Treatment of Middle-up Part Long-segment Femoral Fracture with Long Proximal Femoral Nail Antirotation.

OBJECTIVE: To investigate the outcomes of treating middle-up part long-segment fractures of the femur by long proximal femoral nail antirotation (PFNA-long). METHODS: From June 2006 to December 2013, 139 cases (35 women, 104 men; mean age 48.8, range, 18-86 years) of long-segment femoral fracture in middle-up part were treated with long proximal femoral nail antirotation (PFNA, 320-380 mm) by minimally invasive percutaneous fixation and autogenous iliac bone graft. Fifty-eight cases were graded as type IA long-segment femoral fractures (41.73%), 25 type IB (17.99%), four type IC (2.88%), 28 type II (20.14%), 12 type IIIA (8.63%), five type IIIB (3.60%), and seven type IV (5.04%). Clinical efficacy was evaluated with Harris hip function scores and postoperative pain with visual analogue scale. RESULTS: The operative time was 35-90 min (mean, 45 min) and mean intraoperative blood loss 78.6 mL (range 30-200 mL). Most patients were walking with assistance 4-10 days postoperatively. All patients were followed up for 3-37 months (mean, 19 months). There were no serious complications. All fractures healed after 2.8-6.8 months (mean, 3.9 months). According to Harris criteria, the clinical results were excellent in 108 patients, good in 22, fair in eight and poor in one. Ninety-three cases had no pain, 33 mild pain, 13 moderate pain and 25 occasionally needed non-steroidal analgesics. CONCLUSION: Closed reduction or limited open reduction with PFNA-long is an effective treatment for long-segment femoral fracture in middle-up part, with good strength in fixation, high rate of fracture union, early functional recovery and low rate of complications.

[Reconstruction for knee dislocation with multiple ligaments injury at stage I].

OBJECTIVE: To investigate clinical outcomes of tendon allograft reconstruction with arthroscopy minimally invasive technique at stage I for the treatment of knee dislocation with multiple ligaments injury. METHODS: Forty-eight patients with knee dislocation were reconstructed anterior and posterior ligament under arthroscopy at stage I from January 2008 to January 2012, and repaired ligaments injury of knee joint by minimally invasive technique. There were 38 males and 10 females aged from 20 to 59 years old with an average of 35.6 years old; 22 cases on the left side and 26 cases on the right side; the time from injury to operation ranged from 2 d to 2 weeks. Two cases combined with anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), medial collateral ligament (MCL) and posterolateral complex injuries, 36 cases combined with ACL, PCL, and MCL injuries, 10 cases combined with ACL, PCL and PLC injuries; 4 cases combined with peroneal nerve injury. Lysholm scoring were used to compared the cases before operation and final following-up to evaluate knee function. RESULTS: All patients were followed up from 12 to 30 months with an average of (18.2 ± 6.3) months. Activity and stability of joint were obviously improved. Lysholm score were improved from 40.3 ± 4.1 before operation to 87.0 ± 6.4 at final following-up. CONCLUSION: Reconstruction with arthroscopy minimally invasive technique at stage I for the treatment of knee dislocation with multiple ligaments injury could recover stability of joint better,reserve joint function. Preoperative training and postoperative individualized rehabilitation treatment is the key point of recover knee joint function.

NF-κB p65/p52 plays a role in GDNF up-regulating Bcl-2 and Bcl-w expression in 6-OHDA-induced apoptosis of MN9D cell.

Glial-cell-line-derived neurotrophic factor (GDNF) has been shown to protect dopaminergic (DA) neurons against 6-hydroxydopamine (6-OHDA) toxicity. The mechanism underlying the antiapoptosis role of GDNF still needs further studies. We previously observed that nuclear factor-kappaB (NF-κB) signaling pathway, i.e. p65/p52, mediated the antiapoptosis role of GDNF in MN9D cells. Here, the DA cell line MN9D was used to explore the mechanisms underlying NF-κB p65/p52-mediated protection role of GDNF in DA neurons. The results showed that GDNF pretreatment blocked the apoptotic effects induced by 6-OHDA, with the upregulation of the antiapoptotic protein, Bcl-2 and Bcl-w, as well as the downregulation of the proapoptotic proteins, Bax and Bad. Furthermore, when sip100 plasmids were transfected into MN9D cells to inhibit the expression of p100, which was the precursor of p52, the effects of GDNF on upregulating Bcl-2 and Bcl-w were attenuated. These results indicated that GDNF could protect MN9D cells from apoptosis induced by 6-OHDA via upregulating Bcl-2 and Bcl-w expressions and downregulating Bax and Bad expressions. Moreover, NF-κB p65/p52 signaling mediated the effects of GDNF on Bcl-2 and Bcl-w expressions.