTP) to mediate Ca2+ mobilization, resulting in downstream signalling to promote inflammation and pain. However, little is understood regarding these receptors in canine macrophages. To establish a macrophage model of canine P2 receptor signalling, the expression of these receptors in the DH82 canine macrophage cell line was determined by reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemistry. P2 receptor function in DH82 cells was pharmacologically characterised using nucleotide-induced measurements of Fura-2 AM-bound intracellular Ca2+. RT-PCR revealed predominant expression of P2X4 receptors, while immunocytochemistry confirmed predominant expression of P2Y2 receptors, with low levels of P2X4 receptor expression. ATP and UTP induced robust Ca2+ responses in the absence or presence of extracellular Ca2+. ATP-induced responses were only partially inhibited by the P2X4 receptor antagonists, 2′,3′-O-(2,4,6-trinitrophenyl)-ATP (TNP-ATP), paroxetine and 5-BDBD, but were strongly potentiated by ivermectin. UTP-induced responses were near completely inhibited by the P2Y2 receptor antagonists, suramin and AR-C118925. P2Y2 receptor-mediated Ca2+ mobilization was inhibited by U-73122 and 2-aminoethoxydiphenyl borate (2-APB), indicating P2Y2 receptor coupling to the phospholipase C and inositol triphosphate signal transduction pathway. Together this data demonstrates, for the first time, the expression of functional P2 receptors in DH82 canine macrophage cells and identifies a potential cell model for studying macrophage-mediated purinergic signalling in inflammation and pain in dogs. [ABSTRACT FROM AUTHOR]