Machine Learning and Structural Design to Optimize the Flame Retardancy of Polymer Nanocomposites with Graphene Oxide Hydrogen Bonded Zinc Hydroxystannate.

Designing flame-retardant polymers with high performance is a long-standing challenge, partly because of the time-consuming traditional approaches based on experiential intuition and trial-and-error screenings. Inspired by the effective new paradigm of data-driven material discovery, we used machine learning to analyze experimental data to accelerate the development of new flame-retardant polymers. To explore the relationship between limit oxygen index (LOI) and components, we prepared 20 composites and then trained a simple equation for the LOI using the method sure independence screening and sparsifying operator (SISSO). The data analysis allows us for a better understanding of the flame-retardant mechanism and components, and the equation has good accuracy in guiding the design of composites with high flame-retardant performance. Meanwhile, the increasing structural design of flame retardants is crucial to flame-retardant polymer composites. We proposed a structure of nano graphene oxide (GO) wrapped micro zinc hydroxystannate (ZHS) in a simple but effective way as a novel flame-retardant agent to enhance the flame retardancy and mechanical properties of polypropylene (PP) composites. The GO sheets were like "light yarns" wrapped onto the ZHS via hydrogen bonding in an ethanol solution. The selected samples were analyzed to confirm the predictive LOI model. The resultant composites with the substitution of intumescent flame retardant (IFR) by 1.0, 2.0, and 4.0 wt % ZHS@GO conferred better flame retardancy compared with PP composite containing only IFR, reflected by the efficient increase of LOI value and V0 rating of UL-94 vertical tests. The analysis principles and facile fabrication strategies proposed in this work could be important for developing highly flame retardant composites.

Highly sensitive colorimetric sensor for detection of iodine ions using carboxylated chitosan-coated palladium nanozyme.

Although a massive research has been devoted on the exploration of noble metal-based nanozyme, less progress has been made in the investigation of palladium (Pd) nanozyme and the interaction between ions and Pd nanozyme. In this study, a new type of Pd nanozyme was prepared by a facile one-pot approach by using carboxylated chitosan as the stabilizer. Owing to the synergistic effect of carboxylated chitosan stabilized Pd nanoparticles (CC-PdNPs) can effectively catalyze the H2O2-mediated oxidation of 3,3',5,5'-tetramethylbenzidine sulfate (TMB) accompanied by a blue color change (oxidized TMB), indicating the peroxidase-like activity of CC-PdNPs. Furthermore, the Michaelis-Menten constants and catalytic stability of CC-PdNPs render them suitable for environmental analysis and bio-detection. Here, we found that while introducing the iodine ions (I-) into the reaction medium, the peroxidase-like activity of CC-PdNPs has been rapidly and effectively inhibited through the formation of Pd-I bond; thus, the active sites of PdNPs can be blocked by I-. Based on this specific inhibition by I-, a facile colorimetric assay has been performed for the detection of I- with an extremely low limit of detection (0.19 nM). Furthermore, the practicality of the proposed sensor also has been demonstrated in tap water, and the satisfactory recoveries were obtained. Our study not only demonstrated a novel Pd-based nanozyme but also provided guidance for I- sensing for environmental analysis, food inspection, and bio-detection. Graphical abstract.

Effect of protein oxidation on kinetics of droplets stability probed by microrheology in O/W and W/O emulsions of whey protein concentrate.

Whey protein concentrate (WPC) was oxidized by peroxyl radicals derived from 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) and the kinetics of droplet stability in O/W and W/O emulsions stabilized by oxidized WPC were evaluated by studying the micro-rheology. Degrees of protein oxidation were indicated by carbonyl concentration and emulsion types were distinguished by fluorescence microscopy. Oxidation resulted in free sulfhydryl groups degradation and surface hydrophobicity decrease. Moderate protein oxidation promoted to form diminutive droplets, which aggregated quickly to gel-network structure and decreased the motion rate of droplets, leading to the increased elasticity and viscosity, which led to better stability. Over-oxidation underwent severe droplet aggregation and sediment with increased motion rate, which resulted in instability of emulsions. The W/O emulsions of oxidized WPC were more inclined to block the motion of droplets and form a stable structure with higher viscosity, compared with the O/W emulsions.

Effects of tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on the activation of ERK1/2 MAP kinases and the proliferation of human mammary epithelial cells.

Cigarette smoking is a risk factor in the developing of various cancers including breast tumors. There are more than 60 chemical carcinogens in the cigarette smoke; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) being one of the strongest tobacco-specific carcinogens. In this study, we demonstrated that NNK rapidly activated ERK1 and ERK2 MAP kinases and stimulated proliferation in human normal mammary epithelial cells. MEK1/2 specific inhibitor UO126 completely blocked NNK-induced ERK1/2 activation and cell proliferation, whereas nicotinic receptor nAchR antagonist mecamylamine partially and the selective α(7)-nAchR antagonist α-bungarotoxin essentially inhibited the NNK-induced ERK1/2 activation and cell proliferation. Surprisingly, receptor tyrosine kinase inhibitor genistein, the selective ß(1)-adrenergic antagonist atenolol, and the selective ß(2)-adrenergic antagonist ICI118.551 had a strong inhibitory effect on ERK1/2 activation and cell proliferation induced by NNK. These results suggest that there are at least two different routes in activating ERK1/2 by NNK. One is through nicotinic receptor α(7)-nAchR to MEK1/2; the other is from ß(1)/ß(2)-adrenergic transactivation of tyrosine kinase containing receptor(s) to MEK1/2. In human cancer mammary epithelial cell lines, we found that ERK MAPK signaling pathway was deregulated: (1) ERK1/2 was constitutively activated at various levels; (2) ERK1/2 was further significantly activated in response to NNK induction; (3) UO126 partially or totally failed to inhibit ERK1/2 activation induced by NNK; (4) The expression levels of ERK1/2 in the cancer cell lines were much higher than those in the normal mammary epithelial cells. The tobacco-specific carcinogen NNK showed a strong proliferative effect on human normal and cancer mammary epithelial cells; the proliferation multitudes of these cells are well correlated with the activation levels of ERK1/2 MAP kinases.