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Additional file 1. Additional table and supplementary figures.

Comb-like aluminum (Al) doped ZnO (ZnO:Al) nanostructures were synthesized on Al/silicon substrate by thermal evaporation at 650 °C. A pre-deposited Al layer on the Si substrate was employed to provide the Al dopant into ZnO nanostructures. High-resolution transmission electron microscopy (HRTEM) images displayed that ZnO:Al nanostructures were grown along the [0001] axis. Energy dispersive X-ray spectroscopy (EDS) mapping showed that the Al element was highly scattered and dispersed throughout the ZnO nanostructures. Photoluminescence (PL) spectrum revealed that the ZnO:Al and pure ZnO nanostructures have a blue band emission at 382 nm and 385 nm, respectively. The Al doping did increase the concentration of the oxygen vacancies, therefore a high intensity of green emission band was obtained in ZnO:Al nanostructures as compared to that of pure ZnO nanostructures. The field emission properties of ZnO:Al and ZnO nanostructures were also investigated in this work. The turn-on field of ZnO:Al and pure ZnO nanostructures were found to be 3.8 and 5 V/μm, respectively; the current density was 1 µA/cm 2 . The thresholds field for ZnO:Al and ZnO nanostructures were estimated around 25 and 47 V/μm, respectively; the current density was 1 mA/cm 2 .

Histone deacetylase (HDAC) inhibitors (HDACIs) have long been studied and shown promises in the treatment of various neurodegenerative disorders including Huntington’s disease (HD). Based on many demonstrated potentials of HDACIs in mitigating various diseases, we evaluated the utility of [18F]FAHA, a radiolabeled derivative of suberoylanilide hydroxamic acid (SAHA), as a PET imaging agent for characterizing HDAC activity in a non-human primate model and a R6/2 transgenic mouse model of HD. We were aiming at HD as a potential first application, and therefore also examined the expression of HDAC and acetyl histone (AH) in brains of HD patients. This thesis describes that [18F]FAHA was metabolized rapidly to [18F]FACE in both blood plasma and brain. Kinetic analysis indicated that peripherally generated [18F]FACE contributed to the total brain activity. We therefore used a dual-input function model to analyze the kinetics of tracer accumulation and inhibition by SAHA in rhesus monkeys. Parametric images demonstrated the inhibition of HDAC activity in the brain by SAHA in a dose-dependent manner. Huntington’s mice (R6/2) showed a gradual increase of [18F]FAHA accumulation in all organs including the brain with age. In human tissue we found significant losses of acetyl histons expression from cells in the caudate nucleus and Purkinje cells of the cerebellum in HD, while the level of HDAC 5 was increased in these cells. The data obtained in rhesus monkeys indicated that PET imaging with [18F]FAHA could be used as a pharmacodynamic biomarker of the inhibition of class IIa HDACs by HDACIs in the brain and facilitate the development and clinical translation of novel class-IIa HDACIs.