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

Author

Contreras-Muñoz, P., Fernández-Martín, A., Torrella, R., Serres, X., De la Varga, M., Viscor, G., Järvinen, T. A. H., Martínez-Ibáñez, V., Peiró, J. L., Rodas, G., and Marotta, M.

Subjects
TRAUMA surgery, SKELETAL muscle, ATHLETES, BIOLOGICAL models, FLUORESCENT antibody technique, HISTOLOGY, MAGNETIC resonance imaging, NEEDLE biopsy, RATS, REGENERATION (Biology), TENDONS, SURGERY
Abstract

Skeletal muscle injuries are the most common sports-related injuries in sports medicine. In this work, we have generated a new surgicallyinduced 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. [ABSTRACT FROM AUTHOR]

Published
2016
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7. Long-Pentraxin 3 Derivative as a Small-Molecule FGF Trap for Cancer Therapy.

Author

Ronca R, Giacomini A, Di Salle E, Coltrini D, Pagano K, Ragona L, Matarazzo S, Rezzola S, Maiolo D, Torrella R, Moroni E, Mazzieri R, Escobar G, Mor M, Colombo G, and Presta M

Subjects
Animals, Blotting, Western, C-Reactive Protein metabolism, Cell Cycle drug effects, Cell Cycle genetics, Cell Line, Tumor, Cell Survival drug effects, Cell Survival genetics, Cells, Cultured, Female, Fibroblast Growth Factors metabolism, Fibroblast Growth Factors pharmacology, Humans, Kaplan-Meier Estimate, Male, Mice, Inbred C57BL, Mice, Nude, Mice, Transgenic, Molecular Structure, Neoplasms metabolism, Neoplasms therapy, Neovascularization, Pathologic genetics, Neovascularization, Pathologic metabolism, Reverse Transcriptase Polymerase Chain Reaction, Serum Amyloid P-Component metabolism, Small Molecule Libraries chemistry, Small Molecule Libraries pharmacology, Tumor Burden drug effects, Tumor Burden genetics, Xenograft Model Antitumor Assays methods, C-Reactive Protein genetics, Fibroblast Growth Factors genetics, Gene Expression Regulation, Neoplastic, Neoplasms genetics, Serum Amyloid P-Component genetics
Abstract

The fibroblast growth factor (FGF)/FGF receptor (FGFR) system plays a crucial role in cancer by affecting tumor growth, angiogenesis, drug resistance, and escape from anti-angiogenic anti-vascular endothelial growth factor therapy. The soluble pattern recognition receptor long-pentraxin 3 (PTX3) acts as a multi-FGF antagonist. Here we demonstrate that human PTX3 overexpression in transgenic mice driven by the Tie2 promoter inhibits tumor growth, angiogenesis, and metastasis in heterotopic, orthotopic, and autochthonous FGF-dependent tumor models. Using pharmacophore modeling of the interaction of a minimal PTX3-derived FGF-binding pentapeptide with FGF2, we identified a small-molecule chemical (NSC12) that acts as an extracellular FGF trap with significant implications in cancer therapy., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Published
2015
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8. [Factor V deficiency; apropos of a case].

Author

Hernández Pérez E, Carnicer de la Pardina J, Badía Torrella RM, Melo Valls M, Comas Sans MA, and Toll Costa MT

Subjects
Child, Preschool, Diagnosis, Differential, Hemorrhage diagnosis, Humans, Joint Diseases diagnosis, Male, Pain diagnosis, Purpura diagnosis, Purpura etiology, Factor V Deficiency diagnosis, Hemorrhage etiology, Joint Diseases etiology, Pain etiology
Published
1989

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