The neuroprotective effect of ceria nanoparticles in the context of brain disorders has been explained by their antioxidant effect. However, the in-depth mechanism remains unknown. As resident immune cells in the brain, microglia exert a variety of functional reprogramming termed as polarization in response to stress stimuli. Herein, custom-made ceria nanoparticles were developed and found to scavenge multiple reactive oxygen species with extremely high efficiency. These nanoparticles drove microglial polarization from a pro-inflammatory phenotype to an anti-inflammatory phenotype under pathological conditions. Pretreatment of these nanoparticles changed the microglial function from detrimental to protective for the neuronal cells by blocking the pro-inflammatory signaling. This work not only helps to elucidate the mechanism of ceria-nanoparticle-mediated neuroprotection but also provides a new strategy to rebalance the immuno-environment by switching the equilibrium of the phenotypic activation of microglia.

Flexible ferroelectrics being exploited as energy harvesting and conversion materials are highly desirable for wearable and skin-mountable electronic devices. As one of the most typical ferroelectric polymers, poly(vinylidene fluoride) (PVDF) has been widely used in modern electronic systems and devices, whose ferroelectric performance relies heavily on its β phase content. In this work, to achieve high-β-phase-content PVDF, we first introduced CoFe2O4 nanoparticles into PVDF. With the incorporation of CoFe2O4 nanoparticles used as an effective polymer nucleation agent, the percentage of the β phase in the PVDF has been significantly enhanced, e.g., 84% in the nanocomposite with 5 wt. % CoFe2O4 versus only 73% in the pure PVDF. In order to further increase the β phase content in PVDF, we subsequently proposed an easily realized strategy. By applying DC magnetic fields during the solution-casting process of the PVDF/CoFe2O4 nanocomposites, a further improved β phase content as high as 95% can be achieved. The further improvement of the β phase content is attributable to the tensile stress at the CoFe2O4/PVDF interfaces created by the coupling of magnetic field and CoFe2O4 by means of the magnetostriction effect. The high β-phase content makes the PVDF/CoFe2O4 nanocomposites a promising candidate for flexible and wearable electronic device applications.

Nb‐doped 0.9BaTiO3–0.1Bi0.5Na0.5TiO3 (0.9BT–0.1BNT) ceramics were prepared by conventional solid‐state method. The dielectric and the structural properties were investigated. It was found that the temperature–capacitance characteristics greatly depended on Nb2O5 content. With the addition of 2.0 mol% Nb2O5, 0.9BT–0.1BNT ceramic sample could satisfy the EIA X9R specification. This material was promising for high‐temperature MLCC application. Microstructure element distribution was studied using TEM and EDS. The Bi and Na were almost homogeneously distributed except grain‐boundary segregation of Bi. The Nb exhibited a nonuniform distribution from the grain boundary to the interior, showing the simultaneous presence of Nb‐rich and Nb‐poor regions. Such microheterogeneity gave rise to the temperature stability of permittivity. The solution‐precipitation mechanism was introduced to elucidate the evolution of microstructures. Degradation and recovery of insulation resistance were observed under a dc bias at 200°C, which was attributed to the electromigration and diffusion of Na+.

Development of pharmacologic agents that protect podocytes from injury is a critical strategy for the treatment of kidney glomerular diseases. Retinoic acid reduces proteinuria and glomerulosclerosis in multiple animal models of kidney diseases. However, clinical studies are limited because of significant side effects of retinoic acid. Animal studies suggest that all trans retinoic acid (ATRA) attenuates proteinuria by protecting podocytes from injury. The physiological actions of ATRA are mediated by binding to all three isoforms of the nuclear retinoic acid receptors (RARs): RARα, RARβ, and RARγ. We have previously shown that ATRA exerts its renal protective effects mainly through the agonism of RARα. Here, we designed and synthesized a novel boron-containing derivative of the RARα-specific agonist Am580. This new derivative, BD4, binds to RARα receptor specifically and is predicted to have less toxicity based on its structure. We confirmed experimentally that BD4 binds to RARα with a higher affinity and exhibits less cellular toxicity than Am580 and ATRA. BD4 induces the expression of podocyte differentiation markers (synaptopodin, nephrin, and WT-1) in cultured podocytes. Finally, we confirmed that BD4 reduces proteinuria and improves kidney injury in HIV-1 transgenic mice, a model for HIV-associated nephropathy (HIVAN). Mice treated with BD4 did not develop any obvious toxicity or side effect. Our data suggest that BD4 is a novel RARα agonist, which could be used as a potential therapy for patients with kidney disease such as HIVAN.