We report on an experiment that demonstrates the frequency up-conversion of telecommunication wavelength single-photon-level pulses to be resonant with a + Pr 3 :Y SiO 2 5 crystal. We convert the telecom photons at 1570 nm to 606 nm using a periodically-poled potassium titanyl phosphate nonlinear waveguide. The maximum device efficiency (which includes all optical loss) is inferred to be η = ± 22 1% dev max (internal efficiency η = ± 75 8% int ) with a signal to noise ratio exceeding 1 for single-photon-level pulses with durations of up to 560 ns. The converted light is then stored in the crystal using the atomic frequency comb scheme with storage and retrieval efficiencies exceeding η = 20% AFC for predetermined storage times of up to μ 5 s. The retrieved light is time delayed from the noisy conversion process allowing us to measure a signal to noise ratio exceeding 100 with telecom single-photon-level inputs. These results represent the first demonstration of single-photon-level optical storage interfaced with frequency up-conversion.

Quantum error correction (QEC) is a crucial step towards long coherence times required for efficient quantum information processing (QIP). One major challenge in this direction concerns the fast real-time analysis of error syndrome measurements and the associated feedback control. Recent proposals on autonomous QEC (AQEC) have opened new perspectives to overcome this difficulty. Here, we design an AQEC scheme based on quantum reservoir engineering adapted to superconducting qubits. We focus on a three-qubit bit-flip code, where three transmon qubits are dispersively coupled to a few low-Q resonator modes. By applying only continuous-wave drives of fixed but well-chosen frequencies and amplitudes, we engineer an effective interaction Hamiltonian to evacuate the entropy created by eventual bit-flip errors. We provide a full analytical and numerical study of the protocol, while introducing the main limitations on the achievable error correction rates.

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Adrenalectomy permits a late, local TNF-a release in LPS-challenged rat airways. A. Miller-Larsson, A. Runstro Èm, R. Brattsand. #ERS Journals Ltd 1999. ABSTRACT: The normal rise of circulating endogenous glucocorticosteroids (GCS), in response to immunological stimuli, can be impaired in patients with inflammatory diseases. The aim of this study was to investigate whether abolition of the endogenous GCS response promotes local production of the pro-inflammatory cytokine, tumour necrosis factor (TNF)-a, in challenged airways and affects the cellular response in rats.In adrenalectomized or sham operated rats, the trachea and main bronchi were lavaged at various times after intratracheal instillation of low dose lipopolysaccharide (LPS). TNF-a in lavage fluid and plasma corticosterone were measured, and cells were differentiated.In adrenalectomized rats, LPS-induced in the airways a biphasic TNF-a release peaking at 2 and 6 h, whereas in sham operated rats the second peak was absent; probably inhibited by the strong rise of plasma corticosterone. The second peak was abolished in adrenalectomized rats by pretreatment with exogenous GCS. The LPSinduced neutrophil influx and a decrease in mononuclear cells were prolonged in adrenalectomized rats.In conclusion, abolition of the endogenous glucocorticosteroid response promotes the late release of tumour necrosis factor-a in the airways and prolongs the cellular response. This suggests that a normal rise of endogenous glucocorticosteroid after an immunological trigger contributes to a dampening of the late inflammatory activity. Eur Respir J 1999; 13: 1310±1317.

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