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We have successfully controlled the shape of gold nanocrystals through a simple and low‐cost hydrothermal method based on a modified polyol process. Well‐defined gold nanocrystals of icosahedral shape were synthesized in high yields by the rapid reduction of gold precursors with ethylene glycol (EG) in the presence of poly(vinyl pyrrolidone) (PVP) under hydrothermal conditions for 1 h. Truncated icosahedra (football‐shaped) have been prepared for the first time by prolonging the reaction time to 4 h. Both nanocrystal shapes were obtained quantitatively. Addition of citric acid inhibits the shape‐change process (from icosahedron to truncated icosahedron) by blocking oxidative etching, while addition of Fe(III) facilitates the shape‐change process by enhancing oxidative etching. We propose that growth of truncated icosahedra can be induced and maintained through interplay of the following processes: generation of multiple twinned seeds, shape‐ and size‐focusing by Ostwald ripening, and oxidative etching and preferential growth on the {100} face.

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Nanorods provide distinct advantages over their spherical counterparts for targeted drug delivery. Here, a novel method is described for the synthesis of biocompatible protein nanorods from spherical polystyrene templates using the layer-by-layer (LBL) technique. These nanorods can be used as a vehicle for the delivery of therapeutic agents to diseased sites.

Approximately 10–15% of all bone fractures do not heal properly, causing patient morbidity and additional medical care expenses. Therefore, better mechanism-based fracture repair approaches are needed. In this study, a reduced number of osteoclasts (OCs) and autophagosomes/autolysosomes in OC can be observed in GPCR kinase 2-interacting protein 1 (GIT1) knockout (KO) mice on days 21 and 28 post-fracture, compared with GIT1 wild-type (GIT1 WT) mice. Furthermore, in vitro experiments revealed that GIT1 contributes to OC autophagy under starvation conditions. Mechanistically, GIT1 interacted with Beclin1 and promoted Beclin1 phosphorylation at Thr119, which induced the disruption of Beclin1 and Bcl2 binding under starvation conditions, thereby, positively regulating autophagy. Taken together, the findings suggest a previously unappreciated role of GIT1 in autophagy of OCs during fracture repair. Targeting GIT1 may be a potential therapeutic approach for bone fractures.