Single photon Mach-Zehnder interferometer for quantum networks based on the Single Photon Faraday Effect: principle and applications

Combining the recent progress in semiconductor nanostructures along with the versatility of photonic crystals in confining and manipulating light, quantum networks allow for the prospect of an integrated and low power quantum technology. Within quantum networks, which consist of a system of waveguides and nanocavities with embedded quantum dots, it has been demonstrated in theory that many-qubit states stored in electron spins could be teleported from one quantum dot to another via a single photon using the Single Photon Faraday Effect. However, in addition to being able to transfer quantum information from one location to another, quantum networks need added functionality such as (1) controlling the flow of the quantum information and (2) performing specific operations on qubits that can be easily integrated. In this paper, we show how in principle a single photon Mach-Zehnder interferometer, which uses the concept of the single photon Faraday Effect to manipulate the geometrical phase of a single photon, can be operated both as a switch to control the flow of quantum information inside the quantum network and as various single qubit quantum gates to perform operations on a single photon. Our proposed Mach-Zehnder interferometer can be fully integrated as part of a quantum network on a chip. Given that the X gate, the Z gate, and the XZ gate are essential for the implementation of quantum teleportation, we show explicitly their implementation by means of our proposed single photon Mach-Zehnder interferometer. We also show explicitly the implementation of the Hadamard gate and the single-qubit phase gate, which are needed to complete the universal set of quantum gates for integrated quantum computing in a quantum network.Comment: 25 pages, 16 figure

Single-photon Mach-Zehnder interferometer for quantum networks based on the single-photon Faraday effect

Combining the recent progress in semiconductor nanostructures along with the versatility of photonic crystals in confining and manipulating light, quantum networks allow for the prospect of an integrated and low power quantum technology. Within quantum networks, which consist of a system of waveguides and nanocavities with embedded quantum dots, it has been demonstrated in theory that many-qubit states stored in electron spins could be teleported from one quantum dot to another via a single photon using the single-photon Faraday effect. However, in addition to being able to transfer quantum information from one location to another, quantum networks need added functionality such as (1) controlling the flow of the quantum information and (2) performing specific operations on qubits that can be easily integrated. In this paper, we show how a single-photon Mach-Zehnder interferometer (SMZI), that uses the concept of the single-photon Faraday effect to manipulate the polarization of a single photon, can be operated both as a switch to control the flow of quantum information inside the quantum network and as various single-qubit quantum gates to perform operations on a single photon. Given that the X gate, the Z gate, and the XZ gate are essential for the implementation of quantum teleportation, we show explicitly their implementation by means of our proposed SMZI. We also present the implementation of the Hadamard gate and the single-qubit phase gate, which are needed to complete the universal set of quantum gates for integrated quantum computing in a quantum network. Finally, the expected fidelity and robustness of the proposed SMZI are quantitatively explored by considering the phase errors within the SMZI

CPT spectroscopy on low-temperature sealed MEMS rubidium vapour cells

In recent years there has been a strong effort to reduce the size and power consumption of vapour cell atomic clocks [1,2]. The progress in this direction is driven by several factors such as the use low power laser diodes (VCSEL), Coherent Population Trapping resonances (CPT), and micro-fabricated (MEMS) alkali-vapour cells. Here the micro-fabrication of vapour cells has proven a challenging task. All results reported on this task use anodic bonding at high-temperatures (>300°C) to seal the cell [3]. However, the low melting point and high vapour pressure of the alkali-metal combined with long bonding-times (>1hour) complicate this process. We have recently developed a low temperature (~150°C) sealing technique with fast process time (<1min) based on soldering [4]. We report here on the measurement of 85Rb σ+ CPT resonance in low temperature sealed MEMS-fabricated vapour cells containing natural rubidium and buffer gas. The resonance is recorded on the rubidium D1-line (795nm) using a circular polarized and current-modulated VCSEL. We record the resonance shift, linewidth and amplitude as function of several experimental parameters such as light intensity, cell-temperature, and buffer gas pressure- and mixture. In addition we perform noise measurements on the resonance signal to characterize the cell for clock-applications. Preliminary results show a contrast of 1.7% and linewidth of 900Hz for a 4mm long cell with 70mbar of nitrogen buffer gas. Finally we present and characterize two problems related to the application of 85Rb resonance in clock-applications. First, the low modulation frequency of the VCSEL (1.5GHz) leads to a strong asymmetry in the first order sideband spectrum due to the combined effect of AM- and FM modulation. Second, the buffer gas broadening of the absorption spectrum combined with the small separation between VCSEL carrier and sideband reduces the CPT contrast due to off-resonant absorption. We demonstrate that the impact of both these effects can be reduced by modulating the VCSEL at 3GHz and probing the CPT resonance with the carrier and first order sideband. We acknowledge support from the European Space Agency ESA (ESTEC contract number 20794/07/NL/GLC), the Conference Universitaire Suisse CUS (project CIMENT), the Swiss Space Office SSO, and SpectraTime SA (Neuchâtel, Switzerland)

