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.

A radiological investigation of enzootic pneumonia in the pig.

Twenty normal piglets were radiographed and necropsied. Bronchography was performed in seven of the animals. In dorso-ventral radiographs the borders of the heart are clearly outlined by the adjacent lung lobes. In lateral films the lung fields may be divided into a cranial portion extending from the thoracic inlet to the third pair of ribs and a triangular shaped caudal portion with its base the caudal border of the heart and its apex the phrenico-vertebral angle. Nine field cases of enzootic pneumonia and nine experimentally induced cases were examined radiologically. They were then necropsied and the radiological and pathological findings related to each other. Pulmonary consolidation was identified radiologically as areas of unaerated lung which caused loss of the borders of the heart and diaphragm (silhouette sign) and enhancement of the image of the segmental and smaller bronchi (air bronchogram sign). The silhouette sign correctly predicted pulmonary consolidation of lobes in 77 per cent of field cases and in 54 per cent of lobes of experimental cases. The air bronchogram sign correctly predicted consolidation in 73 per cent of lobes of field cases and 76 per cent of lobes of experimental cases. A radiological examination has limitations for determining whether pigs are free of enzootic pneumonia because foci of consolidation less than 2 cm3 may not be detected.

A complement-fixation test for enzootic pneumonia of pigs using a complement dilution method.

Complement-fixing antibody to Mycoplasma hyopneumoniae in the serums of pigs experimentally infected with enzootic pneumonia was demonstrated by comparing the haemolytic titre of guinea-pig complement titrated in the presence of heated test serum, M. hyopneumoniae antigen and unheated normal pig serum with the titre obtained when the antigen was omitted. The haemolytic titres against sensitised sheep erythrocytes were determined after a fixation period of 16 to 18 hours at 5 degrees C. When serums, collected at intervals of 3 to 7 days, from 43 pigs exposed to pigs experimentally infected with enzootic pneumonia were tested, 4.6 or more complement units were first fixed 14 to 44 (mean 23.4) days after contact began. Serums collected subsequently fixed from 4.6 to more than 31 complement units. This positive reaction usually persisted until the pigs were killed 4 to 35 weeks after contact began. Thirty-three had gross enzootic pneumonia lesions and 9 had lung lesions detected microscopically. Serum antibody was not detected in 73 weaned pigs aged 7 weeks in a pneumonia-free herd but serums from 9 of 15 unweaned piglets aged 9 to 14 days in the same herd, fixed between 3 and 7 complement units.

Isolation of Mycoplasma hyopneumoniae from lesions in experimentally infected pigs.

Pigs aged 6 to 9 weeks from enzootic pneumonia-free herds were inoculated intranasally with a suspension of pneumonic lung containing Mycoplasma hyopneumoniae or were placed in contact with such inoculated pigs. All the inoculated pigs had gross lesions of enzootic pneumonia when killed 27 to 42 days after inoculation. The culture methods described enabled M. hyopneumoniae to be isolated from all 29 inoculated pigs. Of 45 pigs in contact with inoculated pigs 35 had gross lesions of enzootic pneumonia when killed 28 to 71 days later and M. hyopneumoniae was isolated from 33. Another 9 had lesions, detected only microscopically, and M. hyopneumoniae was recovered from 3 of these when killed 75 to 98 days after contact began. In a separate experiment M. hyopneumoniae isolated from experimentally infected pigs, and adapted to the culture medium after 6 passages, caused gross lesions of enzootic pneumonia in 1 of 4 pigs inoculated intranasally.

Acute respiratory, circulatory and pathological changes in the calf after intravenous injections of the galactan from Mycoplasma mycoides subsp. mycoides.

Twenty of 28 calves, 10-12 weeks of age when given intravenous injections of the galactan from Mycoplasma mycoides subsp. mycoides, showed transient apnoea, increased pulmonary arterial and decreased systemic arterial blood pressures, and increased packed-cell volume. Necropsy revealed haemorrhages associated with alveolar ducts and vessel walls, areas of pulmonary oedema, usually associated with the haemorrhages, dilated airways and, in some, capillary thrombosis. Animals that had shown changes in blood pressure and respiration in response to a dose of galactan did not react to a second dose an hour later. One goat tested died, four lambs were mildly affected and a cat and several rats and guinea-pigs did not respond. It is suggested that the galactan released biogenic amines that produced the effects listed. Immunological mechanisms were discounted on the grounds that only a small amount of antigenic material was injected at the time the reaction occurred, and neither serological nor skin tests produced any evidence of prior sensitisation to the galactan or a similar substance. A relationship between reactivity to the galactan and susceptibility to the natural disease has been suggested. This, together with the pulmonary oedema found in galactan-treated calves and in natural lesions of contagious bovine pleuropneumonia (CBPP), and the possibility that contraction of blood vessels could be an initiating cause of thrombosis indicates the role that galactan may play in the pathogenesis of CBPP.

Studies on the origin of false positive reactions to the complement-fixation test for contagious bovine pleuropneumonia.

Serums of cattle free from contagious bovine pleuropneumonia (CBPP) were tested in complement fixation (CF) tests using 3 antigens; these were the standard antigen (SA) used to test to CBPP in Australia, an ethanol extract antigen (EA) also prepared from Mycoplasma mycoides subsp. mycoides (M. mycoides) and an antigen prepared from a Group 7 bovine mycoplasma isolated from arthritis (AA). The serums included 146 which fixed complement with SA. Eighty percent of these false-positive serums reacted with AA but not with EA; the other 20% were positive at low titre with EA but gave no reaction with AA. Attempts were made to produce false-positive serums experimentally by inoculating 3 Group 7 mycoplasmas and 2 Mycoplasma bovigenitalium strains into cattle. Serums from 3 of 9 cattle inoculated with strain L2917 (Group 7) reacted with SA but differed from the false-positive serums of field cattle by reacting with all 3 antigens. Tests with serums from cattle experimentally infected with CBPP gave similar titres with SA and EA, but the results with AA were mostly negative or less than 10% of the titres obtained with SA and EA. The results of CF tests on serums from the experimental cattle, after absorptions with suspensions of the mycoplasmas, showed that there was a one-way serological relationship between strain L2917 and M. mycoides and between this Group 7 strain and M. bovigenitalium. The CF tests with 3 antigens have assisted in demonstrating the false-positive nature of the reacting field serums encountered in the course of routine CF tests for CBPP in cattle in Australia.

Secretory and structural changes in the parotid salivary gland of sheep and lambs after parasympathetic denervation.

The effect of the parasympathetic nerve supply on the development of the parotid gland in the immature lamb and its maintenance in the adult sheep has been investigated by unilateral postganglionic denervation. Seventy-seven to ninety-three days after denervation secretory activity of the gland was examined and material taken for histological examination. The adult denervated glands secreted at lower rates than the innervated and their atropine-resistant secretory flow was reduced to as low as one fifth of that of the innervated glands. In two lambs an atropine-resistant flow did not develop in the denervated glands: in another two, flows of saliva from the denervated glands were present but were much less than in the contralateral innervated glands. After denervation glands were, with one exception, smaller than the contralateral innervated glands. The acinar cells of the denervated adult and lamb glands were smaller than the cells of the innervated glands but similar in size to those of 7-14 day old unoperated control lambs. Acinar cells in denervated glands had periodic acid Schiff staining material but the staining reaction to pyronin-methyl green was similar in the innervated and denervated. The results indicate that the integrity of the parasympathetic innervation is essential for the development of the parotid gland of the sheep and for its maintenance in the adult animal.