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[Display omitted] • Using self-assembly and in-situ reduction strategy, the stable Pt nanoblocks were simply synthesized. • The growth of the rGO/(PLL/PASP) n -PtNB nanocomposites can be controlled by adjusting the concentrations of K 2 PtCl 6 solution, the bilayers number and concentrations of the rGO/(PLL/PASP) n nanofilms.. • The rGO/(PLL/PASP) 3 -PtNB nanocomposites can efficiently transform 4-nitrophenol into 4-aminophenol completely within 4.5 min (k app is 0.962 min−1) and keep good long-term stability. To develop Pt nanomaterials with facile approach is of great significance for the improvement of their catalytic properties for organic pollutants degradation. In this study, we report a simple in-situ reduction strategy to prepare Pt nanoblocks based on graphene/ polyamino acid self-assembly nanofilms. Polyamino acid modified graphene nanofilms severed as the nanoreactor and reducing agent for further fabrication of Pt nanoblocks. The as-prepared complex efficiently transformed 4-nitrophenol into 4-aminophenol completely within 4.5 min (k app is 0.962 min−1) and kept good long-term stability. We expect this work to offer a new valuable insight for facile preparation of Pt materials as efficient and recyclable catalysts for water pollution remediation. [ABSTRACT FROM AUTHOR]

Streptococcus equi ssp. zooepidemicus (S. zooepidemicus, SEZ) is a zoonotic bacterial pathogen that can cause various inflammation, including pneumonia. As the most abundant leukocytes in the circulation, neutrophils are the first wave of leukocytes to arrive in the lung upon infection. This study aims to evaluate the effect of caspase-1 on the host response to SEZ infection in a mouse model. Intranasal exposure to SEZ induced the expression of caspase-1 in wild-type mice lung, and increased the number of neutrophils in the alveolar cavity and alveolar wall. In addition, caspase-1 deficiency reduced the transcription levels of IL-1α, IL-1β, IL-6, and TNF-α in the lungs of infected mice, which was accompanied by decreased recruitment of pulmonary neutrophils. Moreover, knocking out caspase-1 decreased the bactericidal activity of neutrophils and promoted the pulmonary bacterial load. In line with this, the mortality of caspase-1−/− mice infected with SEZ was significantly increased compared with those of caspase-1+/+ mice. Collectively, recruiting neutrophils and enhancing the bactericidal ability of neutrophils are important means for caspase-1 to promote bacterial clearance. • SEZ exposure induces caspase-1 activation and neutrophil recruitment. • Caspase-1 deficiency impairs neutrophil recruitment and bacterial clearance. • Caspase-1 affects the transcription of pulmonary inflammatory factors during SEZ infection. • Caspase-1 was demonstrated to play an indispensable role in mice against SEZ infection. [ABSTRACT FROM AUTHOR]