Duchenne muscular dystrophy (DMD) is a prevalent childhood neuromuscular disease characterized by progressive skeletal and cardiac muscle degeneration due to dystrophin protein deficiency. Despite ongoing drug development efforts, no cure exists, with limited success in preclinical studies. To expedite DMD drug development, we introduce an innovative organ-on-a-chip (OOC) platform. This microfluidic device sustains up to six 3D patient-derived skeletal muscle tissues, enabling real-time evaluation of anti-DMD treatments. Our in vitro model recreates myotube integrity loss, a hallmark of DMD, by encapsulating myogenic precursors in a fibrin-composite matrix using a PDMS casting mold. Continuous contractile regimes mimic sarcolemmal instability, monitored through tissue contractibility and Creatine Kinase (CK) levels—an established marker of muscle damage. We further enhance our platform with a nanoplasmonic CK biosensor, enabling rapid, label-free, and real-time sarcolemmal damage assessment. Combining these elements, our work demonstrates the potential of OOCs in accelerating drug development for DMD and similar neuromuscular disorders.
mixed FAI in 26 cases, pure cam FAI in 6 cases and pure pincer FAI in 13 cases. 42 hips where graded as Tönnis 0 and 2 as Tönnis 1. All patients where evaluated according to the non arthritic hip score (NAHS – McCarthy et all) before and after the surgery at 3, 6, 12, 24 and 36 months. Osyrix® software was used to measure radiographic parameters. The numeric variables where treated using SPSS for windows (paired t student test).
We had no avascular necrosis so far and no neurovascular damage. Trochanteric screw removal was done in 3 cases for local irritation. We had 2 capsule adhesions, released shortly after using arthroscopy.