In this study the fabrication and characterization of an electrically conductive composite material comprised of poly(epsilon-caprolactone) (PCL), polyaniline (PANi), and bioactive mesoporous silicon (BioSilicon) is discussed. The influence of PANi and silicon on calcium phosphate induction was assessed via ex vitro calcification analyses (by acellular simulated body fluid (SBF) exposure) both with and without electrical bias. Acceleration of calcium phosphate formation is one possible desirable feature of "smart" synthetic scaffolds for selected orthopedic-relevant applications. In addition, electrical stability assays were performed in growth medium (DMEM) to determine the stability of such structures to bias in an authentic electrolyte during a typical cell experiment. The cytocompatibility of the composites was evaluated in vitro using human kidney fibroblasts (HEK 293) cell proliferation assays, along with more orthopedically relevant mesenchymal stem cells from mouse stroma. Importantly, these composites demonstrate accelerated calcification in SBF when electrical bias is applied cathodically to the scaffold. Furthermore, these scaffolds exhibit noncytotoxic behavior in the presence of fibroblasts over an 8-day culture period, and attachment of stromal cells to the semiconducting scaffold was directly imaged via scanning electron microscopy. Overall, these results suggest that materials of this type of composition have potential merit as a biomaterial.
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http://dx.doi.org/10.1002/jbm.a.31547 | DOI Listing |
J Mech Behav Biomed Mater
January 2025
School of Materials Science and Engineering, Colorado State University, 700 Meridian Ave, Fort Collins, 80523, CO, USA. Electronic address:
Hyaluronic acid-enhanced polyethylene polymeric TAVR shows excellent in vivo anti-calcific, anti-thrombotic, and in vitro hydrodynamic performance. However, during durability testing, impact wear and fatigue cause early valve failure. Heart valve durability can be improved by strengthening the leaflet with fiber reinforcement.
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Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
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Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute; and Emory University School of Medicine, Atlanta, GA (L.S.S.).
There is a new awareness of the widespread nature of metabolic dysfunction-associated steatotic liver disease (MASLD) and its connection to cardiovascular disease (CVD). This has catalyzed collaboration between cardiologists, hepatologists, endocrinologists, and the wider multidisciplinary team to address the need for earlier identification of those with MASLD who are at increased risk for CVD. The overlap in the pathophysiologic processes and parallel prevalence of CVD, metabolic syndrome, and MASLD highlight the multisystem consequences of poor cardiovascular-liver-metabolic health.
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Department of Orthopedic, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.
Low back pain (LBP) caused by nucleus pulposus degeneration and calcification leads to great economic and social burden worldwide. Unexpectedly, no previous studies have demonstrated the association and the underlying mechanism between nucleus pulposus tissue degeneration and calcification formation. Secreted Phosphoprotein 1 (SPP1) exerts crucial functions in bone matrix mineralization and calcium deposition.
View Article and Find Full Text PDFFront Cell Dev Biol
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Department of Spine Surgery and Innovative Laboratory of Orthopedics, Shenzhen Nanshan People's Hospital, Shenzhen, Guangdong, China.
Intervertebral disc degeneration (IVDD) is the leading cause of low back pain, where degeneration and death of nucleus pulposus cells within the intervertebral disc (IVD) can be obviously revealed. This degeneration can result in an imbalance in the extracellular matrix due to the loss of proteoglycans and water content, which can further lead to catabolic and anabolic dysfunction of the IVD. Recently, the dysfunction of cartilage endplate (CEP) during aging has drawn large attention due to its essential functions in contributing nutrient exchange and maintaining IVD homeostasis.
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