The operative treatment of Ruedi II-III Pilon fractures with the ventr-lateral approach / 中国骨伤

<p><b>OBJECTIVE</b>To investigate the effects of the ventralateral approach in treating severe Pilon fracture.</p><p><b>METHODS</b>From February 2002 to March 2008, 63 patients with Ruedi II-III Pilon fractures were treated with the ventralateral approach, including 36 males and 27 females with an average age of 37 years ranging from 19 to 71 years. The mean time from injury to operation was 8 days (ranged for 2 h-19 d). According to the Ruedi classification system, type II was 32 cases (6 cases of them combined with soft tissue lesion, 4 with open fracture) and type III was 31 cases (9 cases of them combined with soft tissue lesion, 8 with open fracture). The clinical effects were evaluated according to Helfet criteria and the complications were observed including condition of wound healing, infection, bone union, deformity union, motion of the ankle, the degree of the pain and so on.</p><p><b>RESULTS</b>The first intention achieved in 59 cases, the delayed healing in 4 cases. Stiffness of the ankle was found in 5 cases because of bone disunion. All patients were followed up from 8 to 31 months with an average of 15.3 months. The ranging in bone healing time was from 8 to14 weeks with an average of 10 weeks. According to the Helfet criteria, 28 cases obtained excellent results, 30 good, 5 poor.</p><p><b>CONCLUSION</b>The operative treatment of Ruedi I-III Pilon fractures with the ventralateral approach can obtain satisfactory results and avoid complications effectively.</p>

The mechanisms of p21WAF1/Cip-1 expression in MOLT-4 cell line induced by TSA / 中国实验血液学杂志

To investigate the function and molecular mechanism of p21(WAF1/Cip-1) expression in MOLT-4 cells induced by HDAC inhibitor TSA, the expression pattern of p21(WAF1/Cip-1) and the distribution of cell cycle in TSA treated cells were analyzed. The results showed that TSA could effectively induce G(2)/M arrest and apoptosis of MOLT-4 cells. Kinetic experiments demonstrated that p21(WAF1/Cip-1) were upregulated quickly before cell arrested in G(2)/M and began decreasing at the early stage of apoptosis. Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses. This study also identified that the protein level of p21(WAF1/Cip-1) was highly associated with the cell cycle change induced by TSA. Compared to cells treated by TSA only, exposure MOLT-4 cells to TSA meanwhile treatment with MG-132 increased the protein level of p21(WAF1/Cip-1) and increased the numbers of cell in G(2)/M-phase, whereas the cell apoptosis were delayed. It is concluded that p21(WAF1/Cip-1) plays a significant role in G(2)/M arrest and apoptosis signaling induced by TSA in MOLT-4 cells.