Ruiqi Zhao

Humour is regarded as an adaptive coping strategy which could effectively reduce negative emotions. To fundamentally evaluate the function of humour reappraisal, our study aimed to explore the emotion-regulatory advantage effect of humour reappraisal from the perspective of memory mechanisms. Using a learning-testing paradigm, we examined the memory effects of humour reappraisal: first presented humour (or non-humour) reappraisal interpretations of the negative pictures during the learning phase and tested the memory performance from three aspects: free recall, recognition, and implicit memory in the test phase. The results found a superior effect of humorous reappraisal in free recall performance but reduced memory performance for negative stimuli in the recognition and implicit tests. This may be due to the refined processing of humour reappraisal during encoding, the memory content being updated and transformed after cognitive reconstruction, and the original negative pictures no longer being familiar during recognition. The dissociable result in free recall and implicit/recognition of humorous reappraisal suggested that humour reappraisal was an optimal strategy for coping with negative stimuli by fundamentally regulating negative emotions through “cognitive restructuring” rather than “forgetting.” This provided advantageous evidence for the humour reappraisal as an adaptive emotion regulation strategy from a memory perspective.

© 2015 by The American Society for Biochemistry and Molecular Biology Inc. Plasminogen activator inhibitor 1 level is extremely elevated in the edematous fluid of acutely injured lungs and pleurae. Elevated PAI-1 specifically inactivates pulmonary urokinase-type and tissue-type plasminogen activators. We hypothesized that plasminogen activation and fibrinolysis may alter epithelial sodium channel activity, a key player in clearing edematous fluid. Two-chain urokinase has been found to strongly stimulate heterologous human αβγ ENaC activity in a dose- and time-dependent manner. This activity of tcuPA was completely ablated by PAI-1. Furthermore, a mutation of the active site of the enzyme also prevented ENaC activation. By comparison, three truncation mutants of the amino-terminal fragment of tcuPA still activated ENaC. uPA enzymatic activity was positively correlated with ENaC current amplitude prior to reaching the maximal level. In sharp contrast to uPA, neither single-chain tPA nor derivatives, including two-chain tPA and tenecteplase, affected ENaC activity. Furthermore, γ but not α subunit of ENaC was proteolytically cleaved at by tcuPA. In summary, the underlying mechanisms of urokinase-mediated activation of ENaC include release of self-inhibition, proteolysis of γ ENaC, incremental increase in opening rate, and activation of closed channels. This study for the first time demonstrates multifaceted mechanisms for uPA-mediated up-regulation of ENaC, which form the cellular and molecular rationale for the beneficial effects of urokinase in mitigating mortal pulmonary edema and pleural effusions.