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AIM:To evaluate the effectiveness of three-dimensional endoanal ultrasound (3D-EAUS) in the assessment of anal fistulae with and without H2O2 enhancement. METHODS:Sixty-one patients (37 males, aged 17-74 years) with anal fistulae, which were not simple low types, were evaluated by physical examination and 3D-EAUS with and without enhancement. Fistula classification was determined with each modality and compared to operative findings as the reference standard. RESULTS:The accuracy of 3D-EAUS was significantly higher than that of physical examination in detecting the primary tract (84.4% vs 68.7%, P = 0.037) and secondary extension (81.8% vs 62.1%, P = 0.01) and localizing the internal opening (84.2% vs 59.7%, P = 0.004). A contrast study with H2O2 detected several more fistula components including two primary suprasphincteric fistula tracks and one supralevator secondary extension, which were not detected on non-contrast study. However, there was no significant difference in accuracy between 3D-EAUS and H2O2-enhanced 3D-EAUS with respect to classification of the primary tract (84.4% vs 89.1%, P = 0.435) or secondary extension (81.8% vs 86.4%, P = 0.435) or localization of the internal opening (84.2% vs 89.5%, P = 0.406).CONCLUSION: 3D-EAUS was highly reliable in the diagnosis of an anal fistula. H2O2 enhancement was helpful at times and selective use in difficult cases may be economical and reliable.

Cell migration is essential to embryonic development, wound healing, and cancer cell dissemination. Cells move via leading-edge protrusion, substrate adhesion, and retraction of the cell's rear. The molecular mechanisms by which extracellular cues signal to the actomyosin cytoskeleton to control these motility mechanics are poorly understood. The growth factor-responsive and oncogenically activated protein extracellular signal-regulated kinase (ERK) promotes motility by signaling in actin polymerization-mediated edge protrusion. Using a combination of immunoblotting, co-immunoprecipitation, and myosin-binding experiments and cell migration assays, we show here that ERK also signals to the contractile machinery through its substrate, p90 ribosomal S6 kinase (RSK). We probed the signaling and migration dynamics of multiple mammalian cell lines and found that RSK phosphorylates myosin phosphatase–targeting subunit 1 (MYPT1) at Ser-507, which promotes an interaction of Rho kinase (ROCK) with MYPT1 and inhibits myosin targeting. We find that by inhibiting the myosin phosphatase, ERK and RSK promote myosin II–mediated tension for lamella expansion and optimal edge dynamics for cell migration. These findings suggest that ERK activity can coordinately amplify both protrusive and contractile forces for optimal cell motility.

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