Miniemulsion polymerization of styrene using carboxylated graphene quantum dots as surfactant

Carboxylated graphene quantum dots (cGQDs) were synthesized from dextrose and sulfuric acid via a hydrothermal process, and subsequently used as sole surfactant in miniemulsion polymerization of styrene

Miniemulsion polymerization using carboxylated graphene quantum dots as surfactants: Effects of monomer and initiator type

Graphene quantum dots (GQDs) are building blocks of emerging interest for fabrication of polymeric nanocomposite materials with a range of potential applications. In the present work, we have conducted a detailed investigation into the use of carboxylated GQDs as surfactants in aqueous miniemulsion polymerization. The cGQDs were prepared by carbonization of dextrose according to a bottom-up hydrothermal approach. It is demonstrated that cGQDs can satisfactorily stabilize miniemulsions of a variety of vinyl monomers including styrene, acrylates and methacrylates. The nature of the initiation system plays a pivotal role in regards to monomer conversion-the water soluble initiator 2,2'-azobis[2-(2-imidazolin-2-yl)propane]dihydrochloride (VA-044) resulted in substantially higher conversions than the oil soluble initiator azobisisobutyronitrile (AIBN). The present results illustrate that these cGQDs have the ability to function as surfactants in miniemulsion polymerization for various vinyl monomer types, which has implications for hybrid nanocomposite nanoparticles and materials synthesis

The Probiotic Mixture VSL#3 Dampens LPS-Induced Chemokine Expression in Human Dendritic Cells by Inhibition of STAT-1 Phosphorylation

VSL#3, a mixture of 8 different probiotic bacteria, has successfully been used in the clinic to treat Ulcerative Colitis. We previously identified the modulation of chemokines as a major mechanism in the protective effect of the VSL#3 in a mouse model of colitis. This was supported by in vitro studies that implicated a role for VSL#3 in the suppression of LPS-induced chemokine production by mouse bone marrow-derived dendritic cells (DC). Herein, we validated these findings employing human monocyte-derived DC. Stimulation of human DC with LPS, VSL#3, or a combination of both resulted in their maturation, evident from enhanced expression of activation markers on the cell-surface, as well as the induction of various chemokines and cytokines. Interestingly, a set of LPS-induced chemokines was identified that were suppressed by VSL#3. These included CXCL9, CXCL10, CCL2, CCL7, and CCL8. In silico approaches identified STAT-1 as a dominant regulator of these chemokines, and this was confirmed by demonstrating that LPS-induced phosphorylation of this transcription factor was inhibited by VSL#3. This indicates that VSL#3 may contribute to the control of inflammation by selective suppression of STAT-1 induced chemokines