In this study, the copolymerization of sulfobetaine methacrylate (SBMA) and acrylic acid (AA) was carried out by atmospheric pressure plasma jet (APPJ) treatment. By applying APPJ on the precursor solutions, OH radicals and the other reactive species were generated to induce the polymerization processes in solutions. The molecular weight and composition of the resultant poly(SBMA‐co‐AA) can be easily modulated by varying the plasma parameters including treatment time and applied power. The anti‐biofouling effects of the resultant poly(SBMA‐co‐AA) against biomolecules including lysozyme, bovine serum albumin (BSA), and L‐929 mouse fibroblast cells revealed excellent fouling resistance. This study demonstrated that APPJ‐assisted copolymerization is a chemical initiator free process and can provide a simpler alternative route for the preparation of copolymers with designated compositions and advantageous functions.

Previously a model was reported on the simulation of a SF6 plasma generated wettability gradient by considering only the diffusion of the reactive species in plasma. This study proposed a modified model to describe the wettability gradient created by SF6 plasma by further considering the chemical reactions between the plasma species and the substrate. The wettability gradient was prepared by applying SF6 plasma on the O2 plasma pretreated polypropylene film that was covered with a mask. Experimentally, the chemical composition and surface wettability along the gradient was characterized by electron spectroscopy for chemical analysis, contact angle measurements and atomic force microscopy. For the mathematical model, two main assumptions were made for the formation of gradient on the surface of substrate: (i) the dissociation and ionization of SF6 plasma in the vacuum chamber followed the diffusion‐adsorption‐reaction processes and (ii) the fluorine radicals were the principle reactive species. The computation of the numerical solutions was facilitated by the finite element method. The simulated surface fluorine content and surface wettability matched exceptionally (≈95%) with the experimental results. The numerical evaluation of the spatial distribution of plasma reactive species in the mask in y‐ and z‐directions and t‐domain also assisted the understanding of the surface interactions on the gradients.

Oxygen free radicals have been implicated in the pathogenesis of toxic liver injury and are thought to be involved in cardiac dysfunction in the cirrhotic heart. Therefore, direct evidence for the electron spin resonance (ESR) detection of how D‑galactosamine (GalN), an established experimental hepatotoxic substance, induced free radicals formation in platelets and primary hepatocytes is presented in the present study. ESR results demonstrated that GalN induced hydroxyl radicals (OH•) in a resting human platelet suspension; however, radicals were not produced in a cell free Fenton reaction system. The GalN‑induced OH• formation was significantly inhibited by the cyclooxygenase (COX) inhibitor indomethasin, though it was not affected by the lipoxygenase (LOX) or cytochrome P450 inhibitors, AA861 and 1‑aminobenzotriazole (ABT), in platelets. In addition, the present study demonstrated that baicalein induced semiquinone free radicals in platelets, which were significantly reduced by the COX inhibitor without affecting the formed OH•. In the mouse primary hepatocytes, the formation of arachidonic acid (AA) induced carbon‑centered radicals that were concentration dependently enhanced by GalN. These radicals were inhibited by AA861, though not affected by indomethasin or ABT. In addition, GalN did not induce platelet aggregation prior to or following collagen pretreatment in human platelets. The results of the present study indicated that GalN and baicalein may induce OH• by COX and LOX in human platelets. GalN also potentiated AA induced carbon‑centered radicals in hepatocytes via cytochrome P450. The present study presented the role of free radicals in the pathophysiological association between platelets and hepatocytes.