Creation and annihilation of topological meron pairs in in-plane magnetized films.

Merons which are topologically equivalent to one-half of skyrmions can exist only in pairs or groups in two-dimensional (2D) ferromagnetic (FM) systems. The recent discovery of meron lattice in chiral magnet Co8Zn9Mn3 raises the immediate challenging question that whether a single meron pair, which is the most fundamental topological structure in any 2D meron systems, can be created and stabilized in a continuous FM film? Utilizing winding number conservation, we develop a new method to create and stabilize a single pair of merons in a continuous Py film by local vortex imprinting from a Co disk. By observing the created meron pair directly within a magnetic field, we determine its topological structure unambiguously and explore the topological effect in its creation and annihilation processes. Our work opens a pathway towards developing and controlling topological structures in general magnetic systems without the restriction of perpendicular anisotropy and Dzyaloshinskii-Moriya interaction.

Magnetic coupling of vortices in a two dimensional lattice.

We investigated the magnetization reversal of magnetic vortex structures in a two-dimensional lattice. The structures were formed by permalloy (Py) film deposition onto large arrays of self assembled spherical SiO(2)-particles with a diameter of 330 nm. We present the dependence of the nucleation and annihilation field of the vortex structures as a function of the Py layer thickness(aspect ratio) and temperature. By increasing the Py thickness up to 90 nm or alternatively by lowering the temperature the vortex structure becomes more stable as expected. However, the increase of the Py thickness results in the onset of strong exchange coupling between neighboring Py caps due to the emergence of Py bridges connecting them. In particular, we studied the influence of magnetic coupling locally by in-field scanning magne to-resistive microscopy and full-field magnetic soft x-ray microscopy, revealing a domain-like nucleation process of vortex states, which arises via domain wall propagation due to exchange coupling of the closely packed structures. By analyzing the rotation sense of the reversed areas, large connected domains are present with the same circulation sense. Furthermore, the lateral core displacements when an in-plane field is applied were investigated, revealing spatially enlarged vortex cores and a broader distribution with increasing Py layer thickness. In addition, the presence of some mixed states, vortices and c-states, is indicated for the array with the thickest Py layer.

Dynamic switching of the spin circulation in tapered magnetic nanodisks.

Magnetic vortices are characterized by the sense of in-plane magnetization circulation and by the polarity of the vortex core. With each having two possible states, there are four possible stable magnetization configurations that can be utilized for a multibit memory cell. Dynamic control of vortex core polarity has been demonstrated using both alternating and pulsed magnetic fields and currents. Here, we show controlled dynamic switching of spin circulation in vortices using nanosecond field pulses by imaging the process with full-field soft X-ray transmission microscopy. The dynamic reversal process is controlled by far-from-equilibrium gyrotropic precession of the vortex core, and the reversal is achieved at significantly reduced field amplitudes when compared with static switching. We further show that both the field pulse amplitude and duration required for efficient circulation reversal can be controlled by appropriate selection of the disk geometry.

Scaling behavior of the first arrival time of a random-walking magnetic domain.

We report a universal scaling behavior of the first arrival time of a traveling magnetic domain wall into a finite space-time observation window of a magneto-optical microscope enabling direct visualization of a Barkhausen avalanche in real time. The first arrival time of the traveling magnetic domain wall exhibits a nontrivial fluctuation and its statistical distribution is described by universal power-law scaling with scaling exponents of 1.34+/-0.07 for CoCr and CoCrPt films, despite their quite different domain evolution patterns. Numerical simulation of the first arrival time with an assumption that the magnetic domain wall traveled as a random walker well matches our experimentally observed scaling behavior, providing an experimental support for the random-walking model of traveling magnetic domain walls.

The p53 mutation which abrogates trans-activation while maintaining its growth-suppression activity.

The p53 tumor suppressor protein functions as a transcription factor. It has, however, been previously reported that some p53 mutants are able to suppress cell growth independent of their transcriptional activity [Kaneuchi et al., (1999)]. In order to investigate the correlations between the trans-activation and growth-suppressive functions of p53, we have analyzed five p53 mutants by CAT reporter assay, colony formation assay, and growth-rate analysis. Five p53 mutants [Oh et al., (2000)]--199stop (Gly-->stop), 240ile (Ser-->Ile), 250ala (Pro-->Ala), 285lys (Glu-->Lys), and 291asn (Lys-->Asn)--were cotransfected with a reporter construct containing a p53-responsive element and then tested for their trans-activational activity in p53-null Saos-2 cells. As a result of a change in the protein structure, trans-activational activity was negated in 199stop, 240ile, 285lys, and 291asn, while 250ala retained its activity. Colony formation assay revealed that mutants 240ile and 250ala retained their growth suppression, while 199stop, 285lys, and 291asn did not. To study the features of these proteins, a group of isogenic cell lines that express mutant forms of p53 was generated from HeLa cells, and their growth rate was then examined: one group, containing 199stop, 285lys, and 291asn, showed a rapid growth rate, similar to that of the original HeLa cells; the other group, containing 240ile and 250ala, however, exhibited a slow growth rate. In conclusion, mutant p53 240ile, which completely lost its trans-activational activity, nevertheless continued to exhibit its growth-suppressive activity. Further work is required to understand how 240ile is involved in growth suppression.

Identification of p53 gene mutations in breast cancers and their effects on transcriptional activation function.

Somatic mutations in the p53 tumor suppressor gene are the most common genetic alterations found in human malignancies. In the present study, we studied 36 primary human breast carcinomas, using a polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and sequencing analysis of exons 2 through 9 for the presence of p53 gene mutations. Six of 36 (17%) breast cancers contained mutations within the core domain of the p53 protein responsible for sequence-specific DNA binding (codons 102-292); all 5 missense mutations clustered between codons 240 and 291 (codons 240, 243, 250, 285, and 291), whereas one nonsense mutation occurred at codon 199. By using recombinant PCR in vitro mutagenesis, we introduced point mutations at codons 199 from Gly to stop (gly199stop), 240 from Ser to Ile (ser240Ile), 250 from Pro to Ala (pro250ala), 285 from Glu to Lys (glu285lys), and 291 from Lys to Asn (lys291asn), and all the p53 sequences were subcloned into the CMVneoBam vector under the control of the cytomegalovirus (CMV) promoter. To test whether the mutants p53 were functionally wild-type (wt) or mutant, we transfected them to p53-null Saos-2 cells with a reporter plasmid containing a p53-responsive element, and performed chloramphenicol acetyltransferase (CAT) assay. Transient CAT assay for transcriptional activation revealed that one group, including gly199stop, ser240ile, glu285lys, and lys291asn, abolished the transcriptional activity, whereas the other group, including pro250ala, retained stronger transcriptional transactivation activity than that of wt p53.