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ObjectiveTo evaluate the diagnostic value of the Inlet-to-outlet median nerve area ratio (IOR) in patients with clinically and electrophysiologically confirmed carpal tunnel syndrome (CTS).MethodsForty-six wrists in 46 consecutive patients with clinical and electrodiagnostic evidence of CTS and forty-four wrists in 44 healthy volunteers were examined with ultrasonography. The cross-sectional area (CSA) of the median nerve was measured at the carpal tunnel inlet (the level of scaphoid-pisiform) and outlet (the level of the hook of the hamate), and the IOR was calculated for each wrist. Ultrasonography and electrodiagnostic tests were performed under blinded conditions. Electrodiagnostic testing combined with clinical symptoms were considered to be the gold standard test. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic value between the inlet CSA and IOR.ResultsThe study population included 16 men and 30 women (mean age, 45.3 years; range, 18–83 years). The control population included 18 men and 26 women (mean age, 50.4 years; range, 18–79 years). The mean inlet CSA was 8.7 mm2 in healthy controls and 14.6mm2 in CTS group (P<0.001). The mean IOR in healthy volunteers (1.0) was smaller than that in patients (1.6, P<0.001). Receiver operating characteristic analysis revealed a diagnostic advantage to using the IOR rather than the inlet CSA (P<0.01). An IOR cutoff value of ≥ 1.3 would yield 93% specificity and 91% sensitivity in the diagnosis of CTS.ConclusionThe IOR of median nerve area promises to be an effective means in the diagnosis of CTS. A large-scale, randomized controlled trial is required to determine how and when this parameter will be used.

Keloids are tumor-like skin scars that grow as a result of the aberrant healing of skin injuries, with no effective treatment. The molecular mechanism underlying keloid pathogenesis is still largely unknown. In this study, we compared microRNA (miRNA) expression profiles between keloidderived fibroblasts and normal fibroblasts (including fetal and adult dermal fibroblasts) by miRNA microarray analysis. We found that the miRNA profiles in keloid-derived fibroblasts are different with those in normal fibroblasts. Nine miRNAs were differentially expressed, six of which were significantly up-regulated in keloid fibroblasts (KFs), including miR-152, miR-23b-3p, miR-31-5p, miR-320c, miR-30a-5p, and hsv1-miR-H7, and three of which were significantly down-regulated, including miR-4328, miR-145-5p, and miR-143-3p. Functional annotations of differentially expressed miRNA targets revealed that they were enriched in several signaling pathways important for scar wound healing. In conclusion, we demonstrate that the miRNA expression profile is altered in KFs compared with in fetal and adult dermal fibroblasts, and the expression profile may provide a useful clue for exploring the pathogenesis of keloids. miRNAs might partially contribute to the etiology of keloids by affecting several signaling pathways relevant to scar wound healing.