Can't wait to pay: The desire for goal closure increases impatience for costs.

We explore whether the desire to achieve psychological closure on a goal creates impatience. If so, people should choose an earlier (vs. later) option, even when it does not deliver a reward. For example, they may prefer to pay money or complete work earlier rather than later. A choice to incur earlier costs seems to violate the preference for positive discounting (indeed, it may appear like negative time discounting), unless people value earlier goal closure. Across seven studies, we consistently find that people preferred to pay more money sooner over less money later (Study 1) and complete more work sooner over less work later (Studies 2-5) more when they had a stronger desire for goal closure, such as when the sooner option allowed them to achieve goal closure and when the goal would otherwise linger on their minds (compared to when it would not). The implications of goal closure extend to impatience for gains (Studies 6-7), as people preferred less money sooner (vs. more later) when it allowed them to achieve goal closure. These findings suggest that the desire to achieve goal closure is an important aspect of time preferences. Taking this desire into account can explain marketplace anomalies and inform interventions to reduce impatience. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

The psychology of negative-sum competition in strategic interactions.

Many real-life examples-from interpersonal rivalries to international conflicts-suggest that people actively engage in competitive behavior even when it is negative sum (benefiting the self at a greater cost to others). This often leads to loss spirals where everyone-including the winner-ends up losing. Our research seeks to understand the psychology of such negative-sum competition in a controlled setting. To do so, we introduce an experimental paradigm in which paired participants have the option to repeatedly perform a behavior that causes a relatively small gain for the self and a larger loss to the other. Although they have the freedom not to engage in the behavior, most participants actively do so and incur substantial losses. We propose that an important reason behind the phenomena is shallow thinking-focusing on the immediate benefit to the self while overlooking the downstream consequences of how the behavior will influence their counterparts' actions. In support of the proposition, we find that participants are less likely to engage in negative-sum behavior, if they are advised to consider the downstream consequences of their actions, or if they are put in a less frenzied decision environment, which facilitates deeper thinking (acting in discrete vs. continuous time). We discuss how our results differ from prior findings and the implications of our research for mitigating negative-sum competition and loss spirals in real life. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

On the role of similarity in mental accounting and hedonic editing.

The theory of mental accounting is often used to understand how people evaluate multiple outcomes or events. However, a model predicting which outcomes are associated with the same mental account and evaluated jointly, versus different accounts and evaluated separately, has remained elusive. We develop a framework that incorporates an online, bottom-up process of similarity and categorization into mental accounting operations. In this categorization-based model of mental accounting, outcomes that overlap on salient attributes are automatically categorized and assigned to the same mental account while outcomes that do not overlap on salient attributes are assigned to different accounts. We use this model to derive the hedonic accounting hypothesis, which generates testable behavioral predictions on people's preferences over the timing of outcomes given similarity-based constraints on mental accounting operations. Six studies provide support for the predictions: People prefer to experience similar losses close together in time and spread dissimilar losses apart; the reverse is true for gains, with a preference for dissimilar gains close together in time and similar gains spread apart across time. Importantly, our model is able to rationalize prior evidence that has found only limited support for the predictions of mental accounting and hedonic editing. Once the psychological process of similarity and categorization is explicitly incorporated into a formal model of mental accounting, its predictions are supported by the data. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

The impact of agency on time and risk preferences.

Scholars have long argued for the central role of agency-the size of one's choice set-in the human experience. We demonstrate the importance of agency in shaping people's preferences. We first examine the effects of resource scarcity-which has been associated with both impatience and a lack of agency-on patience and risk tolerance, successfully replicating the decrease in patience among those exposed to scarcity. Critically, however, we show that endowing individuals with agency over scarcity fully moderates this effect, increasing patience substantially. We further demonstrate that agency's impact on patience is partly driven by greater risk tolerance. These results hold even though nearly all individuals with greater agency do not exercise it, suggesting that merely knowing that one could alleviate scarcity is sufficient to change behavior. We then demonstrate that the effects of agency generalize to other adverse states, highlighting the potential for agency-based policy and institutional design.

Materazzi effect and the strategic use of anger in competitive interactions.

We propose that individuals use anger strategically in interactions. We first show that in some environments angering people makes them more effective in competitions, whereas in others, anger makes them less effective. We then show that individuals anticipate these effects and strategically use the option to anger their opponents. In particular, they are more likely to anger their opponents when anger negatively affects the opponents' performances. This finding suggests people understand the effects of emotions on behavior and exploit them to their advantage.

Plasminogen activator inhibitor-1 regulates integrin alphavbeta3 expression and autocrine transforming growth factor beta signaling.

Fibrosis is characterized by elevated transforming growth factor beta (TGFbeta) signaling, resulting in extracellular matrix accumulation and increased PAI-1 (plasminogen activator inhibitor) expression. PAI-1 induces the internalization of urokinase plasminogen activator/receptor and integrin alphavbeta3 from the cell surface. Since increased alphavbeta3 expression correlates with increased TGFbeta signaling, we hypothesized that aberrant PAI-1-mediated alphavbeta3 endocytosis could initiate an autocrine loop of TGFbeta activity. We found that in PAI-1 knock-out (KO) mouse embryonic fibroblasts), alphavbeta3 endocytosis was reduced by approximately 75%, leaving alphavbeta3 in enlarged focal adhesions, similar to wild type cells transfected with PAI-1 small interfering RNA. TGFbeta signaling was significantly enhanced in PAI-1 KO cells, as demonstrated by a 3-fold increase in SMAD2/3-containing nuclei and a 2.9-fold increase in TGFbeta activity that correlated with an increase in alphavbeta3 and TGFbeta receptor II expression. As expected, PAI-1 KO cells had unregulated plasmin activity, which was only partially responsible for TGFbeta activation, as evidenced by a mere 25% reduction in TGFbeta activity when plasmin was inhibited. Treatment of cells with an alphavbeta3-specific cyclic RGD peptide (GpenGRGD) led to a more profound (59%) TGFbeta inhibition; a nonspecific RGD peptide (GRGDNP) inhibited TGFbeta by only 23%. Human primary fibroblasts were used to confirm that PAI-1 inhibition and beta3 overexpression led to an increase in TGFbeta activity. Consistent with a fibrotic phenotype, PAI-1 KO cells were constitutively myofibroblasts that had a 1.6-fold increase in collagen deposition over wild type cells. These data suggest that PAI-1-mediated regulation of alphavbeta3 integrin is critical for the control of TGFbeta signaling and the prevention of fibrotic disease.