Natural bio-based monomers for biomedical applications: a review.

In recent years, synthetic and semi-synthetic polymer materials have been widely used in various applications. Especially concerning biomedical applications, their biocompatibility, biodegradability, and non-toxicity have increased the interest of researchers to discover and develop new products for the well-being of humanity. Among the synthetic and semi-synthetic materials, the use of natural bio-based monomeric materials presents a possible novel avenue for the development of new biocompatible, biodegradable, and non-toxic products. The purpose of this article is to review the information on the role of natural bio-based monomers in biomedical applications. Increased eco-friendliness, biocompatibility, biodegradability, non-toxicity, and intrinsic biological activity are some of the attributes which make itaconic, succinic, citric, hyaluronic, and glutamic acids suitable potential materials for biomedical applications. Herein, we summarize the most recent advances in the field over the past ten years and specifically highlight new and interesting discoveries in biomedical applications. Natural origin acid-based bio-monomers for biomedical applications.

Surface Coating with Hyaluronic Acid-Gelatin-Crosslinked Hydrogel on Gelatin-Conjugated Poly(dimethylsiloxane) for Implantable Medical Device-Induced Fibrosis.

Polydimethylsiloxane (PDMS) is a biocompatible polymer that has been applied in many fields. However, the surface hydrophobicity of PDMS can limit successful implementation, and this must be reduced by surface modification to improve biocompatibility. In this study, we modified the PDMS surface with a hydrogel and investigated the effect of this on hydrophilicity, bacterial adhesion, cell viability, immune response, and biocompatibility of PDMS. Hydrogels were created from hyaluronic acid and gelatin using a Schiff-base reaction. The PDMS surface and hydrogel were characterized using nuclear magnetic resonance, X-ray photoelectron spectroscopy, attenuated total reflection Fourier-transform infrared spectroscopy, and scanning electron microscopy. The hydrophilicity of the surface was confirmed via a decrease in the water contact angle. Bacterial anti-adhesion was demonstrated for Pseudomonas aeruginosa, Ralstonia pickettii, and Staphylococcus epidermidis, and viability and improved distribution of human-derived adipose stem cells were also confirmed. Decreased capsular tissue responses were observed in vivo with looser collagen distribution and reduced cytokine expression on the hydrogel-coated surface. Hydrogel coating on treated PDMS is a promising method to improve the surface hydrophilicity and biocompatibility for surface modification of biomedical applications.

Triclosan Resistance in a Bacterial Fish Pathogen, Aeromonas salmonicida subsp. salmonicida, is Mediated by an Enoyl Reductase, FabV.

Triclosan, the widely used biocide, specifically targets enoyl-acyl carrier protein reductase (ENR) in the bacterial fatty acid synthesis system. Although the fish pathogen Aeromonas salmonicida subsp. salmonicida exhibits triclosan resistance, the nature of this resistance has not been elucidated. Here, we aimed to characterize the triclosan resistance of A. salmonicida subsp. salmonicida causing furunculosis. The fosmid library of triclosan-resistant A. salmonicida subsp. salmonicida was constructed to select a fosmid clone showing triclosan resistance. With the fosmid clone showing triclosan resistance, a subsequent secondary library search resulted in the selection of subclone pTSR-1. DNA sequence analysis of pTSR-1 revealed the presence of a chromosomal-borne fabV-encoding ENR homolog. The ENR of A. salmonicida (FabVas) exhibited significant homology with previously known FabV, including the catalytic domain YX(8)K. fabVas introduction into E. coli dramatically increased its resistance to triclosan. Heterologous expression of FabVas might functionally replace the triclosan-sensitive FabI in vivo to confer E. coli with triclosan resistance. A genome-wide search for fabVas homologs revealed the presence of an additional fabV gene (fabVas2) paralog in A. salmonicida strains and the fabVas orthologs from other gram-negative fish pathogens. Both of the potential FabV ENRs expressed similarly with or without triclosan supplement. This is the first report about the presence of two potential FabV ENRs in a single pathogenic bacterium. Our result suggests that triclosan-resistant ENRs are widely distributed in various bacteria in nature, and the wide use of this biocide can spread these triclosan-tolerant ENRs among fish pathogens and other pathogenic bacteria.

Jeju ground water containing vanadium induced immune activation on splenocytes of low dose γ-rays-irradiated mice.

Vanadium, an essential micronutrient, has been implicated in controlling diabetes and carcinogenesis and in impeding reactive oxygen species (ROS) generation. γ-ray irradiation triggers DNA damage by inducing ROS production and causes diminution in radiosensitive immunocytes. In this study, we elucidate the immune activation capacities of Jeju water containing vanadium on immunosuppression caused by γ-ray irradiation, and identify its mechanism using various low doses of NaVO(3). We examined the intracellular ROS generation, DNA damage, cell proliferation, population of splenocytes, and cytokine/antibody profiles in irradiated mice drinking Jeju water for 180 days and in non-irradiated and in irradiated splenocytes both of which were treated with NaVO(3). Both Jeju water and 0.245 µM NaVO(3) attenuated the intracellular ROS generation and DNA damage in splenocytes against γ-ray irradiation. Splenocytes were significantly proliferated by the long-term intake of Jeju water and by 0.245 µM NaVO(3) treatment, and the expansion of B cells accounted for the increased number of splenocytes. Also, 0.245 µM NaVO(3) treatment showed the potency to amplify the production of IFN-γ and total IgG in irradiated splenocytes, which correlated with the expansion of B cells. Collectively, Jeju water containing vanadium possesses the immune activation property against damages caused by γ-irradiation.

Experimental autoimmune encephalomyelitis: association with mutual regulation of RelA (p65)/NF-κB and phospho-IκB in the CNS.

Recently emerging evidence that the NF-κB family plays an important role in autoimmune disease has produced very broad and sometimes paradoxical conclusions. In the present study, we elucidated that the activation of RelA (p65) of NF-κB and IκB dissociation assumes a distinct role in experimental autoimmune encephalomyelitis (EAE) progression by altering IκB phosphorylation and/or degradation. In the present study of factors that govern EAE, the presence and immunoreactivity of nuclear RelA and phospho-IκB were recorded at the initiation and peak stage, and degradation of IκBα progressed rapidly at an early stage then stabilized during recovery. The immunoreactivity to RelA and phospho-IκB occurred mainly in inflammatory cells and microglial cells but only slightly in astrocytes. Subsequently, the blockade of IκB dissociation from NF-κB reduced the severity of disease by decreasing antigen-specific T cell response and production of IL-17 in EAE. Thus, blocking the dissociation of IκB from NF-κB can be utilized as a strategy to inhibit the NF-κB signal pathway thereby to reduce the initiation, progression, and severity of EAE.