Recently reported metamaterial analogues of electromagnetically induced transparency enable a unique route to endow classical optical structures with aspects of quantum optical systems. This method opens up many fascinating prospects on novel optical components, such as slow light units, highly sensitive sensors and nonlinear devices. In particular, optical control of electromagnetically induced transparency in metamaterials promises essential application opportunities in optical networks and terahertz communications. Here we present active optical control of metamaterial-induced transparency through active tuning of the dark mode. By integrating photoconductive silicon into the metamaterial unit cell, a giant switching of the transparency window occurs under excitation of ultrafast optical pulses, allowing for an optically tunable group delay of the terahertz light. This work opens up the possibility for designing novel chip-scale ultrafast devices that would find utility in optical buffering and terahertz active filtering.

Metasurfaces have attracted large interest in recent years due to their relatively simple fabrication, compact design, and ability to control the wavefront of incident light. Ohmic loss attributed to bulk metal metamaterials are not a primary issue, whereby the meta-atom or plasmonic structure is typically only as thin as a fraction of the operation wavelength. Numerous novel applications have been demonstrated by metasurfaces, including an ultrathin metasurface flat lens, and 3D holography.Here, by combining the freedom of both the structural design and the orientation of split ring resonator antennas, we demonstrate Terahertz metasurfaces that are capable of controlling both the phase and amplitude profiles over a very broad bandwidth at~1THz under linearly-polarised incidence. As an example, we show that these phase-amplitude metasurfaces can be engineered to control the diffraction orders arbitrarily.

SUMMARY Cardiac contractility is mediated by variable flux in intracellular calcium (Ca2+), thought to be integrated into mitochondria via the mitochondrial calcium uniporter (MCU) channel to match energetic demand. Here we examine a conditional, cardiomyocyte-specific, mutant mouse lacking Mcu, the pore-forming subunit of the MCU channel, in adulthood. Mcu−/− mice display no overt baseline phenotype and are protected against mCa2+-overload in an in vivo myocardial ischemia-reperfusion injury model by preventing the activation of the mitochondrial permeability transition pore, decreasing infarct size, and preserving cardiac function. In addition, we find that Mcu−/− mice lack contractile responsiveness to acute β-adrenergic receptor stimulation and in parallel are unable to activate mitochondrial dehydrogenases and display reduced bioenergetic reserve capacity. These results support the hypothesis that MCU may be dispensable for homeostatic cardiac function but required to modulate Ca2+-dependent metabolism during acute stress.