Polariton lattices as binarized neuromorphic networks.

We introduce a novel neuromorphic network architecture based on a lattice of exciton-polariton condensates, intricately interconnected and energized through nonresonant optical pumping. The network employs a binary framework, where each neuron, facilitated by the spatial coherence of pairwise coupled condensates, performs binary operations. This coherence, emerging from the ballistic propagation of polaritons, ensures efficient, network-wide communication.

Stochastic circular persistent currents of exciton polaritons.

We monitor the orbital degree of freedom of exciton-polariton condensates confined within an optical trap and unveil the stochastic switching of persistent annular polariton currents under pulse-periodic excitation. Within an elliptical trap, the low-lying in energy polariton current states manifest as a two-petaled density distribution with a swirling phase. In the stochastic regime, the density distribution, averaged over multiple excitation pulses, becomes homogenized in the azimuthal direction.

Steady state oscillations of circular currents in concentric polariton condensates.

Concentric ring exciton polariton condensates emerging under non-resonant laser pump in an annular trapping potential support persistent circular currents of polaritons. The trapping potential is formed by a cylindrical micropillar etched in a semiconductor microcavity with embedded quantum wells and a repulsive cloud of optically excited excitons under the pump spot. The symmetry of the potential is subject to external control via manipulation by its pump-induced component.

GRHL2 and AP2a coordinate early surface ectoderm lineage commitment during development.

Ectodermal dysplasias including skin abnormalities and cleft lip/palate result from improper surface ectoderm (SE) patterning. However, the connection between SE gene regulatory networks and disease remains poorly understood. Here, we dissect human SE differentiation with multiomics and establish GRHL2 as a key mediator of early SE commitment, which acts by skewing cell fate away from the neural lineage.