Biomechanical Strategies for Obstacle Crossing in Patients with Anterior Cruciate Ligament Deficiency

The current study aimed to investigate the biomechanical control strategies in patients with anterior cruciate ligament deficiency (ACLD) when crossing obstacles of different heights. Eighteen patients with unilateral ACLD and sixteen age-matched healthy controls were recruited. They crossed obstacles of heights of 10%, 20% and 30% of their leg lengths at a self-selected pace while the kinematic and kinetic data were measured and analyzed using inverse dynamics analysis. Patients with ACLD were found to avoid using the quadriceps on both affected and unaffected sides during stance phase. Training programs on both quadriceps are needed for more efficient rehabilitation of the patients with unilateral ACLD

VALIDITY OF A MAKER-BASED LOCATOR FOR MEASURING IN VIVO THREEDIMENSIONAL SCAPULAR STATIC POSES USING STEREOPHOTOGRAMMETRY

The study aimed to (1) develop a marker-based scapular locator for measuring scapular poses and (2) to design an in vivo experimental procedure for this static marker-based measurement method to decrease measurement errors, and (3) to validate this scapular locator and the experimental procedure. Six young male adults were implanted into the spine of the scapula with two bone-pins that were attached with a cluster of four retroreflective markers (bone markers). The scapular poses were measured simultaneously using the developed scapular locator and the bone markers. The results showed that very high validity for scapular rotations and for the acromial angle (AA), the root of spine (RS) and the inferior angle (IA) of the scapular translation were achieved. Two main reasons contributed to the results: (1) the adjustable scapular locator and (2) careful palpation of the bony landmarks over the scapula

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

Chemokine (C-C motif) ligand 3 (CCL3), also known as macrophage inflammatory protein-1α, is a cytokine involved in inflammation and activation of polymorphonuclear leukocytes. CCL3 has been detected in infiltrating cells and tumor cells. Chondrosarcoma is a highly malignant tumor that causes distant metastasis. However, the effect of CCL3 on human chondrosarcoma metastasis is still unknown. Here, we found that CCL3 increased cellular migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. Pre-treatment of cells with the MMP-2 inhibitor or transfection with MMP-2 specific siRNA abolished CCL3-induced cell migration. CCL3 has been reported to exert its effects through activation of its specific receptor, CC chemokine receptor 5 (CCR5). The CCR5 and AMP-activated protein kinase (AMPK) inhibitor or siRNA also attenuated CCL3-upregulated cell motility and MMP-2 expression. CCL3-induced expression of MMP-2 and migration were also inhibited by specific inhibitors, and inactive mutants of AMPK, p38 mitogen activated protein kinase (p38 or p38-MAPK), and nuclear factor κB (NF-κB) cascades. On the other hand, CCL3 treatment demonstrably activated AMPK, p38, and NF-κB signaling pathways. Furthermore, the expression levels of CCL3, CCR5, and MMP-2 were correlated in human chondrosarcoma specimens. Taken together, our results indicate that CCL3 enhances the migratory ability of human chondrosarcoma cells by increasing MMP-2 expression via the CCR5, AMPK, p38, and NF-κB pathways

Anti-Neuroinflammatory Effects of the Calcium Channel Blocker Nicardipine on Microglial Cells: Implications for Neuroprotection

Background/Objective Nicardipine is a calcium channel blocker that has been widely used to control blood pressure in severe hypertension following events such as ischemic stroke, traumatic brain injury, and intracerebral hemorrhage. However, accumulating evidence suggests that inflammatory processes in the central nervous system that are mediated by microglial activation play important roles in neurodegeneration, and the effect of nicardipine on microglial activation remains unresolved. Methodology/Principal Findings In the present study, using murine BV-2 microglia, we demonstrated that nicardipine significantly inhibits microglia-related neuroinflammatory responses. Treatment with nicardipine inhibited microglial cell migration. Nicardipine also significantly inhibited LPS plus IFN-γ-induced release of nitric oxide (NO), and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, nicardipine also inhibited microglial activation by peptidoglycan, the major component of the Gram-positive bacterium cell wall. Notably, nicardipine also showed significant anti-neuroinflammatory effects on microglial activation in mice in vivo. Conclusion/Significance The present study is the first to report a novel inhibitory role of nicardipine on neuroinflammation and provides a new candidate agent for the development of therapies for inflammation-related neurodegenerative diseases

An in vitro study glenhumeral performance after suprascapular nerve entrapment

Contains fulltext : mmubn000001_073663255.pdf (publisher's version ) (Open Access)Promotor : J. ThurlingsXII, 236 p

Primary traumatic patellar dislocation

<p>Abstract</p> <p>Acute traumatic patellar dislocation is a common injury in the active and young adult populations. MRI of the knee is recommended in all patients who present with acute patellar dislocation. Numerous operative and non-operative methods have been described to treat the injuries; however, the ideal management of the acute traumatic patellar dislocation in young adults is still in debate. This article is intended to review the studies to the subjects of epidemiology, initial examination and management.</p