A New Surgical Model of Skeletal Muscle Injuries in Rats Reproduces Human Sports Lesions.

Skeletal muscle injuries are the most common sports-related injuries in sports medicine. In this work, we have generated a new surgically-induced skeletal muscle injury in rats, by using a biopsy needle, which could be easily reproduced and highly mimics skeletal muscle lesions detected in human athletes. By means of histology, immunofluorescence and MRI imaging, we corroborated that our model reproduced the necrosis, inflammation and regeneration processes observed in dystrophic mdx-mice, a model of spontaneous muscle injury, and realistically mimicked the muscle lesions observed in professional athletes. Surgically-injured rat skeletal muscles demonstrated the longitudinal process of muscle regeneration and fibrogenesis as stated by Myosin Heavy Chain developmental (MHCd) and collagen-I protein expression. MRI imaging analysis demonstrated that our muscle injury model reproduces the grade I-II type lesions detected in professional soccer players, including edema around the central tendon and the typically high signal feather shape along muscle fibers. A significant reduction of 30% in maximum tetanus force was also registered after 2 weeks of muscle injury. This new model represents an excellent approach to the study of the mechanisms of muscle injury and repair, and could open new avenues for developing innovative therapeutic approaches to skeletal muscle regeneration in sports medicine.

Topoisomerase IIalpha gene (TOP2A) amplification and deletion in cancer--more common than anticipated.

In solid tumours the predominant genetic mechanism for oncogene activation is through amplification of genes. The HER-2 (also known as ErbB2/c-erbB2/HER-2/neu) oncogene is the most frequently amplified oncogene in breast cancer and is also commonly amplified in other forms of cancer. The HER-2 amplicon also contains other biologically relevant genes with altered copy numbers, among these genes is the topoisomerase IIalpha (TOP2A). TOP2A gene is located adjacent to the HER-2 oncogene at the chromosome location 17q12-q21 and is either amplified or deleted, with equal frequency, in almost 90% of HER-2 amplified primary breast tumours. Recent data suggest that amplification and deletion of TOP2A may account for both sensitivity and resistance to topoII-inhibitor-chemotherapy, depending on the specific genetic defect at the TOP2A locus. In this issue of the Cytopathology, Bofin et al. present preliminary evidence for high prevalance of TOP2A amplification and deletion not only in the HER-2 amplified breast tumours, but also in the primary breast tumours without the HER-2 amplification. This finding together with the concept that TOP2A gene amplification and deletion seem to account for both relative chemosensitivity and resistance to topoII-inhibitor therapy further highlights the importance of screening for TOP2A gene copy number aberrations when topoII-inhibitors are considered either alone or in combination of other chemotherapeutic drugs for the treatment of cancer patients.

Basic science and clinical studies coincide: active treatment approach is needed after a sports injury.

The basic response to injury at the tissue level is well known and consists of acute inflammatory phase, proliferative phase, and maturation and remodeling phase. Knowing these phases, the treatment and rehabilitation program of athletes' acute musculoskeletal injuries should use a short period of immobilization followed by controlled and progressive mobilization. Both experimental and clinical trials have given systematic and convincing evidence that this program is superior to immobilization - a good example where basic science and clinical studies do coincide - and therefore active approach is needed in the treatment of these injuries.