Stripe Domain-Structures in a Thin Ferromagnetic Film

Journals published by the American Physical Society can be found at http://journals.aps.org/We present a theory of the stripe domain structure in a thin ferromagnetic film with single-ion easy-axis magnetic anisotropy and long-range dipole interactions, for a wide range of temperatures and applied magnetic field. The domains exist at temperatures below the reorientational phase transition from out-of-plane to in-plane magnetization. The system of stripes can be described as a liquid crystal with a preferred domain-wall orientation. The positional order is destroyed by both thermodynamical meandering of domain walls and by the proliferation of dislocations. Spatial anisotropy generated by the fourth-order exchange energy stabilizes the stripe domain structure and pins its orientation. For any temperature below the reorientational phase transition there exists a critical perpendicular-to-plane magnetic field, which separates multidomain and monodomain states of the film. The theory explains recent experimental observations

High Mutability of the Tumor Suppressor Genes RASSF1 and RBSP3 (CTDSPL) in Cancer

BACKGROUND:Many different genetic alterations are observed in cancer cells. Individual cancer genes display point mutations such as base changes, insertions and deletions that initiate and promote cancer growth and spread. Somatic hypermutation is a powerful mechanism for generation of different mutations. It was shown previously that somatic hypermutability of proto-oncogenes can induce development of lymphomas. METHODOLOGY/PRINCIPAL FINDINGS:We found an exceptionally high incidence of single-base mutations in the tumor suppressor genes RASSF1 and RBSP3 (CTDSPL) both located in 3p21.3 regions, LUCA and AP20 respectively. These regions contain clusters of tumor suppressor genes involved in multiple cancer types such as lung, kidney, breast, cervical, head and neck, nasopharyngeal, prostate and other carcinomas. Altogether in 144 sequenced RASSF1A clones (exons 1-2), 129 mutations were detected (mutation frequency, MF = 0.23 per 100 bp) and in 98 clones of exons 3-5 we found 146 mutations (MF = 0.29). In 85 sequenced RBSP3 clones, 89 mutations were found (MF = 0.10). The mutations were not cytidine-specific, as would be expected from alterations generated by AID/APOBEC family enzymes, and appeared de novo during cell proliferation. They diminished the ability of corresponding transgenes to suppress cell and tumor growth implying a loss of function. These high levels of somatic mutations were found both in cancer biopsies and cancer cell lines. CONCLUSIONS/SIGNIFICANCE:This is the first report of high frequencies of somatic mutations in RASSF1 and RBSP3 in different cancers suggesting it may underlay the mutator phenotype of cancer. Somatic hypermutations in tumor suppressor genes involved in major human malignancies offer a novel insight in cancer development, progression and spread

The effects of mutant Ras proteins on the cell signalome

The genetic alterations in cancer cells are tightly linked to signaling pathway dysregulation. Ras is a key molecule that controls several tumorigenesis-related processes, and mutations in RAS genes often lead to unbiased intensification of signaling networks that fuel cancer progression. In this article, we review recent studies that describe mutant Ras-regulated signaling routes and their cross-talk. In addition to the two main Ras-driven signaling pathways, i.e., the RAF/MEK/ERK and PI3K/AKT/mTOR pathways, we have also collected emerging data showing the importance of Ras in other signaling pathways, including the RAC/PAK, RalGDS/Ral, and PKC/PLC signaling pathways. Moreover, microRNA-regulated Ras-associated signaling pathways are also discussed to highlight the importance of Ras regulation in cancer. Finally, emerging data show that the signal alterations in specific cell types, such as cancer stem cells, could promote cancer development. Therefore, we also cover the up-to-date findings related to Ras-regulated signal transduction in cancer stem cells. © 2020, The Author(s)

Excess resistivity in graphene superlattices caused by umklapp electron–electron scattering

In electronic transport, umklapp processes play a fundamental role as the only intrinsic mechanism that allows electrons to transfer momentum to the crystal lattice and, therefore, provide a finite electrical resistance in pure metals1,2. However, umklapp scattering is difficult to demonstrate in experiment, as it is easily obscured by other dissipation mechanisms1–6. Here we show that electron–electron umklapp scattering dominates the transport properties of graphene-on-boron-nitride superlattices over a wide range of temperature and carrier density. The umklapp processes cause giant excess resistivity that rapidly increases with increasing superlattice period and are responsible for deterioration of the room-temperature mobility by more than an order of magnitude as compared to standard, non-superlattice graphene devices. The umklapp scattering exhibits a quadratic temperature dependence accompanied by a pronounced electron–hole asymmetry with the effect being much stronger for holes than electrons. In addition to being of fundamental interest, our results have direct implications for design of possible electronic devices based on heterostructures featuring superlattices. © 2018, The Author(s), under exclusive licence to Springer Nature Limited

Cosmid contig and cDNA map of the human chromosome 13q14 region frequently lost in B-cell chronic lymphocytic leukemia

We constructed a fine physical map of human chromosome 13q14 region between D13S1168 and D13S25 loci consisting of cosmid and cDNA clones. This interval had been shown to be in the center of the genome region frequently lost in a human blood malignancy known as B-cell chronic lymphocytic leukemia (BCLL), Mapping of the genome region is a step in searching for a putative tumor suppressor gene for BCLL. A chr13-specific cosmid library (LA13NC01) was screened with four YAC and seven WI-STS markers belonging to the above 13q14 interval, yielding a cosmid subset of more than 400 clones representing the region. Cosmids between D13S1168 and D13S25 loci were arranged in contigs. Seven different clones were found in cDNA libraries by hybridization screening with YAC ICRF66c1 and two cosmids covering the D13S319 locus, which is the central point for BCLL-associated deletions, The cDNA clones were mapped against the contigous cosmids