Atomically engineered electron spin lifetimes of 30 s in silicon.

Scaling up to large arrays of donor-based spin qubits for quantum computation will require the ability to perform high-fidelity readout of multiple individual spin qubits. Recent experiments have shown that the limiting factor for high-fidelity readout of many qubits is the lifetime of the electron spin. We demonstrate the longest reported lifetimes (up to 30 s) of any electron spin qubit in a nanoelectronic device. By atomic-level engineering of the electron wave function within phosphorus atom quantum dots, we can minimize spin relaxation in agreement with recent theoretical predictions. These lifetimes allow us to demonstrate the sequential readout of two electron spin qubits with fidelities as high as 99.8%, which is above the surface code fault-tolerant threshold. This work paves the way for future experiments on multiqubit systems using donors in silicon.

Donor hyperfine Stark shift and the role of central-cell corrections in tight-binding theory.

Atomistic tight-binding (TB) simulations are performed to calculate the Stark shift of the hyperfine coupling for a single arsenic (As) donor in silicon (Si). The role of the central-cell correction is studied by implementing both the static and the non-static dielectric screenings of the donor potential, and by including the effect of the lattice strain close to the donor site. The dielectric screening of the donor potential tunes the value of the quadratic Stark shift parameter (η2) from -1.3 × 10(-3) µm(2) V(-2) for the static dielectric screening to -1.72 × 10(-3) µm(2) V(-2) for the non-static dielectric screening. The effect of lattice strain, implemented by a 3.2% change in the As-Si nearest-neighbour bond length, further shifts the value of η2 to -1.87 × 10(-3) µm(2) V(-2), resulting in an excellent agreement of theory with the experimentally measured value of -1.9 ± 0.2 × 10(-3) µm(2) V(-2). Based on our direct comparison of the calculations with the experiment, we conclude that the previously ignored non-static dielectric screening of the donor potential and the lattice strain significantly influence the donor wave function charge density and thereby leads to a better agreement with the available experimental data sets.

Induction of enzootic pneumonia in pigs by the administration of an aerosol of in vitro-cultured Mycoplasma hyopneumoniae.

The aim of this study was to establish whether enzootic pneumonia could be induced reliably in piglets by administering an aerosolised culture of Mycoplasma hyopneumoniae. Groups of five M hyopneumoniaefree Landrace x Large White piglets weaned at 11 to 14 days of age were exposed to aerosols of in vitro cultures of a virulent strain of M hyopneumoniae. In three separate trials, 14 of 15 pigs exposed to the bacteria developed pneumonia, but pigs exposed to the culture medium alone did not develop the disease. Lung pathology, both gross and histological, indicated acute disease. Ten of the pigs were tested for seroconversion by Western blot and they were all positive. The growth rates of the infected pigs were significantly reduced and the water consumption of the infected groups was also depressed. M hyopneumoniae was recovered from eight of the 15 infected pigs.

Protection against enzootic pneumonia of pigs: intraperitoneal inoculation with live LKR strain of Mycoplasma hyopneumoniae.

Pigs obtained from a mycoplasma-free piggery were randomised into 4 groups of 9. Groups 1 and 2 were injected by the intraperitoneal route with liquid culture of the LKR strain of Mycoplasma hyopneumoniae. Group 1 was injected once and group 2 twice. Group 3 was made up of pigs inoculated by the intranasal route with the virulent Beaufort strain of M. hyopneumoniae; they served as the source of infection for the challenge. Group 4 were uninfected, uninjected controls. Six weeks after the last injection, groups from 1 to 4 were placed in contact. Seven of the pigs in the 1-dose group and 6 in the 2-dose group were free of lesions at necropsy 6 weeks after challenge. Of the two pigs with lesions in the 1-dose group one had only a small lesion but the other had extensive lesions; it had not shown an antibody response after injection of culture. The lesions in the 3 pigs in the 2-dose group were all small. All 9 control pigs had lesions which varied from medium to large in size. The difference in the incidence of pneumonia between the injected and control groups was significant (P less than 0.05) and the proportion of severely affected pigs in the vaccinated groups was significantly lower (P greater than 0.01). There was no difference between those given one dose of vaccine and those receiving 2 doses.

