An analysis of the electrical conductivity in BaSO4-added Ag2SO4 solid electrolyte system

The compositions (1 −x)Ag₂SO₄−(x)BaSO₄, wherex=0·01 to 0·6, were prepared by slow cooling of the melt. The extent of the solid solubility of Ba²⁺ in Ag₂SO₄ was determined by X-ray powder diffraction and scanning electron microscopy. The bulk conductivity of each sample was obtained using a detailed impedance analysis. The partial substitution of Ba²⁺ results in the enhancement of conductivity in compliance with the classical aliovalent doping theory. A simplistic model based on lattice distortion (expansion) due to partial substitution of Ag⁺ by the bigger Ba²⁺ has been considered to explain enhanced conductivity. Beyond solid-solubility limit (5·27 mole%) the BaSO₄-dispersed Ag₂SO₄ conductivity follows the usual trend seen in binary systems. An increase in conductivity in this case is discussed in the light of interfacial reactions and surface defect chemistry. The maximum conductivity in 20 mole% BaSO₄ dispersed Ag₂SO₄ is due to percolation threshold.     

A fast-settling GaAs-enhanced frequency synthesizer

An indirect, phase-locked-loop (PLL), GaAs-enhanced frequency synthesizer with 700 ns loop settling time has been developed. The two-chip GaAs insertion reduced the size of an existing synthesizer from 90 in³ to only 30 in³. The 6.0 in×5.5 in.×0.9 in module contains a 400 gate GaAs programmable divider and a sample and hold (S/H) which improved the settling time by 77% and reduced the size by 67% over the current state-of-the-art synthesizer. Furthermore, the divider reduced power dissipation by 9.7 W and the S/H reduced power dissipation by 1.3 W     

Bone marrow and renal injury associated with haloalkene cysteine conjugates in calves

Almost 40 years ago, it was reported that cattle-feed which had been extracted with hot trichloroethylene and then fed to calves produced renal injury and a fatal aplastic anaemia. The toxic factor was subsequently identified as S-(1,2-dichlorovinyl)-L-cysteine (DCVC). These original findings have been confirmed, a single intravenous dose of DCVC at 4 mg/kg, or 0.4 mg/kg intravenously per day administered for 10 days to calves produced aplastic anaemia, and renal injury after a single dose of 4 mg/kg. The toxicity to calves of a number of other haloalkene cysteine conjugates has been examined to ascertain whether, like DCVC, they produce bone marrow and renal injury. Intravenous administration of the N-acetyl cysteine conjugate of DCVC produced renal but not bone marrow injury at a molar equivalent dose to DCVC, indicating that the calf can deacetylate the mercapturic acid and further that sufficient chemical had reached the kidney to be a substrate for the enzyme cysteine conjugate beta-lyase. However, intravenous administration of the alpha-methyl analogue of DCVC, which cannot undergo metabolism via the enzyme cysteine conjugate beta-lyase, was without toxicity at doses about five-fold higher than DCVC. These latter findings provide strong evidence that metabolism of DCVC via the enzyme beta-lyase is necessary for bone marrow and renal injury to occur. The cysteine conjugates of perchloroethylene and hexachloro-1,3-butadiene(HCBD) when given intravenously to calves at molar equivalent doses to DCVC, or above, did not produce either bone marrow or renal injury. In contrast, intravenous administration of the cysteine conjugate of tetrafluoroethylene (TFEC) produced severe renal tubular injury in calves without affecting the bone marrow. In vitro studies with these haloalkene cysteine conjugates showed, like DCVC, that they were good substrates for calf renal cysteine conjugate beta-lyase and toxic to renal cells as judged by their ability to reduce organic anion and cation transport by slices of calf renal cortex and inhibit the renal enzyme glutathione reductase. Calves were also dosed either orally or intravenously with HCBD to assess its toxicity. HCBD at higher molar equivalent doses than DCVC produced mid-zonal necrosis in the liver, renal tubular necrosis but no bone marrow injury in calves. The key findings emerging from these studies are (1) that none of the other cysteine conjugates, at molar equivalent doses to DCVC and above, produce bone marrow injury in calves, (2) TFEC produced only renal injury, suggesting that sufficient of the other conjugates had not reached the kidney for metabolism by beta-lyase to produce cytotoxicity and (3) that HCBD itself is more toxic than its cysteine or mercapturic acid conjugate, suggesting that pharmaco-kinetics and disposition are important factors in determining the toxicity of these conjugates to calves. Further studies are needed to understand the basis for the selective toxicity of DCVC to the bone marrow of calves.     

Response spectrum analysis of piping systems with elastic-plastic gap supports

A new seismic support device and its application in piping systems is described. The device, E-BAR (patented), can be cost effectively used for snubber replacement programs, mitigation of hydraulic transients, pipe whip and as a thermal stop. The device has pre-set gaps to allow free thermal movement. During a seismic or other dynamic load event, if the pipe movement exceeds the gap dimension, the device acts as an elastic or elastic-plastic restraint. The device also has a unique design feature for not exceeding the restraint force beyond a specified limit design value. To analyze piping systems with gap supports having elastic-plastic characteristics, modal analysis procedures for both response spectrum and time history methods are developed. The comparison of responses obtained from the procedures with nonlinear time history analysis and test results available in the literature shows excellent correlation. A pilot program conducted for snubber replacement with E-BARs demonstrates that the limit force feature of E-BAR makes them very attractive for snubber replacement. This is because a particular E-BAR with a specified limit design force can be selected, such that, the E-BAR replacing the snubber does not require any modifications be made to the existing support steel and hardware.     

