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Notes: Introduction of a ferromagnetic quantum well in a ferromagnetic tunnel junction is shown to greatly enhance the tunneling magnetoresistance (TMR) effect, due to spin filtering as well as energy filtering. We have theoretically analyzed resonant transmission probability of a magnetic double barrier heterostructure consisting of III–V based ferromagnetic semiconductor GaMnAs, and nonmagnetic semiconductor AlAs. Experimentally, we have observed very large TMR effect of such a system grown by low-temperature molecular-beam epitaxy, and have shown that some of the measured tunneling features are attributed to spin-dependent resonant tunneling. © 2000 American Institute of Physics.

Notes: We have succeeded in growing MnAs/GaAs/MnAs ferromagnet/semiconductor trilayer heterostructures on GaAs(111)B substrates by molecular-beam epitaxy. Double-step features were observed in magnetization characteristics due to the difference in coercive force between the top and bottom MnAs layers. Magnetoresistance (MR) curves in current-in-plane geometry showed the spin-valve effect, which was caused by the change of the magnetic alignment of the two ferromagnetic MnAs layers from parallel to antiparallel orientation. Temperature dependence of the MR was also investigated. We infer that the positive temperature coefficient of the MR by the spin-valve effect suggests the heat (carrier) induced interlayer exchange coupling. © 2000 American Institute of Physics.

Notes: Filamentless negative ion beam production was investigated with a compact microwave ion source (2.45 GHz). One of the key points for negative ion production is the magnetic configuration. A magnetic filter field to lower electron temperature was generated in a negative ion production cell, which was shielded magnetically from a discharge cell with a magnetic field to couple microwave to plasma. Production of H− beam was studied with this source. H− was extracted through a grid slit (2×16 mm2) from plasma and accelerated to 20–40 keV. H− beam current was measured with a Faraday cup after magnetic mass separation. Continuous H− beam current of 73 μA (0.23 mA/cm2) was obtained with a magnetron power of 700 W. H− beam current was increased around 1.4 times by adding Xe gas to the H2 gas. Other negative ion species, which have a potential for applications to industrial ion beam processing with little charge-up problem, were also investigated. Carbon and hydrocarbon negative ion beams were produced using boron alkoxide (B(OCH3)3) and methane. C2H2− beams (22 μA) were obtained with the alkoxide. C2−(1.6 μA), C2H−(2.3 μA), C2H2−(0.6 μA), and H−(6.9 μA) beams were produced with methane. SiF4 and BF3 were used to generate F−, Si−, SiF3− and B− beams. Beam currents of these ion species were 17, 0.25, 1.5, and 0.03 μA, respectively. © 2000 American Institute of Physics.

Notes: Computer-assisted area measurement of skin lesions would be useful for the assessment of disease severity. Difficulties can be encountered, however, when lesions cannot simply be separated using the normal threshold tool of an image analyser. Owing to body curvature, peripheral sites are usually shadowed. To obtain a well-fitting curved line to account for body curvature-induced glare and shadow, we devised a simple C-programme for averaging neighbouring pixels on the same horizontal line. An image was captured from a colour slide to the image analysis system. C++ was used for programming. Execution of the averaging programme with the original image resulted in a background brightness image file. When this was subtracted from the original image, the lesions were easily detected using the standard threshold tool and the percentage of area involved was calculated. This method is sufficiently accurate for the assessment of disease severity.

Notes: Background: Different authors have postulated both toxic and protective effects for nitric oxide (NO) in the pathophysiology of active inflammation. Aim: To examine the role of NO, especially that produced by the inducible form of nitric oxide synthase (iNOS), by investigating the effects of NOS inhibitors and NO donors on inflammation in experimental acute colitis. Methods: Acute colitis was induced in rats by dextran sulphate sodium (DSS). White blood cell counts and levels of thiobarbituric acid reactants in the portal blood were determined, as were histological changes in the colonic mucosa. We then evaluated the effects of NG-nitro- l-arginine methyl ester ( l-NAME), aminoguanidine (AG) and an NO donor on DSS-induced changes in these inflammatory parameters. Results and Conclusions: Inhibition of NO production by either l-NAME or AG worsened DSS-induced inflammation, suggesting a protective role for NO in acute colitis. On the other hand, a NO donor also exaggerated DSS-induced inflammatory parameters, suggesting that acute colitis may be aggravated by either too much or too little NO. These results suggest that medical treatment of ulcerative colitis must aim for maintenance of appropriate NO levels in the intestinal mucosa.

Notes: Abstract The resistance mechanisms to fluoroquinolones in Staphylococcus aureus were clarified by analyzing mutations in the genes encoding target enzymes, and examining the expression of the efflux pump, and determining the inhibitory activities of fluoroquinolones against the altered enzymes. Mutations in the grlA and gyrA genes of 344 clinical strains of S. aureus isolated in 1994 in Japan were identified by combinations of methods – single-strand conformation polymorphism analysis, restriction fragment length analysis, and direct sequencing – to identify possible relationships with fluoroquinolone resistance. Five types of single-point mutations and four types of double mutations were observed in the grlA gene in 204 strains (59.3%). Four types of single-point mutations and four types of double mutations were found in the gyrA gene in 188 strains (54.7%). Among these mutations, the grlA mutation of TCC → TTC or TAC (Ser-80 → Phe or Tyr) and the gyrA mutation of TCA → TTA (Ser-84 → Leu) were the principal ones, being detected in 137 (39.8%) and 121 (35.2%) isolates, respectively. A total of 15 types of mutation combinations within both genes were related to ciprofloxacin resistance (MIC ≧3.13 μg/ml) and were present in 193 mutants (56.1%). Strains containing mutations in both genes were highly resistant to ciprofloxacin (MIC50 =50 μg/ml). Those strains with the Ser-80 → Phe or Tyr alteration in grlA, but wild type in gyrA showed a lower level of ciprofloxacin resistance (MIC50≦12.5 μg/ml). Levofloxacin was active against 68 of 193 isolates (35.2%) with mutations at codon 80 of grlA in the presence or absence of concomitant mutations at codons 73, 84, or 88 in gyrA (MIC ≦6.25 μg/ml). Sitafloxacin (DU-6859a) showed good activity in 186 of 193 isolates (96.4%), with an MIC of ≦6.25 μg/ml. The contribution of membrane-associated multidrug efflux protein (NorA) expression to fluoroquinolone resistance was clarified by the checker-board titration method for determining the MIC of norfloxacin alone and in combination with carbonyl cyanide m-chlorophenylhydrazone. Among 344 clinical isolates, 139 strains (40.4%), in which the MIC of norfloxacin varied from 1.56 to 〉800 μg/ml, overexpressed the NorA protein. GrlA and GrlB proteins of topoisomerase IV, and GyrA and GyrB proteins of DNA gyrase encoded by genes with or without mutations were purified separately. The inhibitory activities of fluoroquinolones against the topoisomerase IV which contained a single amino acid change (Ser → Phe at codon 80, Glu → Lys at codon 84 of grlA, and Asp → Asn at codon 432 of grlB) were from 5 to 95 times weaker than the inhibitory activities against the non-altered enzyme. These results suggest that the mutations in the corresponding genes may confer quinolone resistance; the active efflux pump, NorA, was considered to be the third quinolone-resistance mechanism. The numerous and complicated mutations seen may explain the rapid and widespread development of quinolone resistance described in S. aureus. Sitafloxacin showed good antibacterial activity against ciprofloxacin- or levofloxacin-resistant mutants because of its high inhibitory activity against both topoisomerase IV and DNA gyrase.