No abstract

Two-dimensional transition-metal dichalcogenides (TMDCs) with intrinsically broken crystal inversion symmetry and large second-order nonlinear responses have shown great promise for future nonlinear light sources. However, the sub-nanometer monolayer thickness of such materials limits the length of their nonlinear interaction with light. Here, we experimentally demonstrate the enhancement of the second-harmonic generation from monolayer MoSe2 by its integration onto a 220-nm-thick silicon waveguide. Such on-chip integration allows for a marked increase in the interaction length between the MoSe2 and the waveguide mode, further enabling phase matching of the nonlinear process. The demonstrated TMDC–silicon photonic hybrid integration opens the door to second-order nonlinear effects within the silicon photonic platform, including efficient frequency conversion, parametric amplification and the generation of entangled photon pairs.

We demonstrate that a dielectric anapole resonator on a metallic mirror can enhance the third harmonic emission by two orders of magnitude compared to a typical anapole resonator on an insulator substrate. By employing a gold mirror under a silicon nanodisk, we introduce a novel characteristic of the anapole mode through the spatial overlap of resonantly excited Cartesian electric and toroidal dipole modes. This is a remarkable improvement on the early demonstrations of the anapole mode in which the electric and toroidal modes interfere off-resonantly. Therefore, our system produces a significant near-field enhancement, facilitating the nonlinear process. Moreover, the mirror surface boosts the nonlinear emission via the free-charge oscillations within the interface, equivalent to producing a mirror image of the nonlinear source and the pump beneath the interface. We found that these improvements result in an extremely high experimentally obtained efficiency of 0.01%.

Optical nanoantennas have shown a great capacity for efficient extraction of photons from the near to the far-field, enabling directional emission from nanoscale single-photon sources. However, their potential for the generation and extraction of multi-photon quantum states remains unexplored. Here we demonstrate experimentally the nanoscale generation of two-photon quantum states at telecommunication wavelengths based on spontaneous parametric down-conversion in an optical nanoantenna. The antenna is a crystalline Al-GaAs nanocylinder, possessing Mie-type resonances at both the pump and the bi-photon wavelengths and when excited by a pump beam generates photonpairs with a rate of 35 Hz. Normalized to the pump energy stored by the nanoantenna, this rate corresponds to 1.4 GHz/Wm, being one order of magnitude higher than conventional on-chip or bulk photon-pair sources. Our experiments open the way for multiplexing several antennas for coherent generation of multi-photon quantum states with complex spatial-mode entanglement and applications in free-space quantum communications and sensing.

Prostate cancer (CaP) subtypes are poorly defined and functional validation of drivers of ETS rearrangement-negative CaP has not been conducted. Here, we identified an ETS− subtype of aggressive CaP (ERG−MAP3K7delCHD1del) and used a novel developmental model and a cell line xenograft model to show that co-suppression of MAP3K7 and CHD1 expression promotes aggressive disease. Analyses of publicly available CaP datasets revealed that MAP3K7 and CHD1 were significantly co-deleted in 10–20% of localized tumors and combined loss correlated with poor disease-free survival. To evaluate the functional impact of dual MAP3K7-CHD1 loss, we suppressed Map3k7 and/or Chd1 expression in mouse prostate epithelial progenitor/stem cells (PrP/SCs) and performed tissue recombination experiments in vivo. Dual shMap3k7-shChd1 PrP/SC recombinants displayed massive glandular atypia with regions of prostatic intraepithelial neoplasia (PIN) and carcinoma apparent. Combined Map3k7-Chd1 suppression greatly disrupted normal prostatic lineage differentiation; dual recombinants displayed significant AR loss, increased neuroendocrine differentiation, and increased neural differentiation. Clinical samples with dual MAP3K7-CHD1 loss also displayed neuroendocrine and neural characteristics. Additionally, dual Map3k7-Chd1 suppression promoted E-cadherin loss and mucin production in recombinants. MAP3K7 and CHD1 protein loss also correlated with Gleason grade and E-cadherin loss in clinical samples. To further validate the phenotype observed in the PrP/SC model, we suppressed MAP3K7 and/or CHD1 expression in LNCaP prostate cancer cells. Dual shMAP3K7-shCHD1 LNCaP xenografts displayed increased tumor growth and decreased survival compared to shControl, shMAP3K7, and shCHD1 xenografts. Collectively, these data identify coordinate loss of MAP3K7 and CHD1 as a unique driver of aggressive CaP development.