Vascular endothelial cells derived from transgene-free pig induced pluripotent stem cells for vascular tissue engineering.

Induced pluripotent stem cells (iPSCs) hold great promise for the treatment of cardiovascular diseases through cell-based therapies, but these therapies require extensive preclinical testing that is best done in species-in-species experiments. Pigs are a good large animal model for these tests due to the similarity of their cardiovascular system to humans. However, a lack of adequate pig iPSCs (piPSCs) that are analogous to human iPSCs has greatly limited the potential usefulness of this model system.

Fully biologic endothelialized-tissue-engineered vascular conduits provide antithrombotic function and graft patency.

Tissue-engineered vascular conduits (TEVCs), often made by seeding autologous bone marrow cells onto biodegradable polymeric scaffolds, hold promise toward treating single-ventricle congenital heart defects (SVCHDs). However, the clinical adoption of TEVCs has been hindered by a high incidence of graft stenosis in prior TEVC clinical trials. Herein, we developed endothelialized TEVCs by coating the luminal surface of decellularized human umbilical arteries with human induced pluripotent stem cell (hiPSC)-derived endothelial cells (ECs), followed by shear stress training, in flow bioreactors.

Navigation in Multiligament Knee Reconstruction: A Proof-of-Concept Study on a Femoral Sawbones Model.

Multiligament knee reconstruction surgery is technically challenging, requiring careful planning and execution. Accurate placement of bone tunnels is important for graft function and there is an inherent risk of tunnel collision, which can compromise graft integrity. In this proof-of-concept study, we present a technique using computer navigation to help optimize tunnel placement and to avoid collision during multiligament knee reconstruction.

De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis-Brief Report.

Background: A series of incurable cardiovascular disorders arise due to improper formation of elastin during development. Supravalvular aortic stenosis (SVAS), resulting from a haploinsufficiency of , is caused by improper stress sensing by medial vascular smooth muscle cells, leading to progressive luminal occlusion and heart failure. SVAS remains incurable, as current therapies do not address the root issue of defective elastin.