Single photon production by rephased amplified spontaneous emission

The production of single photons using rephased amplified spontaneous emission is examined. This process produces single photons on demand with high efficiency by detecting the spontaneous emission from an atomic ensemble, then applying a population-inverting pulse to rephase the ensemble and produce a photon echo of the spontaneous emission events. The theoretical limits on the efficiency of the production are determined for several variants of the scheme. For an ensemble of uniform optical density, generating the initial spontaneous emission and its echo using transitions of different strengths is shown to produce single photons at 70% efficiency, limited by reabsorption. Tailoring the spatial and spectral density of the atomic ensemble is then shown to prevent reabsorption of the rephased photon, resulting in emission efficiency near unity

Single photon production by rephased amplified spontaneous emission

The production of single photons using rephased amplified spontaneous emission is examined. This process produces single photons on demand with high efficiency by detecting the spontaneous emission from an atomic ensemble, then applying a population-inverting pulse to rephase the ensemble and produce a photon echo of the spontaneous emission events. The theoretical limits on the efficiency of the production are determined for several variants of the scheme. For an ensemble of uniform optical density, generating the initial spontaneous emission and its echo using transitions of different strengths is shown to produce single photons at 70% efficiency, limited by reabsorption. Tailoring the spatial and spectral density of the atomic ensemble is then shown to prevent reabsorption of the rephased photon, resulting in emission efficiency near unity

Piezo buffers mechanical stress via modulation of intracellular Ca 2+ handling in the Drosophila heart

Throughout its lifetime the heart is buffeted continuously by dynamic mechanical forces resulting from contraction of the heart muscle itself and fluctuations in haemodynamic load and pressure. These forces are in flux on a beat-by-beat basis, resulting from changes in posture, physical activity or emotional state, and over longer timescales due to altered physiology (e.g. pregnancy) or as a consequence of ageing or disease (e.g. hypertension). It has been known for over a century of the heart’s ability to sense differences in haemodynamic load and adjust contractile force accordingly[1-4]. These adaptive behaviours are important for cardiovascular homeostasis, but the mechanism(s) underpinning them are incompletely understood. Here we present evidence that the mechanically-activated ion channel, Piezo, is an important component of the Drosophila heart’s ability to adapt to mechanical force. We find Piezo is a sarcoplasmic reticulum (SR)-resident channel and is part of a mechanism that regulates Ca2+ handling in cardiomyocytes in response to mechanical stress. Our data support a simple model in which Drosophila Piezo transduces mechanical force such as stretch into a Ca2+ signal, originating from the SR, that modulates cardiomyocyte contraction. We show that Piezo mutant hearts fail to buffer mechanical stress, have altered Ca2+ handling, become prone to arrhythmias and undergo pathological remodelling