Antibody surface immobilization is a promising strategy to capture cells of interest from circulating fluids in vitro and in vivo. An application of particular interest in vascular interventions is to capture endothelial progenitor cells (EPCs) on the surface of stents to accelerate endothelialization. The clinical impact of EPC capture stents has been limited by the lack of efficient selective cell capture. Here, we describe a simple method to immobilize a variety of immunoglobulin G antibodies through their fragment crystallizable (Fc) regions via surface-conjugated RRGW peptides for cell capture applications. As an EPC capture model, peripheral blood endothelial colony-forming cells suspended in cell culture medium with up to 70% serum were captured by immobilized anti-CD144, anti-CD34 or anti-CD309 antibodies under laminar flow. The endothelial colony-forming cells were successfully enriched from a mixture with peripheral blood mononuclear cells using surfaces with anti-CD309 but not anti-CD45. This antibody immobilization approach holds great promise to engineer vascular biomaterials with improved EPC capture potential. The ease of immobilizing different antibodies using the same Fc-binding peptide surface grafting chemistry renders this platform suitable to screen antibodies that maximize cell capture efficiency and selectivity.

Dimethyl carbonate (DMC) is an eco-friendly and sustainable compound with widespread industrial applications. Various extensive routes have been exploited in the chemical industry to produce DMC. However, these routes have several environmental and energy drawbacks. In this study, a promising novel industrial scheme for the synthesis of DMC via the oxidative carbonylation of vaporized methanol with dimethyl oxalate (DMO) as a byproduct is investigated. A methanol conversion of 81.86% and a DMC selectivity of 83.47% were achieved using an isothermal fixed-bed reactor at 130 °C. The DMC is withdrawn at a purity of >99 mol% via pressure-swing azeotropic distillations. Heat integration was performed to optimize energy consumption, reducing the energy requirements by 28%. An economic evaluation was performed for estimating the profitability via cash-flow diagrams, predicting a payback period of 3.7 years. The proposed green process exhibits several benefits, including high profitability and being environmentally friendly. It also eliminates the use or production of hazardous materials, and it enhances safety characteristics.

Maximizing the re-endothelialization of vascular implants such as prostheses or stents has the potential to significantly improve their long-term performance. Endothelial progenitor cell capture stents with surface-immobilized antibodies show significantly improved endothelialization in the clinic. However, most current antibody-based stent surface modification strategies rely on antibody adsorption or direct conjugation via amino or carboxyl groups which leads to poor control over antibody surface concentration and/or molecular orientation, and ultimately bioavailability for cell capture. Here, we assess the utility of a bioaffinity-based surface modification strategy to immobilize antibodies targeting endothelial cell surface antigens. A cysteine-tagged truncated protein G polypeptide containing three Fc-binding domains was conjugated onto aminated polystyrene substrates via a bi-functional linking arm, followed by antibody immobilization. Different IgG antibodies were successfully immobilized on the protein G-modified surfaces. Covalent grafting of the protein G polypeptide was more effective than surface adsorption in immobilizing antibodies at high density based on fluorophore-labeled secondary antibody detection, as well as endothelial colony-forming cell capture through anti-CD144 antibodies. This work presents a potential avenue for enhancing the performance of cell capture strategies by using covalent grafting of protein G polypeptides to immobilize IgG antibodies.

While cells are driven to preserve their own survival, they must cooperate to ensure embryo viability. To explore how cellular behaviours shape human development, we intersect evolutionary game theory and in vitro embryo modelling. We focus on cell competition, a conserved cell-cell killing thought to enable embryonic error correction, though few studies directly link it to embryo success. Our collective risk game shows that killing is costly for a cell, but beneficial when the embryo exceeds its target size and the probability of survival is low. Analogously, successful heX-embryoids form within the target size range of the native human embryonic disc and inhibiting cell death produces larger, defective embryoids. Killing and proliferating are responsive cellular behaviours that maintain optimal embryoid size, consistent with their emergence as conditional strategies in our game. Further, conditional killing is a "threat" to restrain over-proliferating cells. Counter-intuitively, cell competition may underpin cooperation in the embryo.