PURPOSE: When flexor tendons are injuried in children, the management is difficult. There are needs to determine the periods of postoperative immobilization. MATERIALS AND METHODS: From April 1994 to March 1998, 40 patients younger than 16 years who had sustained flexor tendon lacerations in zone I or zone II of 52 digits were available for critical evaluation. The average postoperative follow-up period was 24 (range, 3-48) months. RESULTS: All profundus repairs in zone I achieved excellent or good function. Isolated profundus and combined profundus and superficialis repairs in zone II achieved comparable results which managed with a passive motion program immediately after operation (TAM=82%) or motion following immobilization for 3 weeks (TAM =79%) or 4 weeks (TAM=78%) . Immobilization for longer than 4 weeks which resulted in an appreciable deterioration of funtion (5 weeks: TAM=64%, 6 weeks: TAM=61%) . Digital motion following flexor tendon injuries treated with less than 4 weeks of immobilization or early motion was not significantly different. CONCLUSION: We could find no benefits of early mobilization protocols in children. Howerver, it does appear that it is important that postoperative immobilization not be continued beyond 4 weeks.
Child* ; Early Ambulation ; Follow-Up Studies ; Hand* ; Humans ; Immobilization ; Lacerations ; Tendon Injuries ; Tendons*

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.