Monodisperse Gd2O3‐embedded iron oxide (GdIO) nanoparticles can simultaneously enhance the local magnetic field intensities of each other under an external magnetic field and result in synergistic enhancement of T1 and T2 effects. GdIO nanoparticles have the unique property to be both T1 and T2 contrast agents and can potentially lead to higher accuracy in cancer diagnosis, particularly liver tumors.

Controlled synthesis of monodisperse iron oxide (IO) nanostructures with diverse morphology remains a major challenge. In this work, IO nanostructures with various shapes and surface structures were synthesized by thermal decomposition of iron oleate (FeOL) in the presence of sodium oleate (NaOL). In a mild condition using 1octadecene (ODE) as solvent, NaOL may preferentially bind to Fe 3 O 4 {111} facets and lead to the formation of Fe 3 O 4 {111} facet exposed IO plates, truncated octahedrons, and tetrahedrons. While in a high-boiling temperature tri-noctylamine (TOA) solvent, we obtained Fe 3 O 4 {100} facet exposed IO cubes, concaves, multibranches, and assembled structures by varying the molar ratios of NaOL/FeOL. Moreover, we demonstrated that IO nanoparticles (NPs) with metalexposed surface structures have enhanced T 1 relaxation time shortening effects to protons, and IO NPs with anisotropic shapes are superior in protons T 2 relaxation shortening due to the larger effective radii compared to that of spherical IO NPs. This study can provide rational design considerations for the syntheses and applications of IO nanostructures for a broad community of material research fields.

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Autophagy plays a key role in human health and disease, especially in cancer and neurodegeneration. Many autophagy regulators are developed for therapy. Diverse nanomaterials have been reported to induce autophagy. However, the underlying mechanisms and universal rules remain unclear. Here, for the first time, we show a reliable and general mechanism by which nanoparticles induce autophagy and then successfully modulate autophagy via tuning their dispersity. Various well-designed univariate experiments demonstrate that nanomaterials induce autophagy in a dispersity-dependent manner. Aggregated nanoparticles induce significant autophagic effect in comparison with well-dispersed nanoparticles. As the highly stable nanoparticles may block autophagic degradation in autolysosomes, endocytosis and intracellular accumulation of nanoparticles can be responsible for this interesting phenomenon. Our results suggest dispersity-dependent autophagic effect as a common cellular response to nanoparticles, reveal the relationship between properties of nanoparticles and autophagy, and offer a new alternative way to modulate autophagy.

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