Preservation of myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest with 2, 3-butanedione monoxime

One proposed contributory mechanism for depressed ventricular performance after hypothermic, hyperkalemic cardioplegic arrest is a reduction in myocyte contractile function caused by alterations in intracellular calcium homeostasis. Because 2,3-butanedione monoxime decreases intracellular calcium transients, this study tested the hypothesis that 2,3-butanedione monoxime supplementation of the hyperkalemic cardioplegic solution could preserve isolated myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Myocytes were isolated from the left ventricles of six pigs. Magnitude and velocity of myocyte shortening were measured after 2 hours of incubation under normothermic conditions (37 degrees C, standard medium), hypothermic, hyperkalemic cardioplegic arrest (4 degrees C in Ringer's solution with 20 mEq potassium chloride and 20 mmol/L 2,3-butanedione monoxime). Because beta-adrenergic agonists are commonly employed after cardioplegic arrest, myocyte contractile function was examined in the presence of the beta-agonist isoproterenol (25 nmol/L). Hypothermic, hyperkalemic cardioplegic arrest and rewarming reduced the velocity (32%) and percentage of myocyte shortening (27%, p < 0.05). Supplementation with 2,3 butanedione monoxime normalized myocyte contractile function after hypothermic, hyperkalemic cardioplegic arrest. Although beta-adrenergic stimulation significantly increased myocyte contractile function under normothermic conditions and after hypothermic, hyperkalemic cardioplegic arrest, contractile function of myocytes exposed to beta-agonist after hypothermic, hyperkalemic cardioplegic arrest remained significantly reduced relative to the normothermic control group. Supplementation with 2,3-butanedione monoxime restored beta-adrenergic responsiveness of myocytes after hypothermic, hyperkalemic cardioplegic arrest. Thus, supplementation of a hyperkalemic cardioplegic solution with 2,3-butanedione monoxime had direct and beneficial effects on myocyte contractile function and beta-adrenergic responsiveness after cardioplegic arrest. A potential mechanism for the effects of 2,3-butanedione monoxime includes modulation of intracellular calcium transients or alterations in sensitivity to calcium. Supplementation with 2,3-butanedione monoxime may have clinical utility in improving myocardial contractile function after hypothermic, hyperkalemic cardioplegic arrest.     

Aging, encoding specificity, and memory change in the Double Memory Test

Aged and young adults were tested by category cued recall after learning with category cues (CCR) or with item cues (ICR). CCR was about twice ICR for both aged and young adults. The aged recalled less than the young and did not benefit as much from greater encoding specificity and deeper processing in CCR. ICR and CCR were correlated, so that expected CCR can be predicted from ICR. The regression of CCR on ICR was linear for young adults, but was piecewise linear for the aged, showing that the relationship between ICR and CCR was not uniform for the aged adults. Lower than expected CCR by a subset of aged without clinical dementia may be a sign of preclinical dementia.     

A high-current and high-temperature 6H-SiC thyristor

A 6H-SiC thyristor has been fabricated and characterized. A forward breakover voltage close to 100 V and a pulse switched current density of 5200 A/cm² have been demonstrated. The thyristor is shown to operate under pulse gate triggering for turn-on and turn-off, with a rise time of 43 ns and a fall time of less than 100 ns. The forward breakover voltage is found to decrease by only 4% when the operating temperature is increased from room temperature to 300°C. It is found that anode ohmic contact resistance dominates the device forward drop at high current densities     

Evaluation of the recombinant 38-kilodalton antigen of Mycobacterium tuberculosis as a potential immunodiagnostic reagent

The diagnosis of infection caused by Mycobacterium tuberculosis is of increased public health concern following increases in the number of cases in developed countries and major increases in developing countries associated with the spread of human immunodeficiency virus (HIV) infection. The specificity of purified protein derivative skin testing for the detection of infection is compromised by exposure to environmental mycobacteria. Examination of sputum detects the most infectious patients, but not those with extrapulmonary disease. The 38-kDa antigen of M. tuberculosis contains two M. tuberculosis-specific B-cell epitopes. We overexpressed the gene for this antigen in Escherichia coli and evaluated the recombinant product in in vitro assays of T-cell function and as a target for the antibody response in humans. The sensitivity and specificity of the antigen as a skin test reagent were also assessed in outbred guinea pigs. We found that 69% of healthy sensitized humans recognize the antigen in vitro, as manifested by both cell proliferation and the production of gamma interferon. Untreated patients initially have a lower frequency of response (38%); this recovers to 72% during therapy. A total of 292 patients (20 with HIV coinfection) and 58 controls were examined for production of antibody to the 38-kDa antigen by using a commercially available kit. The sensitivity of the test in comparison with that of culture was 72.6%, and the specificity was 94.9%. The antigen was also tested for its ability to induce skin reactions in outbred guinea pigs sensitized by various mycobacterial species. The antigen provoked significant skin reactions in M. tuberculosis-, M. bovis BCG-, and M. intracellulare-sensitized animals. The significance of these findings and the usefulness of this antigen in immunodiagnosis are discussed.