No abstract

In this paper, a simple, but effective method is reported to construct the core−shell gold nanorod@metal–organic frameworks (AuNR@MOFs) as a multifunctional theranostic platform by using functionalized AuNRs as seed crystal for the growth of porphyrinic MOFs on the surface of AuNR. Such a delicate tunable core−shell composite not only possesses the improved drug loading efficiency, near‐infrared light‐trigger drug release, and fluorescence imaging, but also can produce reactive oxygen species as well as photothermal activity to achieve combined cancer therapy. It is further demonstrated that the camptothecin loaded AuNR@MOFs show distinctively synergistic efficiency for damaging the cancer cell in vitro and inhibiting the tumor growth and metastasis in vivo. The development of this high‐performance incorporated nanostructure will provide more perspectives in the design of versatile nanomaterials for biomedical applications.

Magnetic microrobots can be actuated in fuel-free conditions and are envisioned for biomedical applications related to targeted delivery and therapy in a minimally invasive manner. However, mass fabrication of microrobots with precise propulsion performance and excellent therapeutic efficacy is still challenging, especially in a predictable and controllable manner. Herein, we propose a facile technique for mass production of magnetic microrobots with multiple functions using Spirulina (Sp.) as biotemplate. Core−shell-structured Pd@Au nanoparticles (NPs) were synthesized in Sp. cells by electroless deposition, working as photothermal conversion agents. Subsequently, the Fe 3 O 4 NPs were deposited onto the surface of the obtained (Pd@Au)@Sp. particles via a sol−gel process, enabling them to be magnetically actuated. Moreover, the anticancer drug doxorubicin (DOX) was loaded on the (Pd@Au)/Fe 3 O

A significant pathological signature of Alzheimer's disease (AD) is the deposition of amyloid-β (Aβ) plaques in the brain and the synaptic dysfunction and neurodegeneration associated with it. Compounds or drugs that inhibit Aβ fibrillation are thus desirable to develop novel therapeutic strategies against AD. Conventional strategies usually require an elaborate design of their molecular structures. Here we report the size-effect of gold nanoparticles (AuNPs) and nanoclusters (AuNCs) in the inhibition of protein amyloidosis. Using l-glutathione stabilized AuNPs with different sizes and AuNCs as examples, we show that large AuNPs accelerate Aβ fibrillation, whereas small AuNPs significantly suppress this process. More interestingly, AuNCs with smaller sizes can completely inhibit amyloidosis. Dynamic light scattering (DLS) experiments show that AuNCs can efficiently prevent Aβ peptides from aggregation to larger oligomers (e.g. micelles) and thus avoid nucleation to form fibrils. This is crucially important for developing novel AD therapies because oligomers are the main source of Aβ toxicity. This work presents a novel strategy to design anti-amyloidosis drugs, which also provides interesting insights to understand how biological nanostructures participate in vivo in Aβ fibrillation from a new perspective.