Articular cartilage covers and protects the ends of long bones to enable smooth and pain-free joint motion. Within this important tissue, resident cells (chondrocytes) are responsible for maintaining the extracellular matrix (ECM). However, when cartilage is exposed to extreme mechanical forces, chondrocyte death can occur. For example, when the knee is destabilized by an injury to the anterior cruciate ligament (ACL), the resulting abnormal forces in the joint can initiate chondrocyte necrosis and trigger osteoarthritis (OA), a painful and complex joint disease characterized by progressive degeneration of cartilage and surrounding tissues.
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Insertional Achilles tendinopathy (IAT) is a debilitating disorder that responds poorly to conservative (non-surgical) therapies. An effective conservative treatment for this disease must target the fundamental causes of pathological tissue alterations and induce deformations that promote their reversal. Thus, the objective of this study is to elucidate the patterns of mechanical strain (i.e., deformation) that cause and reverse IAT in vitro, and determine how to induce these strain patterns in vivo during exercise-based physical therapy.
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More than 65,000 vision-restoring corneal transplantations take place every year for individuals with corneal disease, injury (e.g., from cataract surgery) and scarring. The most common reason for transplanted corneal grafts to fail is loss of corneal endothelial cells (CECs), the cells that line the inside of the cornea and pump fluid from it to maintain corneal transparency. Many of these cells are killed during transplantation surgery due to physical manipulation of corneal grafts and contact of the donor endothelium with surrounding tissues, surgical tools, tissue injectors, suture material and/or irrigating fluid.
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Under normal intraocular pressure, the cornea takes on a dome-like shape that helps it to focus light onto the retina and enable vision. However, when the mechanical properties of the cornea are altered (e.g., in an individual with keratoconus), the cornea takes on an abnormal shape, causing the path of light passing through the eye to be altered and vision to become blurred. Hence, understanding how the structure and composition of the cornea mediate its mechanical properties is of great scientific and clinical interest.
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Back pain is the leading cause of disability globally and the second most common cause of doctors’ visits. Despite extensive research efforts, the underlying mechanism of back pain has not been fully elucidated. The intervertebral disc (IVD) is a viscoelastic tissue that provides flexibility to the spinal column and acts as a shock absorber in the spine. When viscoelastic materials like IVD are cyclically loaded, they dissipate energy as heat. Thus, daily movements of the vertebral column intermittently deform the IVD and could increase disc temperature through viscoelastic heating. This temperature elevation has the potential to influence cell function, alter enzyme kinetics, drive cell death, and potentially induce nociception in innervating neurons within the IVD.
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