RESUMO
Recreational water use (RWU) injuries span from superficial lacerations to even death. Given the global popularity of RWU, radiologists should be aware of the common mechanisms and key imaging findings related to injuries in this setting. The goal of this article is to depict common RWU injuries and their emergent radiographic findings, which may have both important surgical and management implications. We present a broad review with case illustrations of these injuries seen at our level 1 trauma center showing the breadth of injury that can occur, general mechanisms and sample imaging findings.
Assuntos
Traumatismos em Atletas/diagnóstico por imagem , Recreação , Tomografia Computadorizada por Raios X , Água , Humanos , Lagos , Oceanos e Mares , Navios , PiscinasRESUMO
Despite the understanding of the importance of mitogen-activated protein (MAP) kinase activation in the stimulation of growth, little is known about the role of MAP kinase regulation during contact inhibited growth control. To investigate the role of the MAP kinase extracellular signal-regulated kinase (ERK) during the transition to a contact inhibited state, cultures of normal fibroblasts (BJ) were grown to different stages of confluency. The levels of MAP kinase phosphatase (MKP) expression and the amount of active ERK and MAP ERK kinase (MEK) in these cultures were assessed through western blot analysis and were compared to fibrosarcoma cell cultures (HT-1080), which lack contact inhibition. In normal fibroblasts, the amounts of active MEK and ERK decline at contact inhibition, concurrently with a rise in MKP-1, MKP-2, and MKP-3 protein levels. In contrast, fibrosarcoma cells appear to lack density-dependent regulation of the ERK pathway. Additionally, altering the redox environment of fibrosarcoma cells to a less reducing state, as seen during contact inhibition, results in increased MKP-1 expression. Taken together, these results suggest that the altered redox environment upon contact inhibition may contribute to the regulation of ERK inactivation by MKPs.