The Pulsed Nd:YAG Laser Therapy Enhanced Nerve Regeneration via Apoptosis Inhibition in a Rat Crushed Sciatic Nerve Model.

The study was aimed to validate the efficacy of the pulsed Nd:YAG laser on nerve regeneration in a rat sciatic nerve crushed model. 54 Wistar rats were randomly assigned into three groups: shame control, crush control, and laser treated group. For the laser treated group, the pulsed Nd:YAG laser (10 Hz) with 350 mJ per pulse in energy density and 50 J/cm2 in fluence was applied extracorporeally at the lesion site for 12 min to daily deliver 500 J immediately and consecutive 9 days following the crush injury. At week 1, the apoptosis-related activities in the injured nerve were examined (n = 8/each group). The sciatic functional index (SFI) was measured preoperatively and weekly until 4 weeks after the index procedure. The injured nerve and the innervated gastrocnemius muscle histology were assessed at week 4 (n = 10/each group). At week 1, the laser group showed the significant less TUNEL-positive ratio (P < 0.05), and the lower expression of cleaved caspase3/procaspase-3 and beclin-2/beclin-2-associated protein X ratios compared with the crush control. Furthermore, the laser group revealed significantly better SFI since week 1 and throughout the study (P < 0.05, all) compared with the crush control. At week 4, the laser group showed significantly higher axon density, lower myelin g-ratio, and the corresponding higher glycogen expression (P < 0.05, all) in the gastrocnemius muscle compared with those in the crush control. The pulsed Nd:YAG might enhance the injured nerve regeneration via apoptosis inhibition.

Aeromonas hydrophilia-infected nonunion of a closed tibial fracture in a healthy adolescent: A case report.

Aeromonas hydrophilia can cause soft tissue infection in both immunocompromised and healthy persons. A healthy 15-year-old adolescent fell into a ditch after a scooter accident and sustained a right distal tibial shaft closed fracture, a right femoral shaft closed fracture, and a dirty laceration over the medial aspect of the distal thigh above the right knee. After empiric antibiotics and radical debridement of the contaminated wound, a femoral interlocking nail and tibial external fixator were applied. However, acute osteomyelitis later presented in his femur and tibia, and Aeromonas hydrophilia grew in cultures from the knee wound and the fracture sites. During the follow-up, his tibia became an infected nonunion, and was successfully treated with the induced membrane technique. In an otherwise healthy patient with a closed fracture, Aeromonas hydrophilia can cause acute osteomyelitis and necrotizing fasciitis by spreading from a nearby contaminated wound. Exposure to water is a risk factor for Aeromonas hydrophilia infection.

Jigless knotless internal brace technique for acute Achilles tendon rupture: a case series study.

PURPOSE: To mitigate the risk of poor wound healing and of infection associated with the open repair of Achilles tendon midsubstance ruptures, minimally invasive techniques have been developed. We report our preliminary results after reviewing our "jigless knotless internal brace technique." METHODS: Patients were placed in prone position and a transverse 3-cm incision was made proximal to the palpable ruptured end. The proximal ruptured end was pulled out, gently debrided, and sutured using Krackow locking loops. Percutaneous sutures were crisscrossed through the distal tendon stump and looped around the Krackow sutures over the proximal stump. The ipsilateral Krackow sutures and the contralateral crisscrossed sutures were subcutaneously passed through two mini-incisions over the posterior calcaneus tuberosity and seated at the tuberosity with two 4.5-mm knotless suture anchors. All patients underwent the same post-operative rehabilitation protocol and regular follow-ups for at least 1 year. RESULTS: We recruited 10 patients (mean age, 37.3 years) who scored 100 points on the American Orthopaedic Foot and Ankle Society (AOFAS) scale, and who returned to their preoperative exercise levels 1-year post-operatively with no complications. CONCLUSION: Our method is simple, effective, and requires no special tools. It might be a reliable option for Achilles tendon repair. LEVEL OF EVIDENCE: III.

Inhibition of CD44 induces apoptosis, inflammation, and matrix metalloproteinase expression in tendinopathy.

Apoptosis has emerged as a primary cause of tendinopathy. CD44 signaling pathways exert anti-apoptotic and -inflammatory effects on tumor cells, chondrocytes, and fibroblast-like synoviocytes. The aim of this study was to examine the association among CD44, apoptosis, and inflammation in tendinopathy. Expression of CD44 and apoptotic cell numbers in tendon tissue from patients with long head of biceps (LHB) tendinopathy were determined according to the histological grades of tendinopathy. Primary tenocytes from Achilles tendon of Sprague-Dawley rats 1 week after collagenase injection were cultured with an antagonizing antibody against CD44. Treatment responses were determined by evaluating cell viability and expression of tendon-related proliferation markers, inflammatory mediators, and apoptosis. The expression of CD44 and apoptosis were positively correlated with the severity of tendinopathy in the human LHB tendinopathy. Furthermore, CD44 expression and apoptotic cells were co-stained in tendinopathic tendon. Blocking the CD44 signaling pathways in rat primary tenocytes by OX-50 induced cell apoptosis and the elevated levels of cleaved caspase-3. Furthermore, they had decreased cell viability and expression of collagen type I, type III, tenomodulin, and phosphorylated AKT. In contrast, there were elevated levels of inflammatory mediators, including interleukin (IL)-1ß, IL-6, tumor necrosis factor-α, cyclooxygenase-2, and phosphorylated NF-κB, as well as matrix metalloproteinase (MMP) family members including MMP-1, -3, -9, and -13 in tenocytes upon OX-50 treatment. This study is the first to demonstrate the association of CD44 and apoptosis in tendinopathy. Our data imply that CD44 may play a role in tendinopathy via regulating apoptosis, inflammation, and extracellular matrix homeostasis.

Perturbation of ATP-induced tetramerization of human cytosolic thymidine kinase by substitution of serine-13 with aspartic acid at the mitotic phosphorylation site.

Human cytosolic thymidine kinase (TK1) is tightly regulated in the cell cycle by multiple mechanisms. Our laboratory has previously shown that in mitotic-arrested cells human TK1 is phosphorylated at serine-13, accompanied by a decrease in catalytic efficiency. In this study we investigated whether serine-13 phosphorylation regulated TK1 activity and found that substitution of serine-13 with aspartic acid (S13D), which mimics phosphorylation, not only diminished the ATP-activating effect on the enzyme, but also decreased its thymidine substrate affinity. Our experimental results further showed that the S13D mutation perturbed ATP-induced tetramerization of TK1. Given that the dimeric form of TK1 is less active than the tetrameric, we propose that mitotic phosphorylation of serine-13 is of physiological importance, in that it may counteract ATP-dependent activation of TK1 by affecting its quaternary structure, thus attenuating its enzymatic function at the G2/M phase.