Background: Posterior tibial plateau fractures, including avulsion fractures of the posterior cruciate ligament (PCL) insertion, represent a challenge for the orthopedic trauma surgeon. These injuries have gained a new perspective both diagnostically and therapeutically after the regular use of multiplanar computed tomography. In the herein study, we describe the outcome of patients sustaining a tibial plateau fracture with posterior articular involvement treated by open reduction and internal fixation (ORIF) using our modified gastrocnemius splitting anatomic approach.
Methods: This observational retrospective descriptive study was conducted at Complejo Medico de la Policia Federal Argentina Churruca-Visca. All patients were treated by ORIF by our team through our modified gastrocnemius splitting anatomic approach, and followed-up for a minimum of 12 months.
Results: A total of 18 patients sustaining plateau fracture were treated by this approach. Satisfactory tomographic reduction with articular gap and/or step-off <2 mm was achieved in 16. The mean time to the return to activities of daily living was 192.2 days.
Conclusion: The modified gastrocnemius splitting anatomic approach represents a good alternative for the management of tibial plateau fractures involving the posterior quadrants.
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http://dx.doi.org/10.1016/j.injury.2023.111021 | DOI Listing |
PLoS One
January 2025
Department of Orthopedic Surgery, Asan Medical Center, University of Ulsan College of Medicine, Songpa-gu, Seoul, Republic of Korea.
Objective: Cubital tunnel syndrome is a common peripheral neuropathy of the upper extremity. Anterior transposition of the ulnar nerve is an established surgical treatment option for this condition. This study aimed to introduce a novel musculofascial lengthening technique that uses only a portion of the flexor-pronator muscle mass for submuscular anterior transposition of the ulnar nerve and investigate its clinical outcomes.
View Article and Find Full Text PDFVet Clin North Am Equine Pract
January 2025
Department of Large Animal Clinical Sciences, Michigan State University, East Lansing, MI 48824, USA.
Many myopathies in horses can be managed by exercise regimes and dietary modifications. This includes modifying the amount of nonstructural carbohydrate, fat, amino acids, vitamin E, and selenium based on the horse's specific myopathy, metabolic status, exercise program, and optimal body weight. Because dietary recommendations differ substantially between myopathies, it is imperative to establish a specific diagnosis.
View Article and Find Full Text PDFiScience
January 2025
Museum of Comparative Zoology, Harvard University, Cambridge, MA 02138, USA.
Tunas are high-performance pelagic fishes of considerable economic importance and have a suite of biological adaptations for high-speed locomotion. In contrast to our understanding of tuna body and muscle function, mechanosensory systems of tuna are poorly understood. Here we present the discovery of a remarkable sensory lateral line canal within the bilateral tuna keels with tubules that extend to the upper and lower keel surfaces.
View Article and Find Full Text PDFIntroduction: Several anthropometric indices reflecting cardiometabolic risks have been developed, but the relationship of body composition with arterial stiffness remains unclear. We aimed to determine the interaction between age-related anthropometric changes and progression of arterial stiffness.
Methods: This research analyzed cross-sectional data (N=13,672) and 4-year longitudinal data (N=5,118) obtained from a healthy Japanese population without metabolic disorders.
Biochem Pharmacol
January 2025
Department of Biomedical Sciences, University of Padova, 35131 Padova, Italy,. Electronic address:
Sarcoglycanopathies are rare forms of severe muscular dystrophies currently without a therapy. Mutations in sarcoglycan (SG) genes cause the reduction or absence of the SG-complex, a tetramer located in the sarcolemma that plays a protective role during muscle contraction. Missense mutations in SGCA, which cause α-sarcoglycanopathy, otherwise known as LGMD2D/R3, lead to folding defective forms of α-SG that are discarded by the cell quality control.
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