The speed limit of optoelectronics.

Light-field driven charge motion links semiconductor technology to electric fields with attosecond temporal control. Motivated by ultimate-speed electron-based signal processing, strong-field excitation has been identified viable for the ultrafast manipulation of a solid's electronic properties but found to evoke perplexing post-excitation dynamics. Here, we report on single-photon-populating the conduction band of a wide-gap dielectric within approximately one femtosecond. We control the subsequent Bloch wavepacket motion with the electric field of visible light. The resulting current allows sampling optical fields and tracking charge motion driven by optical signals. Our approach utilizes a large fraction of the conduction-band bandwidth to maximize operating speed. We identify population transfer to adjacent bands and the associated group velocity inversion as the mechanism ultimately limiting how fast electric currents can be controlled in solids. Our results imply a fundamental limit for classical signal processing and suggest the feasibility of solid-state optoelectronics up to 1 PHz frequency.

Carrier frequency tuning of few-cycle light pulses by a broadband attenuating mirror.

We demonstrate the performance of a novel multilayer dielectric reflective thin-film attenuator capable of reshaping the super-octave spectrum of near-single-cycle visible laser pulses without deteriorating the phase properties of the reflected light. These novel broadband attenuating mirrors reshape in a virtually dispersion-free manner the incident spectrum such that the carrier wavelength of the reflected pulses shifts from ∼700 nm (Eγ=1.77 eV) to ∼540 nm (Eγ=2.25 eV) or beyond while maintaining their initial near-single-cycle pulse duration. This constitutes a viable approach to convert a number of established few-cycle ultrafast laser systems into sources with a selectable excitation wavelength to meet the requirements of single-color/multicolor high temporal resolution spectroscopic experiments.

Antiproliferative activity of the human IFN-alpha-inducible protein IFI44.

The interferon-alpha (IFN-alpha)-inducible protein IFI44 is associated with hepatitis C virus (HCV) infection, and its function is unknown. We show here in two human melanoma cell lines (ME15 and D10) that transcription starts 4 h after induction, and peak protein levels are reached 24 h after stimulation. We show by immunofluorescence, viral overexpression, and cellular fractionation that IFI44 is a cytoplasmic protein. Overexpression of IFI44 cDNA induces an antiproliferative state in vitro, even in cells that are not responsive to IFN-alpha. IFI44 contains a perfect GTP binding site but has no homology to known GTPases or G proteins. Based on these results, we propose a model in which IFI44 binds intracellular GTP, and this depletion abolishes extracellular signal-regulated kinase (ERK) signaling and results finally in cell cycle arrest.