Multiple Epiphyseal Dysplasia With Knee Joint Locking Symptoms Caused by Intra-articular Loose Bodies.

Multiple epiphyseal dysplasia (MED) is a congenital disease causing epiphyseal dysplasia in long bones. Herein, we report a case of a middle-aged man with bilateral knee joint locking symptoms who was diagnosed with multiple epiphyseal dysplasia caused by Matrilin-3 (MATN3) pathogenic variants and was successfully treated with arthroscopic loose body removal. A 48-year-old man has had bilateral knee pain since his twenties and underwent loose body removal of both knees in his thirties.

Arthroscopic Reconstruction of the Anterior Tibiotalar Ligament Using a Free Tendon Graft.

Deltoid ligament injuries account for 5.1% to 15.8% of ankle sprains and occur with concomitant lateral ankle sprains.

Anatomical Arthroscopic Anterior Talofibular Ligament and Calcaneofibular Ligament Reconstruction Using an Autogenic Hamstring Tendon: Safe Creation of Anatomical Fibular Tunnel.

Ankle sprains are the most common lower extremity injuries associated with sports activity. Although ligament repair techniques are popular, reconstruction methods using free tendons are considered when the ligament remnant is insufficiently strong, when high-demand athletes sustain repeat ankle sprains, or in revision cases after repair. Recently, some arthroscopic reconstruction techniques have been reported.

Expression of the Nd1 gene is down-regulated by doxorubicin at post-transcriptional level.

Doxorubicin is an anti-neoplastic agent with cardiotoxicity as a side effect. We previously demonstrated that doxorubicin treatment of mice resulted in a selective decrease in expression of the Nd1 gene, which encoded a new kelch family actin binding protein in the heart. Here we show that doxorubicin treatment also reduced the Nd1 expression in various organs of mice and cultured cell lines.

Overexpression of Nd1, a novel Kelch family protein, in the heart of transgenic mice protects against doxorubicin-induced cardiomyopathy.

Doxorubicin is one of the most effective drugs available for cancer chemotherapy. However, the clinical use of doxorubicin has been greatly limited because of severe side effects on cardiomyocytes. Since Nd1-L, a novel actin-binding protein, is expressed most abundantly in the heart of adult mice, we examined a role of Nd1-L in doxorubicin-induced cardiomyopathy.

Overexpression of Nd1-s, a variant form of new kelch family protein, perturbs the cell cycle progression of fibroblasts.

The murine Nd1 gene encodes two forms of protein, Nd1-L and Nd1-S, both of which share the BTB/POZ domain, but Nd1-S lacks the kelch repeats. Although Nd1-L ubiquitously expresses, localizes in the cytoplasm and functions as a stabilizer of actin filaments, expression and function of Nd1-S were unknown. Here we show that Nd1-S were expressed in all tissues examined and localized in the nucleus as a speckled-like pattern.

Protective role of Nd1 in doxorubicin-induced cardiotoxicity.

Objective: The Ndl gene, which encodes a novel kelch family protein, is expressed ubiquitously in mouse tissues. In vitro studies suggest that Ndl protein, which binds to actin filaments, functions as a cytoskeletal stabilizer. In order to elucidate a physiological function of Ndl in vivo, we generated Nd1-deficient (Ndl-/-) mice.