High-speed linear optics quantum computing using active feed-forward

As information carriers in quantum computing, photonic qubits have the advantage of undergoing negligible decoherence. However, the absence of any significant photon-photon interaction is problematic for the realization of non-trivial two-qubit gates. One solution is to introduce an effective nonlinearity by measurements resulting in probabilistic gate operations. In one-way quantum computation, the random quantum measurement error can be overcome by applying a feed-forward technique, such that the future measurement basis depends on earlier measurement results. This technique is crucial for achieving deterministic quantum computation once a cluster state (the highly entangled multiparticle state on which one-way quantum computation is based) is prepared. Here we realize a concatenated scheme of measurement and active feed-forward in a one-way quantum computing experiment. We demonstrate that, for a perfect cluster state and no photon loss, our quantum computation scheme would operate with good fidelity and that our feed-forward components function with very high speed and low error for detected photons. With present technology, the individual computational step (in our case the individual feed-forward cycle) can be operated in less than 150 ns using electro-optical modulators. This is an important result for the future development of one-way quantum computers, whose large-scale implementation will depend on advances in the production and detection of the required highly entangled cluster states.     

Noxious compounds activate TRPA1 ion channels through covalent modification of cysteines

The nervous system senses peripheral damage through nociceptive neurons that transmit a pain signal. TRPA1 is a member of the Transient Receptor Potential (TRP) family of ion channels and is expressed in nociceptive neurons. TRPA1 is activated by a variety of noxious stimuli, including cold temperatures, pungent natural compounds, and environmental irritants. How such diverse stimuli activate TRPA1 is not known. We observed that most compounds known to activate TRPA1 are able to covalently bind cysteine residues. Here we use click chemistry to show that derivatives of two such compounds, mustard oil and cinnamaldehyde, covalently bind mouse TRPA1. Structurally unrelated cysteine-modifying agents such as iodoacetamide (IA) and (2-aminoethyl)methanethiosulphonate (MTSEA) also bind and activate TRPA1. We identified by mass spectrometry fourteen cytosolic TRPA1 cysteines labelled by IA, three of which are required for normal channel function. In excised patches, reactive compounds activated TRPA1 currents that were maintained at least 10 min after washout of the compound in calcium-free solutions. Finally, activation of TRPA1 by disulphide-bond-forming MTSEA is blocked by the reducing agent dithiothreitol (DTT). Collectively, our data indicate that covalent modification of reactive cysteines within TRPA1 can cause channel activation, rapidly signalling potential tissue damage through the pain pathway.     

Angiotensin II in the hippocampus. A histochemical and electrophysiological study

Summary The presence of the renin angiotensin system in the hippocampus is shown by immunohistochemistry. Intra- and extra-cellular recordings revealed that angiotensin II and III excite CA 1 pyramidal cells by disinhibition. The effect is antagonized by [Sar¹, Thr⁸]-A II.This work was supported by grant Nos 3.271.78 and 3.396.78 of the Swiss National Science Foundation and research grant HL-24112 from NIH. T. Inagami was a visiting scientist of the Roche Medical Research Foundation.     

Effects of Gd solutes on hardness and yield strength of Mg alloys

Relative contribution of individual strengthening mechanisms to the yield strength of Mg–0–15 wt%Gd alloys were investigated.Alloys with different grain size were prepared by adding Zr and hot extrusion.Hardness and tensile/compression yield strength were tested on the alloys after solid solution treatment and extrusion.HallPetch constants were calculated with hardness and tensile/compressive data.The results showed that the hardness of Mg–Gd alloys with similar Gd content and different grain size were almost the same,which indicates that grain size had little effect on hardness.The hardness linearly increased with rising Gd content(d H_v/dc≈25 kg mm~(-2)/at%Gd).The tensile and compressive yield strengths enhanced with the increase of Gd content for all alloys in different conditions.In addition,the tensile/compressive(t/c)yield asymmetry of extruded alloys decreased with increasing Gd content.Large t/c yield asymmetry ratio(1.77)was observed for pure Mg,and with increasing Gd content this value decreased to 1.With the increasing of tensile strength,the stress intensity factor,k_y,decreased from 0.27 MPa m~(1/2)for Mg–2 wt%Gd alloy to 0.19 MPa m~(1/2) for Mg–5 wt%Gd alloy,then increased to 0.29 MPa m~(1/2) for Mg–15 wt%Gd alloy.However,k_yincreased linearly form 0.16–0.31 MPa for compression test.The influence of grain size strengthening was eliminated,and the yield strength of tension and compression both linearly increased with c~n,where c is the atom concentration of Gd,and n=1/2 or 2/3.     

Effect of halogenmethylenebisphosphonates on bone cells in culture and on bone resorption in vivo

Summary Dihalogenmethylenebisphosphonates increase alkaline phosphatase activity and fatty acid oxidation in calvaria cells in culture (Cl₂MBP>Br₂MBPF₂MBP). The monohalogen C1MBP and the non-halogenated analogues are less active on phosphatase and inactive on or inhibitory towards fatty acid oxidation. The three dihalogenbisphosphonates and C1MBP inhibit bone resorption in vivo, Cl₂MBP most strongly.Acknowledgments. We thank Miss M.-L. Aebersold, Miss J. Portenier, Mrs I. Tschudi and Mrs Ch. Marti for their skilled technical assistance. This work has been supported by the Swiss National Science Foundation (grant 3.937.82), by the Procter & Gamble Company, Cincinnati, USA, by the Istituto Gentili S.p.A., Pisa, Italy, and by the Ausbildungs- und Förderungsfonds der Arbeitsgemeinschaft für Osteosynthese (AO), Chur, Switzerland.     

An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor

Activation of the aryl hydrocarbon receptor (AHR) by environmental xenobiotic toxic chemicals, for instance 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), has been implicated in a variety of cellular processes such as embryogenesis, transformation, tumorigenesis and inflammation. But the identity of an endogenous ligand activating the AHR under physiological conditions in the absence of environmental toxic chemicals is still unknown. Here we identify the tryptophan (Trp) catabolite kynurenine (Kyn) as an endogenous ligand of the human AHR that is constitutively generated by human tumour cells via tryptophan-2,3-dioxygenase (TDO), a liver- and neuron-derived Trp-degrading enzyme not yet implicated in cancer biology. TDO-derived Kyn suppresses antitumour immune responses and promotes tumour-cell survival and motility through the AHR in an autocrine/paracrine fashion. The TDO-AHR pathway is active in human brain tumours and is associated with malignant progression and poor survival. Because Kyn is produced during cancer progression and inflammation in the local microenvironment in amounts sufficient for activating the human AHR, these results provide evidence for a previously unidentified pathophysiological function of the AHR with profound implications for cancer and immune biology.