Engineering of Human Skeletal Muscle With an Autologous Deposited Extracellular Matrix.

Adult skeletal muscle progenitor cells can be embedded in an extracellular matrix (ECM) and tissue-engineered to form bio-artificial muscles (BAMs), composed of aligned post-mitotic myofibers. The ECM proteins which have been used most commonly are collagen type I and fibrin. Fibrin allows for in vitro vasculogenesis, however, high concentrations of fibrinolysis inhibitors are needed to inhibit degradation of the ECM and subsequent loss of BAM tissue structure. For in vivo implantation, fibrinolysis inhibition may prove difficult or even harmful to the host. Therefore, we adapted in vitro culture conditions to enhance the deposition of de novo synthesized collagen type I gradually replacing the degrading fibrin ECM. The in vitro viscoelastic properties of the fibrin BAMs and deposition of collagen were characterized. BAMs engineered with the addition of proline, hydroxyproline, and ascorbic acid in the tissue culture medium had a twofold increase in Young's Modulus, a 2.5-fold decrease in maximum strain, and a 1.6-fold increase in collagen deposition. Lowering the fibrin content of the BAMs also increased Young's Modulus, decreased maximum strain, and increased collagen deposition. Tissue engineering of BAMs with autologous ECM may allow for prolonged in vivo survival.

Congenital onychodysplasia of the index finger presenting as a congenital bifid nail.

Congenital onychodysplasia of the index finger (COIF) is a rare disorder characterized by various nail dystrophies, often with underlying bony deformity. We report a case of a COIF presenting as a congenital bifid nail deformity with underlying bone deformity.

Intratumoral heterogeneity of chromosome 9 loss and CDKN2A (p16) protein expression in a morphologically challenging spitzoid melanoma.

In young adults and children, spitzoid melanoma carries striking resemblance to spitz nevus clinically and histopathologically. Many have attempted to differentiate between these 2 entities by searching for immunohistochemical and molecular diagnostic differences. Here, the authors report a spitzoid melanoma in a young adult, which was morphologically similar to a spitzoid nevus and carried a loss of chromosome 9 detected by an array-based comparative genomic hybridization. However, the expression of cyclin-dependent kinase inhibitor 2A (p16) protein, encoded on chromosome 9p21, detected by the immunohistochemical study was heterogeneous among tumor cells. This case demonstrates the presence of clonal heterogeneity of losses of chromosome 9 and p16 protein expression within a single spitzoid melanoma, challenging a robust application of p16 expression detected only by immunohistochemical staining in determining the diagnosis of spitzoid melanoma.