Putting our heads together: interpersonal neural synchronization as a biological mechanism for shared intentionality

Shared intentionality, or collaborative interactions in which individuals have a shared goal and must coordinate their efforts, is a core component of human interaction. However, the biological bases of shared intentionality and, specifically, the processes by which the brain adjusts to the sharing of common goals, remain largely unknown. Using functional near infrared spectroscopy (fNIRS), coordination of cerebral hemodynamic activation was found in subject pairs when completing a puzzle together in contrast to a condition in which subjects completed identical but individual puzzles (same intention without shared intentionality). Interpersonal neural coordination was also greater when completing a puzzle together compared to two control conditions including the observation of another pair completing the same puzzle task or watching a movie with a partner (shared experience). Further, permutation testing revealed that the time course of neural activation of one subject predicted that of their partner, but not that of others completing the identical puzzle in different partner sets. Results indicate unique brain-to-brain coupling specific to shared intentionality beyond what has been previously found by investigating the fundamentals of social exchange

Alternatively Activated Macrophages and Collagen Remodeling Characterize the Postpartum Involuting Mammary Gland across Species

Recent pregnancy correlates with decreased survival for breast cancer patients compared with non–pregnancy-associated breast cancer. We hypothesize that postpartum mammary involution induces metastasis through wound-healing programs known to promote cancer. It is unknown whether alternatively activated M2 macrophages, immune cells important in wound-healing and experimental tumorigenesis that also predict poor prognosis for breast cancer patients, are recruited to the normal involuting gland. Macrophage markers CD68, CSF-1R, and F4/80 were examined across the pregnancy and involution cycle in rodent and human mammary tissues. Quantitative immunohistochemistry revealed up to an eightfold increase in macrophage number during involution, which returned to nulliparous levels with full regression. The involution macrophages exhibit an M2 phenotype as determined by high arginase-1 and low inducible nitric oxide synthase staining in rodent tissue, and by mannose receptor expression in human breast tissue. M2 cytokines IL-4 and IL-13 also peaked during involution. Extracellular matrix (ECM) isolated from involuting rat mammary glands was chemotactic for macrophages compared with nulliparous mammary ECM. Fibrillar collagen levels and proteolysis increased dramatically during involution, and denatured collagen I acted as a strong chemoattractant for macrophages in cell culture, suggesting proteolyzed fibrillar collagen as a candidate ECM mediator of macrophage recruitment. M2 macrophages, IL-4, IL-13, fibrillar collagen accumulation, and proteolysis of collagen are all components of tumor promotional microenvironments, and thus may mediate promotion of breast cancers arising in the postpartum setting