Tendinopathy is a tendon pathology often resulting from a failed healing response to tendon injury. Activated protein C (APC) is a natural anti-coagulant with anti-inflammatory and wound healing promoting functions, which are mainly mediated by its receptors, endothelial protein C receptor (EPCR) and protease activated receptors (PARs). This study aimed to determine whether APC stimulates tenocyte healing and if so, to assess the involvement of the receptors. Mouse-tail tenocytes were isolated from 3-week-old wild type (WT), PAR- 1 knockout (KO) and PAR-2 KO mice. The expression of EPCR, PAR-1 and −2 and the effect of APC on tenocytes tendon healing and the underlying mechanisms were investigated by Reverse transcription real time PCR, western blot, 3- (4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay, zymography, and scratch wound healing/ migration assay. When compared to WT cells, PAR-1 KO tenocytes showed increased cell proliferation (3.3-fold, p<0.0001), migration (2.7-fold, p<0.0001) and wound healing (3-fold, p<0.0001), whereas PAR-2 KO cells displayed decreased cell proliferation (0.6-fold, p<0.05) and no change in cell migration or wound healing. APC at 1 μg/ml stimulated WT and PAR-1 KO tenocyte proliferation (~1.3, respectively, p<0.05) and wound healing (~1.3-fold, respectively, p<0.05), and additionally promoted PAR1-KO cell migration (1.4-fold, p<0.0001). APC only increased the migration (2-fold, p<0.05) of PAR-2 KO tenocytes. The activation of AKT, extracellular signal-regulated kinase (ERK)-2, and glycogen synthase kinase (GSK)-β3, the intracellular molecules that are associated with cell survival/growth, and matrix metalloproteinase (MMP)-2 that is related to cell migration and wound healing, were increased in all three cell lines in response to APC treatment. These findings show that PAR-1 and PAR-2 act differentially in tenocyte proliferation/migration/wound healing. APC likely promotes tenocyte proliferation/ wound healing via PAR-2, not PAR-1.
Dystrophic calcification (DC) is the abnormal appearance of calcified deposits in degenerating tissue, often associated with injury. Extensive DC can lead to heterotopic ossification (HO), a pathological condition of ectopic bone formation. The highest rate of HO was found in combat-related blast injuries, a polytrauma condition with severe muscle injury. It has been noted that the incidence of HO significantly increased in the residual limbs of combat-injured patients if the final amputation was performed within the zone of injury compared to that which was proximal to the zone of injury. While aggressive limb salvage strategies may maximize the function of the residual limb, they may increase the possibility of retaining non-viable muscle tissue inside the body. In this study, we hypothesized that residual dead muscle tissue at the zone of injury could promote HO formation. We tested the hypothesis by investigating the cellular and molecular consequences of implanting devitalized muscle tissue into mouse muscle pouch in the presence of muscle injury induced by cardiotoxin.Aims
Methods
The lack of effective treatment for cartilage defects has prompted investigations using tissue engineering techniques for their regeneration and repair. The success of tissue-engineered repair of cartilage may depend on the rapid and efficient adhesion of transplanted cells to a scaffold. Our aim in this study was to repair full-thickness defects in articular cartilage in the weight-bearing area of a porcine model, and to investigate whether the CD44 monoclonal antibody biotin-avidin (CBA) binding technique could provide satisfactory tissue-engineered cartilage. Cartilage defects were created in the load-bearing region of the lateral femoral condyle of mini-type pigs. The defects were repaired with traditional tissue-engineered cartilage, tissue-engineered cartilage constructed with the biotin-avidin (BA) technique, tissue-engineered cartilage constructed with the CBA technique and with autologous cartilage. The biomechanical properties, Western blot assay, histological findings and immunohistochemical staining were explored.Objectives
Methods
Femoral shaft fracture treatment often results in mal-alignment and the high dosage of radiation exposure. The objective of this study is to develop a Parallel Manipulator Robot (PMR) on traction table to overcome these difficulties so as achieve better alignment for the fractured femur and reduce radiation to both patients and physicians. The distal platform of PMR is attached to the central pole on standard traction table by the boot adaptor. A leg model with soft tissue made by Pacific Research Laboratory, Inc. is flexed at the knee with patella on the top. A 2/3 circular ring, with 1/3 open circle down, fixed to the fractured distal femur with one trans-wire and one self-tapping screw, acting as adaptable stirrup fixing scheme. To secure proximal femur, an adapter is assembled on the traction table and fixed on the proximal femur. The distal femur is fixed to the 2/3 circular ring platform of PMR. Surgical planning is performed by first acquiring the bi-planar images from the C-Arm X-ray machine. After simulated fracture on 3-D femoral model is made, proximal and distal segments of the model will be superimposed with background bi-planar images. Finally the pre-fractured length and mechanical axis of 3-D femoral model will be restored. Afterwards, a table of schedule for length adjustments of six struts of PMR is generated. This length adjustment schedule is used to drive the PMR for fractured femur alignment and reduction. When reduction completed, a special designed device is used to fix the reduced femur. Then the PMR is removed from the traction table and the patient can be removed from the traction table.Objectives
Methods
Femoral shaft fracture treatment often results in mal-alignment and the high dosage of radiation exposure. The objective of this study is to develop a Parallel Manipulator Robot (PMR) on traction table to overcome these difficulties so as achieve better alignment for the fractured femur and reduce radiation to both patients and physicians. The distal platform of PMR is attached to the central pole on standard traction table by the boot adaptor. A leg model with soft tissue made by Pacific Research Laboratory, Inc. is flexed at the knee with patella on the top. A 2/3 circular ring, with 1/3 open circle down, fixed to the fractured distal femur with one trans-wire and one self-tapping screw, acting as adaptable stirrup fixing scheme. To secure proximal femur, an adapter is assembled on the traction table and fixed on the proximal femur. The distal femur is fixed to the 2/3 circular ring platform of PMR. Surgical planning is performed by first acquiring the bi-planar images from the C-Arm X-ray machine. After simulated fracture on 3-D femoral model is made, proximal and distal segments of the model will be superimposed with background bi-planar images. Finally the pre-fractured length and mechanical axis of 3-D femoral model will be restored. Afterwards, a table of schedule for length adjustments of six struts of PMR is generated. This length adjustment schedule is used to drive the PMR for fractured femur alignment and reduction. When reduction completed, a special designed device is used to fix the reduced femur. Then the PMR is removed from the traction table and the patient can be removed from the traction table.Objective
Method