Resolution of Joint Molecules by RuvABC and RecG Following Cleavage of the Escherichia coli Chromosome by EcoKI

DNA double-strand breaks can be repaired by homologous recombination involving the formation and resolution of Holliday junctions. In Escherichia coli, the RuvABC resolvasome and the RecG branch-migration enzyme have been proposed to act in alternative pathways for the resolution of Holliday junctions. Here, we have studied the requirements for RuvABC and RecG in DNA double-strand break repair after cleavage of the E. coli chromosome by the EcoKI restriction enzyme. We show an asymmetry in the ability of RuvABC and RecG to deal with joint molecules in vivo. We detect linear DNA products compatible with the cleavage-ligation of Holliday junctions by the RuvABC pathway but not by the RecG pathway. Nevertheless we show that the XerCD-mediated pathway of chromosome dimer resolution is required for survival regardless of whether the RuvABC or the RecG pathway is active, suggesting that crossing-over is a common outcome irrespective of the pathway utilised. This poses a problem. How can cells resolve joint molecules, such as Holliday junctions, to generate crossover products without cleavage-ligation? We suggest that the mechanism of bacterial DNA replication provides an answer to this question and that RecG can facilitate replication through Holliday junctions

Recombination Phenotypes of Escherichia coli greA Mutants

<p>Abstract</p> <p>Background</p> <p>The elongation factor GreA binds to RNA polymerase and modulates transcriptional pausing. Some recent research suggests that the primary role of GreA may not be to regulate gene expression, but rather, to promote the progression of replication forks which collide with RNA polymerase, and which might otherwise collapse. Replication fork collapse is known to generate dsDNA breaks, which can be recombinogenic. It follows that GreA malfunction could have consequences affecting homologous recombination.</p> <p>Results</p> <p><it>Escherichia coli </it>mutants bearing substitutions of the active site acidic residues of the transcription elongation factor GreA, D41N and E44K, were isolated as suppressors of growth inhibition by a toxic variant of the bacteriophage lambda Red-beta recombination protein. These mutants, as well as a D41A <it>greA </it>mutant and a <it>greA </it>deletion, were tested for proficiency in recombination events. The mutations were found to increase the efficiency of RecA-RecBCD-mediated and RecA-Red-mediated recombination, which are replication-independent, and to decrease the efficiency of replication-dependent Red-mediated recombination.</p> <p>Conclusion</p> <p>These observations provide new evidence for a role of GreA in resolving conflicts between replication and transcription.</p

Cortical Layer 1 and Layer 2/3 Astrocytes Exhibit Distinct Calcium Dynamics In Vivo

Cumulative evidence supports bidirectional interactions between astrocytes and neurons, suggesting glial involvement of neuronal information processing in the brain. Cytosolic calcium (Ca2+) concentration is important for astrocytes as Ca2+ surges co-occur with gliotransmission and neurotransmitter reception. Cerebral cortex is organized in layers which are characterized by distinct cytoarchitecture. We asked if astrocyte-dominant layer 1 (L1) of the somatosensory cortex was different from layer 2/3 (L2/3) in spontaneous astrocytic Ca2+ activity and if it was influenced by background neural activity. Using a two-photon laser scanning microscope, we compared spontaneous Ca2+ activity of astrocytic somata and processes in L1 and L2/3 of anesthetized mature rat somatosensory cortex. We also assessed the contribution of background neural activity to the spontaneous astrocytic Ca2+ dynamics by investigating two distinct EEG states (“synchronized” vs. “de-synchronized” states). We found that astrocytes in L1 had nearly twice higher Ca2+ activity than L2/3. Furthermore, Ca2+ fluctuations of processes within an astrocyte were independent in L1 while those in L2/3 were synchronous. Pharmacological blockades of metabotropic receptors for glutamate, ATP, and acetylcholine, as well as suppression of action potentials did not have a significant effect on the spontaneous somatic Ca2+ activity. These results suggest that spontaneous astrocytic Ca2+ surges occurred in large part intrinsically, rather than neural activity-driven. Our findings propose a new functional segregation of layer 1 and 2/3 that is defined by autonomous astrocytic activity

