High quality entanglement on a chip-based frequency comb.

We report an efficient energy-time entangled photon-pair source based on four-wave mixing in a CMOS-compatible silicon photonics ring resonator. Thanks to suitable optimization, the source shows a large spectral brightness of 400 pairs of entangled photons /s/MHz for 500 µW pump power, compatible with standard telecom dense wavelength division multiplexers. We demonstrate high-purity energy-time entanglement, i.e., free of photonic noise, with near perfect raw visibilities (> 98%) between various channel pairs in the telecom C-band. Such a compact source stands as a path towards more complex quantum photonic circuits dedicated to quantum communication systems.

Two-photon interference between disparate sources for quantum networking.

Quantum networks involve entanglement sharing between multiple users. Ideally, any two users would be able to connect regardless of the type of photon source they employ, provided they fulfill the requirements for two-photon interference. From a theoretical perspective, photons coming from different origins can interfere with a perfect visibility, provided they are made indistinguishable in all degrees of freedom. Previous experimental demonstrations of such a scenario have been limited to photon wavelengths below 900 nm, unsuitable for long distance communication, and suffered from low interference visibility. We report two-photon interference using two disparate heralded single photon sources, which involve different nonlinear effects, operating in the telecom wavelength range. The measured visibility of the two-photon interference is 80 ± 4%, which paves the way to hybrid universal quantum networks.

A pilot prospective study of the vascular repair response following red cell transfusion in critically ill patients.

BACKGROUND: Red blood cell transfusion has been associated with adverse outcomes including infection, delayed recovery and increased mortality in some patient populations. Circulating cells that yield endothelial-like vascular progenitor cell (VPC) clusters are correlated with vascular repair and recovery after ischaemic injury. The impact of red cell transfusion on VPC clusters and vascular repair remains uncertain. STUDY DESIGN: We prospectively enrolled patients admitted to intensive care requiring red cell transfusion and subjects at low likelihood of requiring red cell transfusion. Levels of VPC clusters and plasma levels of angiogenic cytokines were compared. A total of 17 patients were recruited and had blood samples collected at time of enrolment and at 24-48 h, 48-72 h and 1 week following transfusion. RESULTS: We could not discern differences in the number of VPC clusters between transfused patients (n = 6) and non-transfused subjects (n = 11) at baseline or throughout the study period. VPC cluster levels demonstrated wide variance and were highest at 24-h post-enrolment in the entire cohort. Furthermore, levels of all 16 cytokines analysed were not significantly different between transfused and non-transfused patients and we did not observe a correlation between cytokine concentrations and levels of circulating VPC-cluster forming cells in the overall study population. CONCLUSIONS: Our data suggest that assessment of vascular repair responses after red blood cell transfusion in critically ill patients is challenging. Although our study did not allow us to discern an influence of red cell transfusion on VPC cluster levels or angiogenic cytokines, new methods evaluating vascular repair mechanisms may be required.

Inhibition of DNA polymerase-alpha by ara-CMP in the presence of a regulatory protein extracted from human promyelocytic leukemic cells (HL-60).

Cytotoxicity of arabinofuranosylcytosine (ara-C) has been related in vitro to the inhibition of the DNA polymerase activities by arabinosylcytosine triphosphate (ara-CTP) and the incorporation of ara-C into the DNA where, acting as a chain terminator, it slows the chain elongation. Induced in vitro cellular resistance to ara-C was shown to be secondary to altered deoxycytidine (dCyd) kinase activity, dCyd deaminase activity, or deoxynucleotides triphosphates (dNTP) pools. Recent studies reported no differences of ara-C metabolism in cells obtained from leukemic patients at diagnosis and at relapse after ara-C therapy, suggesting that unknown cellular biochemical determinants may be involved in acquisition of ara-C resistance. Using dialysed crude extracts of leukemic cells obtained from patients at diagnosis, we observed variable inhibition of their DNA polymerase activities by arabinosylcytosine monophosphate (ara-CMP) at 2 mmol/L (0% to 50% inhibition). In similar conditions, ara-CMP reduced the polymerase activities of human thymus extract by 35% and 55% in extract of HL-60 cells (cultured human promyelocytic cells). The ara-CMP factor responsible for inhibition of DNA polymerase activity was nondialysable, heat labile, proteinase K sensitive, and has an estimated molecular mass of 30 kilodalton by gel filtration. After partial purification, this protein had no DNA polymerase RNA polymerase activities. In presence of the regulator and ara-CMP at 2 mmol/L, we observed no inhibition of the HL-60 3'----5' and 5'----3' exonucleases activities, suggesting the regulator interaction being mainly with the DNA polymerases in presence of ara-CMP. The relevance of the presence or absence of this protein regarding the cell sensitivity to ara-C is under investigation.

The production and characterization of a monoclonal antibody specific for the 94,000 dalton enkephalin-degrading peptidase from rabbit kidney brush border.

We have prepared a monoclonal antibody specific for a major 94,000 dalton protein from the brush border membrane of rabbit kidney cortex. The monoclonal antibody was used for the immunoaffinity purification of this protein after solubilization of brush border membranes with octylglucoside. The 94,000 dalton protein is a peptidase capable of cleaving the Gly3-Phe4 bond of methionine-enkephalin. Identification of this peptidase as a previously described 94,000 dalton enkephalinase of kidney cortex was confirmed by its sensitivity to EDTA and inhibitors such as thiorphan and phosphoramidon.