Demonstration of polarization-insensitive optical filters on silicon photonics platform.

We experimentally demonstrate a polarization-insensitive optical filter (PIOF) using polarization rotator-splitters (PRSs) and microring resonators (MRRs) on the silicon-on-insulator (SOI) platform with complementary metal-oxide-semiconductor (CMOS) compatible fabrication process. The PRS consists of a tapered-rib waveguide and an asymmetrical directional coupler (ADC), which realize the polarization rotation and splitting, to ensure the connected MRRs-based optical filter operating at one desired polarization when light with different polarizations are launched into the device. The measured results show that the optical transmission spectra of the device are identical for TE and TM polarization input. The box-like filtering spectra are also achieved with a 3-dB bandwidth of ∼0.15 nm and a high extinction ratio (ER) over 30 dB.

Ferulic acid amide derivatives with varying inhibition of amyloid-ß oligomerization and fibrillization.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized, in part, by the misfolding, oligomerization and fibrillization of amyloid-ß (Aß). Evidence suggests that the mechanisms underpinning Aß oligomerization and subsequent fibrillization are distinct, and may therefore require equally distinct therapeutic approaches. Prior studies have suggested that amide derivatives of ferulic acid, a natural polyphenol, may combat multiple AD pathologies, though its impact on Aß aggregation is controversial. We designed and synthesized a systematic library of amide derivatives of ferulic acid and evaluated their anti-oligomeric and anti-fibrillary capacities independently. Azetidine tethered, triphenyl derivatives were the most potent anti-oligomeric agents (compound 2i: IC50 = 1.8 µM ± 0.73 µM); notably these were only modest anti-fibrillary agents (20.57% inhibition of fibrillization), and exemplify the poor correlation between anti-oligomeric/fibrillary activities. These data were subsequently codified in an in silico QSAR model, which yielded a strong predictive model of anti-Aß oligomeric activity (κ = 0.919 for test set; κ = 0.737 for validation set).