Exploring what synchronized physiological arousal can reveal about the social regulatory process in a collaborative argumentation activity.

Combining physiological measures with observational data (e.g., video or self-reports) to further capture and understand the temporal and cyclical process of social regulation has become a trend in the field. Synchronized physiological arousal is a particularly meaningful situation in collaboration. However, little attention has been given to synchronized physiological arousal episodes and their relationship with the social regulatory process. In addition, only a few research utilized heart rate (HR) as a physiological measure in the current collaboration literature. More research is necessary to reveal the potential of HR to expand the diversity of physiological indicators in the field. Therefore, the current study aimed to explore what synchronized physiological arousal can further reveal about the social regulatory process. To achieve this goal, this study designed a collaborative argumentation (CA) activity for undergraduates (mean age 20.3). It developed an arousal-regulation analysis platform, which could automatically detect synchronized physiological arousal in HR and align them with coding challenges and social regulation based on the timeline. In total, 14 four-member groups were recruited. After analyzing both videos and HR data, several findings were obtained. First, only one-third of episodes were synchronized physiological arousal episodes, and the situations where four members were all in arousal states were rare during CA. Second, synchronized physiological arousal was more sensitive to socio-emotional aspects of collaboration as the shared physiological arousal more frequently co-occurred with socio-emotional challenges and socio-emotional regulation, while it happened the least under motivational challenges. Third, synchronized physiological arousal has also been found to be associated with the challenges being regulated. Finally, pedagogical implications were suggested.

Extracellular cyclophilin A induces cardiac hypertrophy via the ERK/p47phox pathway.

Excessive reactive oxygen species (ROS) are a critical driver of cardiac hypertrophy developing into heart failure. Cyclophilin A (CyPA), a member of the cyclophilin family, has been highlighted as a main secreted ROS-induced factor. The mechanism by which extracellular CyPA interacts with cardiomyocytes is unclear. We showed that extracellular CyPA is upregulated in cardiac hypertrophy rats and expressed around hypertrophic cardiomyocytes. Cell experiments further confirmed that extracellular CyPA induces H9c2 cardiomyocytes hypertrophy via ROS generation. Extracellular CyPA-induced ROS is derived from nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, and extracellular CyPA activates p47phox membrane translocation through ERK1/2 pathway. When blocking extracellular matrix metalloproteinase inducer (EMMPRIN), most of the extracellular CyPA effects were significantly inhibited. The current study shows that extracellular CyPA is one of the key factors linking oxidative stress and cardiac hypertrophy, and may be a potential target for cardiac hypertrophy therapy.

Role of CyPA in cardiac hypertrophy and remodeling.

Pathological cardiac hypertrophy is a complex process and eventually develops into heart failure, in which the heart responds to various intrinsic or external stress, involving increased interstitial fibrosis, cell death and cardiac dysfunction. Studies have shown that oxidative stress is an important mechanism for this maladaptation. Cyclophilin A (CyPA) is a member of the cyclophilin (CyPs) family. Many cells secrete CyPA to the outside of the cells in response to oxidative stress. CyPA from blood vessels and the heart itself participate in a variety of signaling pathways to regulate the production of reactive oxygen species (ROS) and mediate inflammation, promote cardiomyocyte hypertrophy and proliferation of cardiac fibroblasts, stimulate endothelial injury and vascular smooth muscle hyperplasia, and promote the dissolution of extracellular matrix (ECM) by activating matrix metalloproteinases (MMPs). The events triggered by CyPA cause a decline of diastolic and systolic function and finally lead to the occurrence of heart failure. This article aims to introduce the role and mechanism of CyPA in cardiac hypertrophy and remodeling, and highlights its potential role as a disease biomarker and therapeutic target.