Sphingomyelin is associated with kidney disease in type 1 diabetes (The FinnDiane Study)

Diabetic kidney disease, diagnosed by urinary albumin excretion rate (AER), is a critical symptom of chronic vascular injury in diabetes, and is associated with dyslipidemia and increased mortality. We investigated serum lipids in 326 subjects with type 1 diabetes: 56% of patients had normal AER, 17% had microalbuminuria (20 ≤ AER < 200 μg/min or 30 ≤ AER < 300 mg/24 h) and 26% had overt kidney disease (macroalbuminuria AER ≥ 200 μg/min or AER ≥ 300 mg/24 h). Lipoprotein subclass lipids and low-molecular-weight metabolites were quantified from native serum, and individual lipid species from the lipid extract of the native sample, using a proton NMR metabonomics platform. Sphingomyelin (odds ratio 2.53, P < 10−7), large VLDL cholesterol (odds ratio 2.36, P < 10−10), total triglycerides (odds ratio 1.88, P < 10−6), omega-9 and saturated fatty acids (odds ratio 1.82, P < 10−5), glucose disposal rate (odds ratio 0.44, P < 10−9), large HDL cholesterol (odds ratio 0.39, P < 10−9) and glomerular filtration rate (odds ratio 0.19, P < 10−10) were associated with kidney disease. No associations were found for polyunsaturated fatty acids or phospholipids. Sphingomyelin was a significant regressor of urinary albumin (P < 0.0001) in multivariate analysis with kidney function, glycemic control, body mass, blood pressure, triglycerides and HDL cholesterol. Kidney injury, sphingolipids and excess fatty acids have been linked in animal models—our exploratory approach provides independent support for this relationship in human patients with diabetes

Replication Fork Reversal after Replication–Transcription Collision

Replication fork arrest is a recognized source of genetic instability, and transcription is one of the most prominent causes of replication impediment. We analyze here the requirement for recombination proteins in Escherichia coli when replication–transcription head-on collisions are induced at a specific site by the inversion of a highly expressed ribosomal operon (rrn). RecBC is the only recombination protein required for cell viability under these conditions of increased replication-transcription collisions. In its absence, fork breakage occurs at the site of collision, and the resulting linear DNA is not repaired and is slowly degraded by the RecJ exonuclease. Lethal fork breakage is also observed in cells that lack RecA and RecD, i.e. when both homologous recombination and the potent exonuclease V activity of the RecBCD complex are inactivated, with a slow degradation of the resulting linear DNA by the combined action of the RecBC helicase and the RecJ exonuclease. The sizes of the major linear fragments indicate that DNA degradation is slowed down by the encounter with another rrn operon. The amount of linear DNA decreases nearly two-fold when the Holliday junction resolvase RuvABC is inactivated in recB, as well as in recA recD mutants, indicating that part of the linear DNA is formed by resolution of a Holliday junction. Our results suggest that replication fork reversal occurs after replication–transcription head-on collision, and we propose that it promotes the action of the accessory replicative helicases that dislodge the obstacle

Differential Requirements of Two recA Mutants for Constitutive SOS Expression in Escherichia coli K-12

Background Repairing DNA damage begins with its detection and is often followed by elicitation of a cellular response. In E. coli, RecA polymerizes on ssDNA produced after DNA damage and induces the SOS Response. The RecA-DNA filament is an allosteric effector of LexA auto-proteolysis. LexA is the repressor of the SOS Response. Not all RecA-DNA filaments, however, lead to an SOS Response. Certain recA mutants express the SOS Response (recAC) in the absence of external DNA damage in log phase cells. Methodology/Principal Findings Genetic analysis of two recAC mutants was used to determine the mechanism of constitutive SOS (SOSC) expression in a population of log phase cells using fluorescence of single cells carrying an SOS reporter system (sulAp-gfp). SOSC expression in recA4142 mutants was dependent on its initial level of transcription, recBCD, recFOR, recX, dinI, xthA and the type of medium in which the cells were grown. SOSC expression in recA730 mutants was affected by none of the mutations or conditions tested above. Conclusions/Significance It is concluded that not all recAC alleles cause SOSC expression by the same mechanism. It is hypothesized that RecA4142 is loaded on to a double-strand end of DNA and that the RecA filament is stabilized by the presence of DinI and destabilized by RecX. RecFOR regulate the activity of RecX to destabilize the RecA filament. RecA730 causes SOSC expression by binding to ssDNA in a mechanism yet to be determined