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Notes: We demonstrate that focused Ga+ ion irradiation can comprehensively modify the ferromagnetic properties of Ni80Fe20 thin films. Magneto-optic Kerr effect measurements at room temperature and magnetoresistance measurements at temperatures between 1.5 and 270 K characterized the irradiation effects. Irradiation steadily reduced the films' room temperature coercivity, and a dose of 1.0×1016 ions/cm2 at 30 keV was found sufficient to cause a loss of ferromagnetism at room temperature in films of thickness up to 15.5 nm. In situ end-point detection and postirradiation atomic force microscopy confirmed that the sputtering which accompanied doses up to 1.0×1016 ions/cm2 did not compromise the protective caps on these Ni80Fe20 films. We therefore conclude that the modification of ferromagnetic properties occurred primarily because of direct Ga+ ion implantation. From these results, we speculate that focused Ga+ ion irradiation could be a convenient tool for the nanoscale patterning of magnetic properties in 3d transition metal thin films. © 2001 American Institute of Physics.

Notes: We fabricate a one-dimensional constriction in a shallow, δ-doped GaAs/AlxGa1−xAs two-dimensional electron gas, by locally oxidizing the surface using an atomic force microscope. The channel exhibits ballistic conduction with up to seven conductance plateaus, quantized in units of 2e2/h. The dependence of the device conductance on dc bias voltage reveals the energy separation of the first two subbands to be ΔE1,2=5.5(±0.3) meV, which allows ballistic conduction to be observed up to a temperature of 20 K. A lateral electric field, combined with the hard-walled confinement due to the insulating lines, allows manipulation of the electron wave function in a way which is not possible with surface-gated devices. © 2001 American Institute of Physics.

Notes: To assess the risk of transmission of infectious haematopoietic necrosis virus (IHNV) associated with the movement of processed rainbow trout, Oncorhynchus mykiss, from an area where the virus is endemic, 240 freshly eviscerated fish (225–500 g) exhibiting spinal curvature or spinal compression types of deformities were tested for IHNV by virus isolation and polymerase chain reaction (PCR) techniques. Commercially produced rainbow trout, approximately 1-year-old, that exhibited spinal deformities were considered to have had a high likelihood of having survived an outbreak of IHN. Serological analysis of fish exhibiting spinal curvature or spinal compression types of deformities for anti-IHNV antibodies resulted in 71 and 50% of the serum samples, respectively, with detectable neutralization activity suggesting previous infection with IHNV. A portion of the skin and muscle in the area of the deformity was collected, as well as brain tissue from each commercially processed fish. Tissue homogenates were tested for IHNV using the epithelioma papulosum cyprini (EPC) cell line pretreated with polyethylene glycol and the chinook salmon embryo (CHSE-214) cell line using standard methods. Nested, reverse transcriptase (RT)-PCR for the detection of IHNV used the central 1231 bp portion of the glycoprotein (G) gene. All brain and skin-muscle homogenates were negative for IHNV by virus isolation and by nested RT-PCR. To assess virus clearance experimentally, groups of 100 specific-pathogen-free (SPF) rainbow trout (mean weight, 100 g) were either intraperitoneally injected with IHNV or sham infected and held separately in 385 L aquaria in SPF water at 15 °C. In the first study, a total of 33% of the infected fish died. Ten days after the last mortality or 34 days after post-infection, six fish from each treatment were killed at weekly intervals for 6 weeks. Kidney and brain homogenates from individual fish were tested by virus isolation and nested RT-PCR using the nucleoprotein (N) gene. All tissue homogenates were negative for IHNV. When this study was repeated, 54% of the infected fish died and beginning 34 days post-infection, six fish from each treatment were killed at biweekly intervals for 8 weeks, and kidney and brain homogenates from individual fish were tested by virus isolation and quantitative real-time PCR utilizing primers and fluorescent labelled probes generated for the specific identification of the N and G genes of IHNV. One brain specimen from an IHN survivor obtained 34 days post-infection was positive by both virus isolation and quantitative PCR; however, all remaining tissue specimens were negative over the 8-week period. Intraperitoneal injection of supernatants from pooled kidney or brain tissue obtained from control or IHN survivor fish into SPF rainbow trout (mean weight, 10 g) also failed to establish virus infection. A strong humoral response was detected in the IHN survivors in both challenge studies and is suggested as a mechanism responsible for virus clearance. These results provide scientific information that can be used to assess the risk associated with the movement of processed rainbow trout from an IHNV endemic area.