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Permalloy ([Ni.sub.80][Fe.sub.20]) wire-based structures (30 nm thick and 1 [multiplied by] w [multiplied by] 10 [micro]m wide) with junctions (crosses, networks, H-shapes, rectangular chains and ring chains) prepared on a GaAs (100) substrate were observed in both their demagnetized and remanent states by magnetic force microscopy (MFM) in order to investigate the role of junction geometry in domain formation. Except in ring chains, two classes of domain configuration are found at the junction: (i) a domain wall-like feature due to abrupt spin rotation and (ii) a triangle-shape domain consistent with a flux closure configuration. Ring chains, on the other hand, form vortex domains at every other junction. The MFM observations are compared with micromagnetic calculations which qualitatively support the magnetic domain configurations. Index Terms--Mesoscopic structures, magnetic domain configuration, magnetic force microscopy, micromagnetic calculation.

The magnetization reversal process in mesoscopic permalloy ([Ni.sub.80][Fe.sub.20]) wire structures has been investigated using scanning Kerr microscopy, magnetic force microscopy (MFM) and micromagnetic calculations. We find that the junction offers a site for reversed domain wall nucleation in the narrow part of the wires. As a consequence, the switching field is dominated by the domain nucleation field and the junction region initiates reversal by the wall motion following the nucleation of domains. Our results suggest the possibility of designing structures that can be used to 'launch' reverse domains in narrow wires within a controlled field range. Index Terms--Magnetization reversal, mesoscopic wires, nucleation process, switching field.

The domain configuration in permalloy wires (30 nm thick, 10 μm wide, and 205 μm long) with a wide size range of a narrow central bridge (5 μm long and w μm wide; 0.5≤w≤10 μm) were investigated in both their demagnetized and remanent states using magnetic force microscopy and the results were confirmed by micromagnetic calculations. At the bridge region, domain walls were found to be shifted by a small external field. Scanning magneto-optical Kerr effect revealed that the coercivity in these structures are the same as that in a straight wire, suggesting that domain wall movement is the dominant process in the magnetization reversal of these structures. © 2000 American Institute of Physics. [ABSTRACT FROM AUTHOR]

The domain structures of epitaxial Fe (20 nm)/GaAs(100) circular dot arrays (diameters from 50 to 1 μm) were studied with magnetic force microscopy. A transition from a single domain to a multidomain remanent state was observed upon reducing the dot diameter beneath 10 μm in dot arrays with the separation twice the dot diameter. When the separation is reduced to half the dot diameter, the single domain states were found to “collapse” into stripe-like multidomain states due to local dipole coupling between dots. Micromagnetic simulations further suggest that for ultrathin Fe dots of less than about 2 nm thickness the diameter does not have a significant influence on the domain structures due to a dramatic reduction of the dipole energy. © 2000 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Presents a study that investigated the spin orientation in an exchange coupled iron trilayer using polarized neutron reflection. Characteristics of the iron compound; Details on the experiment; Discussion on the results of the study.

Presents a study which investigated the evolution of magnetic domain in permalloy mesoscopic dots. Significance of mesoscopic structures in magnetoelectronics and devices; Results and discussion; Numerical calculations; Conclusions.

The trp and trpl genes are thought to encode two classes of light-activated ion channels in Drosophila. A previous report indicated that a null trpl mutant does not display any mutant phenotype. This lack of detectable mutant phenotypes made it difficult to suggest functions for the transient receptor potential-like (TRPL) channel in photoreceptor responses. Here, the properties of trpl photoreceptor responses were studied by using electroretinogram (ERG) and intracellular recording techniques in combination with light stimuli of relatively long durations. Distinct mutant phenotypes were detectable under these conditions. These consisted of a reduced sustained component, oscillations superimposed on the response, a poststimulus hyperpolarization, and altered adaptation properties to dim background light. Comparison of photoreceptor responses obtained from wild type, trp, and trpl showed that the responses obtained from the trp and trpl null mutants did not sum up to that of the wild-type response. To explain the nonlinear summation at the peak of the response, Reuss et al. (1997) proposed that Ca(2+) ions entering through the TRP channel modulate TRP and TRPL channel activities differentially. However, nonlinear summation was present not only at the peak but throughout the duration of response. Two lines of evidence are presented to suggest that, in addition to the interaction proposed by Reuss et al. (1997), there are other forms of interactions between TRP and TRPL channels, probably involving the channel proteins themselves.

The trp gene of Drosophila encodes a subunit of a class of Ca(2+)-selective light-activated channels that carry the bulk of the phototransduction current. Transient receptor potential (TRP) homologs have been identified throughout animal phylogeny. In vertebrates, TRP-related channels have been suggested to mediate "store-operated Ca(2+) entry," which is important in Ca(2+) homeostasis in a wide variety of cell types. However, the mechanisms of activation and regulation of the TRP channel are not known. Here, we report on the Drosophila inaF gene, which encodes a highly eye-enriched protein, INAF, that appears to be required for TRP channel function. A null mutation in this gene significantly reduces the amount of the TRP protein and, in addition, specifically affects the TRP channel function so as to nearly shut down its activity. The inaF mutation also dramatically suppresses the severe degeneration caused by a constitutively active mutation in the trp gene. Although the reduction in the amount of the TRP protein may contribute to these phenotypes, several lines of evidence support the view that inaF mutations also more directly affect the TRP channel function, suggesting that the INAF protein may have a regulatory role in the channel function.

