No abstract

Hydrophilic−hydrophobic core−shell microparticles are highly appealing for a variety of industrial applications (foods, pharmaceutics, cosmetics, biomedicines, etc.) owing to their unique properties of moisture resistance and controlled release. However, the fabrication of such structured microparticles proves to be nontrivial due to the difficulty in assembling two materials of distinctly different hydrophilicities and hydrophobicities. This paper reports a facile method to fabricate hydrophilic−hydrophobic core− shell microparticles using all-natural food-grade polysaccharides and proteins, based on a novel principle of gel-networkrestricted antisolvent precipitation. Immersion of microgel beads prepared from hydrophilic polysaccharides (i.e., alginates, κ-carrageenan, agarose) into a hydrophobic protein solution (i.e., zein in 70% aqueous ethanol) enables slow and controllable antisolvent precipitation of a protein layer around the microbead surface, leading to the formation of a hydrophilic−hydrophobic core−shell structure. The method applies to various gelling systems and can easily tailor the particle size and shell thickness. The resulting freeze-dried microparticles demonstrate restricted swelling in water, improved moisture resistance, and sustained release of encapsulants, with great potential in applications such as protection of unstable and/or hygroscopic compounds and delivery and controlled release of drugs, bioactives, flavors, etc. The method is rather universal and can be extended to prepare more versatile core−shell structures using a large variety of hydrophilic and hydrophobic materials.

Biofilms are colonies of bacteria embedded inside a complicated self-generating intercellular. The formation and scatter of a biofilm is an extremely complex and progressive process in constant cycles. Once formed, it can protect the inside bacteria to exist and reproduce under hostile conditions by establishing tolerance and resistance to antibiotics as well as immunological responses. In this article, we reviewed a series of innovative studies focused on inhibiting the development of biofilm and summarized a range of corresponding therapeutic methods for biological evolving stages of biofilm. Traditionally, there are four stages in the biofilm formation, while we systematize the therapeutic strategies into three main periods precisely:(i) period of preventing biofilm formation: interfering the colony effect, mass transport, chemical bonds and signaling pathway of plankton in the initial adhesion stage; (ii) period of curbing biofilm formation:targeting several pivotal molecules, for instance, polysaccharides, proteins, and extracellular DNA (eDNA) via polysaccharide hydrolases, proteases, and DNases respectively in the second stage before developing into irreversible biofilm; (iii) period of eliminating biofilm formation: applying novel multifunctional composite drugs or nanoparticle materials cooperated with ultrasonic (US), photodynamic, photothermal and even immune therapy, such as adaptive immune activated by stimulated dendritic cells (DCs), neutrophils and even immunological memory aroused by plasmocytes. The multitargeted or combinational therapies aim to prevent it from developing to the stage of maturation and dispersion and eliminate biofilms and planktonic bacteria simultaneously.

BackgroundFibroblast-like synoviocytes (FLS) are essential cellular components in inflammatory joint diseases such as osteoarthritis (OA) and rheumatoid arthritis (RA). Despite the growing use of FLS isolated from OA and RA patients, a detailed functional and parallel comparison of FLS from these two types of arthritis has not been performed.MethodsIn the present study, FLS were isolated from surgically removed synovial tissues from twenty-two patients with OA and RA to evaluate their basic cellular functions.ResultsPure populations of FLS were isolated by a sorting strategy based on stringent marker expression (CD45−CD31−CD146−CD235a−CD90+PDPN+). OA FLS and RA FLS at the same passage (P2-P4) exhibited uniform fibroblast morphology. OA FLS and RA FLS expressed a similar profile of cell surface antigens, including the fibroblast markers VCAM1 and ICAM1. RA FLS showed a more sensitive inflammatory status than OA FLS with regard to proliferation, migration, apoptosis, inflammatory gene expression and pro-inflammatory cytokine secretion. In addition, the responses of OA FLS and RA FLS to both the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) and the anti-inflammatory drug methotrexate (MTX) were also evaluated here.ConclusionThe parallel comparison of OA FLS and RA FLS lays a foundation in preparation for when FLS are considered a potential therapeutic anti-inflammatory target for OA and RA.

A supramolecular polyelectrolyte PVA-PAANa-PAH hydrogel with excellent mechanical properties and superior conductive stability has been fabricated for multifunctional applications.