Publications by authors named "Mohammad Abdul Sattar"

The significant rise in end-of-life tires (ELTs) globally poses immediate environmental and human health risks. Therefore, to promote ELTs recycling and to reduce tire industry carbon emissions, herein we present a facile approach for fine-tuning the interfacial interactions between pyrolytic carbon black (P-CB) obtained from ELTs and natural rubber (NR) matrix using phosphonium-based ionic liquid (PIL). The reinforcing effect of PIL-activated P-CB was studied by replacing the furnace-grade carbon black (N330-CB) with varying PIL and P-CB loadings.

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-(1,3-Dimethyl butyl)-'-phenyl--phenylenediamine (6-PPD) is a worldwide antioxidant commonly added to delay the thermo-oxidative degradation of tire rubbers. Unfortunately, 6PPD and its transformation product 6PPD-quinone are toxic to aquatic organisms (e.g.

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Extensive use of zinc oxide and accelerators such as diphenyl guanidine (DPG) in the vulcanization of rubber composites entail potential environmental risks. These are pervasive contaminants of roadway runoff originating from tire wear particles (TWPs). Herein, the effect of phosphonium ionic liquids (PILs) in styrene-butadiene rubber compounds was demonstrated with reduced ZnO loading and no DPG to minimize the environmental footprint of the vulcanization process.

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Polymers and polymer nanocomposites (PNCs) are extensively used in daily life. However, the growing requirement of advanced PNCs laid persistent environmental issues due to deformation-induced damage that once formed, does not vanish at future stages. Therefore, self-healing materials with significantly enhanced long life and safety have been designed to epitomize the forefront of recent advances in materials chemistry and engineering.

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Intermolecular interactions between the constituents of a polymer nanocomposite at the polymer-particle interface strongly affect the segmental mobility of polymer chains, correlated with their glass transition behavior, and are responsible for the improved dynamical viscoelastic properties. In this work, we emphasized on the evolution of characteristic interfaces and their dynamics in silica (SiO NP)-reinforced, solution-polymerized, styrene butadiene rubber (SSBR) composites, whose relative prevalence varied with the phosphonium ionic liquid (PIL) volume fraction, used as an interfacial modifier. The molecular origins of such interfaces were examined through systematic dielectric spectroscopy, molecular dynamics (MD) simulations, and dynamic-mechanical analyses.

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While survival rates have markedly improved following cardiac ischemia-reperfusion (IR) injury, the resulting heart damage remains an important issue. Preserving mitochondrial quality and limiting NLRP3 inflammasome activation is an approach to limit IR injury, in which the mitochondrial deacetylase sirtuin 3 (SIRT3) has a role. Recent data demonstrate cytochrome P450 (CYP450)-derived epoxy metabolites, epoxydocosapentaenoic acids (EDPs), of docosahexaenoic acid (DHA), attenuate cardiac IR injury.

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The preparation of natural rubber (NR)-silica (SiO) elastomeric composites with excellent mechanical properties along with better self-healing ability remains a key challenge. Inspired by the energy dissipation and repairability of sacrificial bonds in biomaterials, a strategy for combining covalent and noncovalent sacrificial networks is engineered to construct a dual hybrid network. Here, the approach used to fabricate the composites was self-assembly of NR, bearing proteins and phospholipids on its outer bioshell, with SiO via metal-ion-mediated heteroaggregation effected by reversible electrostatic and H-bonds.

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Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that causes life threatening renal disease and current therapies are limited with serious side-effects. CYP epoxygenase metabolites of arachidonic acid epoxyeicosatrienoic acids (EETs) demonstrate strong anti-inflammatory and kidney protective actions. We investigated the ability of an orally active EET analog, EET-A to prevent kidney injury in a mouse SLE model.

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