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Tailoring surface characteristics is key to guiding scaffold interaction with the biological environment, promoting successful biointegration while minimizing immune responses and inflammation. In cardiac tissue engineering, polyvinylidene fluoride (PVDF) is a material of choice for its intrinsic piezoelectric properties, which can be enhanced through electrospinning, also enabling the fabrication of nanofibrous structures mimicking native tissue. However, the inherent hydrophobicity of PVDF can hinder its integration with biological tissues. To overcome this limitation, electrospun PVDF patches were subjected to radio-frequency low-pressure O plasma treatment to enhance surface hydrophilicity and overall biocompatibility. A systematic experimental study identified optimal parameters, revealing that higher gas content and prolonged exposure are preferable to high power levels, which deteriorate the patch's morphological and mechanical properties. X-ray photoelectron spectroscopy confirmed the formation of oxygen-containing surface groups, resulting in the patch's superhydrophilicity. Preservation of the fibrous nanostructure and electroactive phase content was verified using scanning electron microscopy and infrared spectroscopy combined with differential scanning calorimetry, respectively. The optimized plasma treatment maintained the patch's elasticity and demonstrated long-term stability for up to 3 months. In vitro biocompatibility was assessed through indirect and direct tests using AC16 human cardiomyocytes and neonatal human dermal fibroblasts, revealing good cell viability, adhesion, and spreading over 7-days. Finally, plasma-treated patches demonstrated strong adhesion to the myocardial tissue and exhibited markedly reduced inflammatory response compared to the untreated controls, as shown by decreased CD45 immune cell infiltration around the patch implanted in infarcted mice, highlighting the surface treatment's effectiveness in enhancing in vivo biocompatibility.
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http://dx.doi.org/10.1016/j.bioadv.2025.214488 | DOI Listing |
J Clin Invest
September 2025
The University of Texas at Austin, Austin, United States of America.
Background: Following SARS-CoV-2 infection, ~10-35% of COVID-19 patients experience long COVID (LC), in which debilitating symptoms persist for at least three months. Elucidating biologic underpinnings of LC could identify therapeutic opportunities.
Methods: We utilized machine learning methods on biologic analytes provided over 12-months after hospital discharge from >500 COVID-19 patients in the IMPACC cohort to identify a multi-omics "recovery factor", trained on patient-reported physical function survey scores.
J Clin Invest
September 2025
Department of Cellular and Molecular Medicine, UCSD, La Jolla, United States of America.
3-O-sulfation of heparan sulfate (HS) is the key determinant for binding and activation of Antithrombin III (AT). This interaction is the basis of heparin treatment to prevent thrombotic events and excess coagulation. Antithrombin-binding HS (HSAT) is expressed in human tissues, but is thought to be expressed in the subendothelial space, mast cells, and follicular fluid.
View Article and Find Full Text PDFJ Thromb Thrombolysis
September 2025
Central Laboratory of Yongchuan Hospital, Chongqing Medical University, No. 439, Xuanhua Road, Yongchuan District, Chongqing, 402160, China.
In vitro assessment of the inhibitory effect of antiplatelet drugs on platelet aggregation is frequently employed to guide personalized antiplatelet therapy in clinical practice. However, existing methods for detecting platelet aggregation rely heavily on high concentrations of exogenous agonists, which may obscure part of the inhibitory effect of antiplatelet drugs and lead to an underestimation of their effects. This study validates a novel analytical strategy for evaluating the effects of antiplatelet drugs by quantifying the microscopic three-dimensional morphological parameters of platelet aggregates formed through spontaneous aggregation on a glass surface.
View Article and Find Full Text PDFMetabolomics
September 2025
Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Introduction: Knockout of the Fmo5 gene in mice led to a lean, slow-ageing phenotype characterised by the presence of 2,3-butanediol isomers in their urine and plasma. Oral treatment of wildtype mice with 2,3-butanediol led to a low cholesterol, low epididymal fat phenotype.
Objectives: Determine if significant, heterozygous coding variations in human FMO5 would give rise to similar clinical and metabolic phenotypes in humans, as in C57BL/6J mice with knockout of the Fmo5 gene and in particular, increased excretion of 2,3-butanediol.
Diabetologia
September 2025
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Aims/hypothesis: Alpha cell dysregulation is an integral part of type 2 diabetes pathophysiology, increasing fasting as well as postprandial glucose concentrations. Alpha cell dysregulation occurs in tandem with the development of insulin resistance and changes in beta cell function. Our aim was to investigate, using mathematical modelling, the role of alpha cell dysregulation in beta cell compensatory insulin secretion and subsequent failure in the progression from normoglycaemia to type 2 diabetes defined by ADA criteria.
View Article and Find Full Text PDF