Optical imaging of diseases represents a highly dynamic and multidisciplinary research area, and second near-infrared window (NIR-II, 1000–1700 nm) imaging is at the forefront of the research on optical imaging techniques.
Anisotropic colloidal hybrid nanoparticles
exhibit superior optical
and physical properties compared to their counterparts with regular
architectures. We herein developed a controlled, stepwise strategy
to build novel, anisotropic, branched, gold nanoarchitectures (Au-tripods)
with predetermined composition and morphology for bioimaging. The
resultant Au-tripods with size less than 20 nm showed great promise
as contrast agents for in vivo photoacoustic imaging
(PAI). We further identified Au-tripods with two possible configurations
as high-absorbance nanomaterials from various gold multipods using
a numerical simulation analysis. The PAI signals were linearly correlated
with their concentrations after subcutaneous injection. The in vivo biodistribution of Au-tripods favorable for molecular
imaging was confirmed using small animal positron emission tomography
(PET). Intravenous administration of cyclic Arg-Gly-Asp-d-Phe-Cys (RGDfC) peptide conjugated Au-tripods (RGD-Au-tripods) to
U87MG tumor-bearing mice showed PAI contrasts in tumors almost 3-fold
higher than for the blocking group. PAI results correlated well with
the corresponding PET images. Quantitative biodistribution data revealed
that 7.9% ID/g of RGD-Au-tripods had accumulated in the U87MG tumor
after 24 h post-injection. A pilot mouse toxicology study confirmed
that no evidence of significant acute or systemic toxicity was observed
in histopathological examination. Our study suggests that Au-tripods
can be reliably synthesized through stringently controlled chemical
synthesis and could serve as a new generation of platform with high
selectivity and sensitivity for multimodality molecular imaging.
Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality, but the molecular underpinnings of this association are poorly understood. Here, we demonstrate in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to increased cellular proliferation and tumour burden. Saturated fat intake (SFI) is also associated with an enhanced MYC transcriptional signature in prostate cancer patients. The SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, switching from a high-fat to a low-fat diet, attenuates the MYC transcriptional program in mice. Our findings suggest that in primary prostate cancer, dietary SFI contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.
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