Early serological responses to Mycoplasma hyopneumoniae infection.

A complement fixation (CF) test for Mycoplasma hyopneumoniae antibody, using the complement dilution method, will detect infection in inoculated pigs at an early stage. The interval between inoculation and the first positive CF response--defined as 4.6 u of complement fixed--was determined for four separate methods of inoculation and for pigs with artificially induced pneumonia. Sera from two groups were tested by the enzyme-linked immunosorbent assay (ELISA). By CF, the i.v. group showed positive titers at 9.8 +/- 0.4 (mean +/- SE) days. All pigs in this group had positive titers, most of them at the maximum level of 31 u fixed. The i.p. group first showed positive titers at 13.3 +/- 1.0; 17 of 70 had no CF response. The s.c. group first showed titers at 21.1 +/- 2.6; 7 of 24 did not respond. Intranasal inoculation first produced a CF response at 14.3 +/- 0.9, and all pigs had positive titers. Pigs in contact with those with induced pneumonia first showed titers at a mean of 27.2 days (SE +/- 1.3), and all pigs exhibited a CF response. There was no significant difference between the CF test and ELISA results.

Assessment of a complement fixation test to detect Mycoplasma hyopneumoniae infection in pigs.

Serums from pigs slaughtered at abattoirs were tested for evidence of Mycoplasma hyopneumoniae infection using a complement fixation (CF) test which avoids the procomplementary effect of pig serum. To establish a diagnosis of enzootic pneumonia, the lungs from all sampled pigs were examined for pathological and histological changes consistent with the disease and cultures were made for mycoplasmas and bacteria. The study was carried out at Parkville and Bendigo 160 km apart at different times and all serums were tested at both laboratories. The results agreed closely. Thirty-six of 97 pigs at Parkville and 46 of 99 at Bendigo had enzootic pneumonia. About 80% were positive in the CF test. Sixteen per cent of porkers and 36% of baconers gave false negative reactors, that is, a negative test though lesions were present. About 18% to 36% gave false positive reactions but the level in the porkers in the Bendigo group was significantly higher (p less than 0.02). Possible explanations include, for the false negatives, loss of reactivity caused by circulating antigen and for the false positives, cross reacting antibody produced by another infection or failure to appreciate that lesions of EP were present in lungs because either they were not identified as such or they were not detected. The validity of any serological test for this disease cannot be established while there is a possibility that the present methods used for diagnosis, gross and microscopic examination and recovery of M. hyopneumoniae, fail to detect some infected animals. Other criteria may have to be adopted.

A method for assessing induced resistance to enzootic pneumonia of pigs.

The resistance induced in pigs by the intravenous, intraperitoneal and subcutaneous inoculation of live Mycoplasma hyopneumoniae was tested by placing inoculated pigs in contact with pigs artificially infected with enzootic pneumonia. Control pigs inoculated by the same routes with sterile culture medium were exposed simultaneously to the infected pigs and the incidence and extent of the pneumonia in both groups were compared. A score derived from the cube root of the calculated or estimated volume of the lung lesion, was used to evaluate severity. Ninety-six per cent of the control pigs developed lesions characteristic of enzootic pneumonia but only 29 per cent of the pigs that had previously been inoculated with M hyopneumoniae developed lesions. Induced lesions differed from those seen in natural cases in extent rather than in character. The method of challenge was satisfactory in that a high proportion of control pigs became infected without the resistance of a majority of inoculated pigs being overwhelmed.

Production of arthritis by intravenous inoculation of Mycoplasma hyopneumoniae: tests on five strains.

Cultures of five strains of Mycoplasma hyopneumoniae (syn, M suipneumoniae) were each inoculated intravenously into four pigs aged eight to nine weeks. One strain produced no response. For two strains two of the four pigs showed complement fixing antibody and mycoplasmaemia and one of these pigs in each group developed arthritis in one limb joint. The response to the other two strains was more severe: all four pigs in each group had a serological response, were mycoplasmaemic and several limb joints were arthritic.