Tamoxifen has been an effective antiestrogen in suppressing breast cancer growth which is estrogen-responsive or dependent. Early studies have provided circumstantial evidence that transforming growth factor-beta (TGF-beta) may be an autocrine mediator of tamoxifen action. Therefore, it is both fundamentally important and clinically relevant to investigate the relationship between tamoxifen and TGF-beta. In this study, we demonstrated that CAMA-1 cells, which are sensitive to tamoxifen inhibition, did not respond to TGF-beta growth inhibition. The type I and II TGF-beta receptors were undetectable by the radio-ligand affinity labeling technique. Despite the presence of a normal TGF-beta type II receptor gene, the mRNA transcript of the gene was undetectable by the extremely sensitive Intron-differential RNA/PCR method. The possibility that the lack of TGF-beta receptors might be intimately linked to the absence of normal retinoblastoma (Rb) gene products, as suggested by previous studies of retinoblastoma cells, was further investigated. The lack of TGF-beta receptor expression was found due to reasons other than the absence, deletion or abnormality of the Rb gene because a normal Rb gene and its hyper- and hypo-phosphorylated protein products were detected in CAMA-1 cells. In conclusion, our results suggest that the TGF-beta system is not obligatory for antiestrogen growth inhibition of CAMA-1 cells.

Voltage-activated Ca channels play a central role in synaptic transmission, control of cell excitability, and many other cellular processes. It is now clear that there are multiple types of Ca channels with various modes of modulation. Drosophila offers exceptional advantages for studying the molecular basis of the diversity and modulation of Ca channels. As a step in this study, we have characterized the single-channel Ba currents recorded from cell-attached patches on cultured embryonic Drosophila nerve and muscle cells. The voltage dependence and selectivity of the channels carrying these Ba currents identify them as Ca channels. All Ca channels found in Drosophila neurons appear to have the same voltage dependence of activation and similar single-channel conductance, 12-17 pS (100 mM Ba2+). However, the kinetic properties of individual Ca channels vary greatly. The mean open time of individual channels ranges from 2 msec to less than 0.2 msec. Some channels completely inactivate during the first half of a 90 msec depolarization, while others are more active in the second half. Many channels open during almost every depolarization, while others open in less than 20% of the depolarizations. Channels with longer open times tend to inactivate and open during a small fraction of depolarizations. When these kinetic properties were quantified, a continuum of values was found, instead of the clustering of values that might be expected for discrete types of channels. Muscle Ca channels form a more homogeneous class than do the neuronal Ca channels. The muscle Ca channel conductance is 18 pS. These channels do not inactivate during 90 msec depolarizations and open during a majority of depolarizations applied. Muscle Ca channels are similar to a subset of neuronal Ca channels. When a purified toxin from the spider Hololena curta is applied to neurons, the number of active Ca channels is reduced, and those channels still active open in a small fraction of depolarization. Since channels that open in a small fraction of depolarizations tend to inactivate, these data support the hypothesis that this toxin selectively blocks noninactivating neuronal Ca channels. This differential toxin sensitivity and the much larger variability observed in kinetic properties of neuronal, compared to muscle, Ca channels suggest that there are at least two types of neuronal Ca channels in Drosophila.

To elucidate the relationship between epidermal growth factor (EGF)/transforming growth factor (TGF-alpha) and estradiol-17 beta (E) in cell proliferation, we examined their effects on the breast cancer cell line, CAMA-1. While E was able to consistently induce cell proliferation under a variety of experimental conditions, EGF/TGF-alpha was without effect. Despite the presence of the receptor (EGFR) gene, mature EGFR protein and mRNA were not detected by radioreceptor assay, 35S Met-labelling, and the Intron Differential RNA/PCR method under conditions in which cells remain responsive to E. Furthermore, TGF-alpha is not an autocrine factor in CAMA-1 cells. We demonstrated unequivocally that EGF/TGF-alpha interaction with EGFR is not an obligatory event in mediating estrogen-stimulated cell proliferation.

Toxins from spider venom, originally purified for their ability to block synaptic transmission in Drosophila, are potent and specific blockers of Ca2+ currents measured in cultured embryonic Drosophila neurons using the whole-cell, patch-clamp technique. Differential actions of toxins from two species of spiders indicate that different types of Drosophila neuronal Ca2+ currents can be pharmacologically distinguished. Hololena toxin preferentially blocks a non-inactivating component of the current, whereas Plectreurys toxin blocks both inactivating and non-inactivating components. These results suggest that block of a non-inactivating Ca2+ current is sufficient to block neurotransmitter release at Drosophila neuromuscular junction.