Arthroscopic Reconstruction of Posterior Cruciate Ligament with Embedded Tibial Tendon Bolt.

OBJECTIVE: To evaluate the effect of newly designed arthroscopic reconstruction of posterior cruciate ligament (PCL) using tibial tendon bolt. METHODS: The effects of embedded tendon pin were observed by X-ray of knee joint. From October 2010 to September 2015, 51 PCL injury patients who met the inclusion criteria were enrolled in this retrospective study. The arthroscopically assisted reconstruction of the PCL with tibial tendon bolt was performed on all patients. Visual Analog Scale (VAS) pain score, Tegner activity score, Lysholm score, International Knee Documentation Committee (IKDC) assessment, posterior drawer test (PDT), and KT-1000 activity score were evaluated preoperatively and at 1-year postoperative and 3-year postoperative. RESULTS: The preoperative, 1-year postoperative, and 3-year postoperative IKDC score (15.8% ± 14.8%, 89.6% ± 5.8%, and 86.8% ± 5.4%), Lysholm score (17.4 ± 10.7, 91.2 ± 2.8, and 88.2 ± 3.1), VAS score (5.8 ± 1.2, 1.3 ± 0.5, and 0.6 ± 0.5), Tegner activity score (1.2 ± 0.8, 8.1 ± 0.8, and 7.4 ± 0.8), and KT-1000 score (15.6 ± 3.6, 4.5 ± 2.4, and 5.4 ± 1.8) were obtained. There were significant differences in these outcomes among preoperative, 1-year postoperative, and 3-year postoperative (all P < 0.0001). After 1- and 3-year surgery, 31 (60.8%) and 26 (51.0%) patients had the negative PDT, indicating that the PCL injury was improved. There were no postoperative complications. CONCLUSION: The application of tendon pin fixed by tibial inlay 8-shaped tibial tunnel to reconstruct PCL was an effective, simple, and safe surgical procedure for PCL injury.

Abrogating ClC-3 Inhibits LPS-induced Inflammation via Blocking the TLR4/NF-κB Pathway.

This study investigated the function of a chloride channel blocker, DIDS. Both in vitro and in vivo studies found that DIDS significantly inhibits lipopolysaccharide (LPS)-induced release of proin flammatory cytokines. Here, we show that DIDS inhibits LPS-induced inflammation, as shown by downregulation of inflammatory cytokines via inhibition of the TLR4/NF-κB pathway. Furthermore, we show that ClC-3siRNA transfection reduces LPS-induced pro-inflammation in Raw264.7 cells, indicating that ClC-3 is involved in the inhibitory effect of DIDS during LPS-induced cytokines release. In vivo, DIDS reduced LPS-induced mortality, decreased LPS-induced organic damage, and down-regulated LPS-induced expression of inflammatory cytokines. In sum, we demonstrate that ClC-3 is a pro-inflammatory factor and that inhibition of ClC-3 inhibits inflammatory induction both in vitro and in vivo, suggesting that ClC-3 is a potential anti-inflammatory target.