Pulse shaping by coupled-cavities: Single photons and qudits

Dynamic coupling of cavities to a quantum network is of major interest to distributed quantum information processing schemes based on cavity quantum electrodynamics. This can be achieved by active tuning a mediating atom-cavity system. In particular, we consider the dynamic coupling between two coupled cavities, each interacting with a two-level atom, realized by tuning one of the atoms. One atom-field system can be controlled to become maximally and minimally coupled with its counterpart, allowing high fidelity excitation confinement, Q-switching and reversible state transport. As an application, we first show that simple tuning can lead to emission of near-Gaussian single-photon pulses that is significantly different from the usual exponential decay in a passive cavity-based system. The influences of cavity loss and atomic spontaneous emission are studied in detailed numerical simulations, showing the practicality of these schemes within the reach of current experimental technology in solid-state environment. We then show that when the technique is employed to an extended coupled-cavity scheme involving a multi-level atom, arbitrary temporal superposition of single photons can be engineered in a deterministic way.Comment: 11 pages, 11 figures, minor revision

High speed quantum gates with cavity quantum electrodynamics

Cavity quantum electrodynamic schemes for quantum gates are amongst the earliest quantum computing proposals. Despite continued progress, and the dramatic recent demonstration of photon blockade, there are still issues with optimal coupling and gate operation involving high-quality cavities. Here we show dynamic control techniques that allow scalable cavity-QED based quantum gates, that use the full bandwidth of the cavities. When applied to quantum gates, these techniques allow an order of magnitude increase in operating speed, and two orders of magnitude reduction in cavity Q, over passive cavity-QED architectures. Our methods exploit Stark shift based Q-switching, and are ideally suited to solid-state integrated optical approaches to quantum computing.Comment: 4 pages, 3 figures, minor revision

Deterministic optical quantum computer using photonic modules

The optical quantum computer is one of the few experimental systems to have demonstrated small scale quantum information processing. Making use of cavity quantum electrodynamics approaches to operator measurements, we detail an optical network for the deterministic preparation of arbitrarily large two-dimensional cluster states. We show that this network can form the basis of a large scale deterministic optical quantum computer that can be fabricated entirely on chip.Comment: 9 pages, 10 figures, minor revision

Architectural design for a topological cluster state quantum computer

The development of a large scale quantum computer is a highly sought after goal of fundamental research and consequently a highly non-trivial problem. Scalability in quantum information processing is not just a problem of qubit manufacturing and control but it crucially depends on the ability to adapt advanced techniques in quantum information theory, such as error correction, to the experimental restrictions of assembling qubit arrays into the millions. In this paper we introduce a feasible architectural design for large scale quantum computation in optical systems. We combine the recent developments in topological cluster state computation with the photonic module, a simple chip based device which can be used as a fundamental building block for a large scale computer. The integration of the topological cluster model with this comparatively simple operational element addresses many significant issues in scalable computing and leads to a promising modular architecture with complete integration of active error correction exhibiting high fault-tolerant thresholds.Comment: 14 Pages, 8 Figures, changes to the main text, new appendix adde

Effect of galactose diet removal on the progression of retinal vessel changes in galactose-fed dogs

PURPOSE. Feeding dogs a diet containing 30% galactose induces experimental galactosemia and results in the formation of diabetes-like microvascular lesions of the retina. The appearance and progression of these retinal lesions can be arrested in a dose-dependent manner by treating these dogs with aldose reductase inhibitors from the onset of galactosemia. To determine whether the elimination of galactosemia can also reduce the progression of retinal lesions, the galactose diet was removed from the galactosemic dogs after either the appearance of pericyte ghosts or formation of microaneurysms. METHODS. Ten control dogs were fed a normal diet, and 50 dogs were fed a diet containing 30% galactose. The galactose diet was removed from 15 dogs after 24 months, the time at which pericyte ghosts had previously been observed to develop, and from another 15 dogs after 31 months, when microaneurysms had previously been observed to develop. Eighteen dogs were continued on a galactose diet. Beginning at 24 months, eyes from each group were enucleated at approximately 6-month intervals. Changes in retinal lesions were quantified by computer image analyses. RESULTS. Significant (P Ͻ 0.05-0.01) increases in the endothelium-pericyte (E-P) ratio and decreases in pericyte density were observed with increased duration of galactose feeding. Although no reversal of retinal lesions occurred, differences in the progression of retinal lesions between the galactose-fed and galactose-deprived groups became evident after 12 to 24 months. CONCLUSIONS. Discontinuation of galactose in the diet at the initial stages of background retinopathy beneficially delays the progression of retinal lesions. (Invest Ophthalmol Vis Sci. 2002;43:1916 -1921 D iabetic retinopathy, a leading cause of blindness, is a major long-term complication of diabetes mellitus that is characterized by vascular changes of the retinal capillary bed. In its early, nonproliferative stage, these changes include the formation of microaneurysms, intraretinal hemorrhages, exudates and altered blood flow. In the later, proliferative stage, neovascularization occurs as retinal vessels break through the inner limiting membrane and grow into the vitreous. 1 A hallmark of this disease is the destruction of pericytes (mural cells) from retinal capillaries and the formation of pericyte ghosts. 2,3 Their loss is associated with vessel dilation, formation of microaneurysm, and endothelial cell proliferation. Retinal vessel changes similar to human retinopathy have been observed to occur in diabetic 4 -6 and galactose-fed Galactosemia is associated with a number of diabetes-like lesions. 10 Galactosemia, both hereditary and experimentally induced with galactose feeding, is associated with the rapid formation of galactitol and, to a lesser extent, the formation of galactonic acid and/or galactonolactone. 11-14 Long-term galactosemia is also associated with increased nonenzymatic glycation, basement membrane thickening, and biochemical changes that include decreased glutathione, taurine, and myoinositol levels, decreased adenosine triphosphate (ATP) and amino acid transport activity, increased PKC and VEGF levels, and altered membrane permeability. Formation of galactitol is catalyzed by the enzyme aldose reductase, and its intracellular accumulation precedes the biochemical changes associated with long-term galactosemia. The administration of aldose reductase inhibitors to animals from the onset of galactose feeding has been observed to reduce galactitol formation and prevent the subsequent formation of diabetes-like lesions. 10 However, aldose reductase inhibitors do not inhibit gulonic acid or formation of galactonolactone, suggesting that the formation of these latter two metabolic intermediates, unlike galactitol, do not contribute to the formation of diabetes-like lesions. 14 Studies using the galactose-fed dog model indicate that degeneration of retinal capillary pericytes is linked to the aldose reductase-catalyzed production of galactitol and that their loss precedes further vascular changes associated with retinopathy. In beagles fed a 30% galactose diet for 36 to 38 months, the onset and progression of destruction of pericytes and the formation of microaneurysms was reduced by the concomitant administration of the aldose reductase inhibitors sorbinil (S-6-fluoro-spirochroman-4-5Ј-imidazolidine-2Ј,4Јdione), its more potent 2-methyl analogue M79175 (2-methyl-6-fluorospirochroman-4-5Ј-imidazolidine-2Ј,4Јdione), or a combination of both inhibitors