Adiabatic optical entanglement between electron spins in separate quantum dots

We present an adiabatic approach to the design of entangling quantum operations with two electron spins localized in separate InAs/GaAs quantum dots via the Coulomb interaction between optically-excited localized states. Slowly-varying optical pulses minimize the pulse noise and the relaxation of the excited states. An analytic "dressed state" solution gives a clear physical picture of the entangling process, and a numerical solution is used to investigate the error dynamics. For two vertically-stacked quantum dots we show that, for a broad range of dot parameters, a two-spin state with concurrence $C>0.85$ can be obtained by four optical pulses with durations $\sim 0.1 - 1$ ns.Comment: 7 pages, 5 figure

Fast initialization of the spin state of an electron in a quantum dot in the Voigt configuration

We consider the initialization of the spin-state of a single electron trapped in a self-assembled quantum dot via optical pumping of a trion level. We show that with a magnetic field applied perpendicular to the growth direction of the dot, a near-unity fidelity can be obtained in a time equal to a few times the inverse of the spin-conserving trion relaxation rate. This method is several orders-of-magnitude faster than with the field aligned parallel, since this configuration must rely on a slow hole spin-flip mechanism. This increase in speed does result in a limit on the maximum obtainable fidelity, but we show that for InAs dots, the error is very small.Comment: 4 pages, 4 figure

Response of two mouse tumours to hyperthermia with CCNU or melphalan.

The in vivo response of B16 melanoma and Lewis lung carcinoma to combinations of hyperthermia and graded doses of CCNU or Melphalan was studied. To obtain dose-response curves and quantitative comparisons of different treatments, an agar-colony assay was used to measure survival of cells from excised tumours. For heating experiments, the use of 2 tumours per animal, one heated and one not, allowed all other factors to be kept constant. When tumours were immersed in a water-bath at 43 degrees C for 1 h, Thermal Enhancement Ratios (TER) measured from the slopes of the dose-response curves were up to 1.6 for CCNU and 2.4 for Melphalan. Direct heat killing of about 1 decade was seen for 1 h at 43 degrees C. The anaesthetic Saffan also enhanced drug cell kill; the largest Dose Modifying Factor (2.7) was measured for Melphalan in the Lewis lung tumour. The duration of heating, and waterbath temperature, both influenced the enhancement of cell killing by CCNU, as did the time of excision of tumours between 0 and 3 1/2 h after treatment. There was no difference in effect between 3 1/2 and 24 h. The interaction between heat and CCNU varied if the interval between them was altered. The maximum effect was found if the heat and drug were given in close sequence

Clonogenic assays in the B16 melanoma: response to cyclophosphamide.

The survival of clonogenic cells in the B16 melanoma has been studied simultaneously by 3 methods: an in vitro assay in soft agar, a lung-colony assay, and the end-point dilution technique. Details of the first 2 methods have previously been reported, but those of the third are described here. The 3 methods have agreed well in investigations of the response of the B16 melanoma to cyclophosphamide

Cell survival in B16 melanoma after treatment with combinations of cytotoxic agents: lack of potentiation.

The extent of tumour, cell kill, produced by treating B16 melanomas with vincristine, cyclophosphamide, 5-fluorouracil and gamma-rays, alone and in combination, was determined using an in vitro colony assay. Cell kill by vincristine was revealed as a reduction in the yield of cells obtained by trypsinization, and as a decrease in the colony-forming ability of the extracted cells. The reduction in cell yield was interpreted as evidence of rapid cell lysis. Cyclophosphamide and gamma-rays also reduced both cell yield and surviving fraction, but in this case the small decrease in cell yield was due to an increase in cell volume. FU had no effect on cell yield, but surviving fraction was reduced. Tumour weight was also measured, and used in conjunction with cell yield and surviving fraction data to calculate the fraction of surviving cells per tumour following treatment with the agents. In combination studies, single doses of two different cytotoxic agents were given either simultaneously, or up to 24 h apart in either sequence, and assays were performed 24 h after the second drug was given. Combinations of vincristine + cyclophosphamide and 5-fluorouracil + gamma-rays were chosen because they had been shown by other workers to exhibit marked schedule dependency, including considerabl potentiation, against leukaemic cell lines. However, in the B16 melanoma there was no evidence of schedule-dependent cell killing with either of these combinations. For all sequences studied, the fraction of surviving cells per tumour was slightly greater than the predicted additive response calculated from single-drug controls

Attacking Group Protocols by Refuting Incorrect Inductive Conjectures

Automated tools for finding attacks on flawed security protocols often fail to deal adequately with group protocols. This is because the abstractions made to improve performance on fixed 2 or 3 party protocols either preclude the modelling of group protocols all together, or permit modelling only in a fixed scenario, which can prevent attacks from being discovered. This paper describes Coral, a tool for finding counterexamples to incorrect inductive conjectures, which we have used to model protocols for both group key agreement and group key management, without any restrictions on the scenario. We will show how we used Coral to discover 6 previously unknown attacks on 3 group protocols