RESUMEN
Donor spins in silicon are highly competitive qubits for upcoming quantum technologies, offering complementary metal-oxide semiconductor compatibility, coherence (T2) times of minutes to hours, and simultaneous initialization, manipulation, and readout fidelities near ~99.9%. This allows for many quantum error correction protocols, which will be essential for scale-up. However, a proven method of reliably coupling spatially separated donor qubits has yet to be identified. We present a scalable silicon-based platform using the unique optical properties of "deep" chalcogen donors. For the prototypical 77Se+ donor, we measure lower bounds on the transition dipole moment and excited-state lifetime, enabling access to the strong coupling limit of cavity quantum electrodynamics using known silicon photonic resonator technology and integrated silicon photonics. We also report relatively strong photon emission from this same transition. These results unlock clear pathways for silicon-based quantum computing, spin-to-photon conversion, photonic memories, integrated single-photon sources, and all-optical switches.
RESUMEN
Cutaneous neurogenic inflammation is a complex biological response of the host immune system to noxious stimuli. Present evidence suggests that zinc metalloproteases may play an important role in the regulation of neurogenic inflammation by controlling the local availability of neuropeptides, such as substance P (SP), that are capable of initiating or amplifying cutaneous inflammation after release from sensory nerves. To address the hypothesis that the dipeptidyl carboxypeptidase angiotensin-converting enzyme (ACE) is capable of modulating skin inflammation, we have analyzed murine allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD) using wild-type C57BL/6J (ACE(+/+)) or genetically engineered mice with a heterozygous deletion of somatic ACE (ACE(+/-)). In 2,4-dinitro-1-fluorobenzene-sensitized ACE(+/-) mice, ACD was significantly augmented in comparison to ACE(+/+) controls as determined by the degree of ear swelling after exposure to hapten. Likewise, systemic treatment of ACE(+/+) mice with the ACE inhibitor captopril before sensitization or elicitation of ACD significantly augmented the ACD response. In contrast, local damage and neuropeptide depletion of sensory nerves following capsaicin, injection of a bradykinin B(2), or a SP receptor antagonist before sensitization significantly inhibited the augmented effector phase of ACD in mice with functionally absent ACE. However, in contrast to ACD, the response to the irritant croton oil was not significantly altered in ACE(+/-) compared with ACE(+/+) mice. Thus, ACE by degrading bradykinin and SP significantly controls cutaneous inflammatory responses to allergens but not to irritants, which may explain the frequently observed exacerbation of inflammatory skin disease in patients under medication with ACE inhibitors.