Competition of perpendicular magnetic anisotropy and exchange magnetic anisotropy in a Pt/Co/α-Cr₂O₃(0001) thin film

We investigated perpendicular magnetic anisotropy and exchange magnetic anisotropy in a Pt/Co/α-Cr₂O₃(0001) thin film grown on an α-Al₂O₃(0001) substrate. The film exhibits perpendicular magnetic anisotropy below a Co thickness of 1.2 nm at room temperature. Independent of the magnetic easy direction of the Co layer, the perpendicular exchange bias (PEB) appears in a direction perpendicular to the film below 80 K. The maximum unidirectional magnetic anisotropy energy estimated from the exchange bias field is 0.33 erg/cm², which is higher than the reported PEB strength. The perpendicular exchange bias is accompanied by the in-plane remanent magnetization and an increase in the in-plane coercivity. We speculate that the increases in the in-plane remanent magnetization and the in-plane coercivity are caused by the spin canting of Cr³⁺ in the α-Cr₂O₃(0001) layer.Yu Shiratsuchia, Hayato Noutomi, Hiroto Oikawa, Toshiaki Fujita, and Ryoichi Nakatani, Journal of Applied Physics 109, 07C101 (2011); https://doi.org/10.1063/1.3535555

Instrumental Utilization to Elevate Puncture Result in Percutaneous Renal Biopsy

In performing percutaneous renal biopsy, it seems that the lesser the amount of the intercalative tissue existing in the space between the derm to the kidney, the more improved the results of puncture would be, with minimal complications of puncture. As we believe such ideal operation may be secured by methods based on open needle biopsy, we have carried out renal puncture by employing the technic which constitutes of insertion of ascites trocar needle in the direction and to the depth as determined by renal explorative needle, followed by removal of the inner trocar needle and insertion of a Tru-Cut needle into the outer trocar. As a result, in 49 out of 50 cases renal tissue could be obtained, the mean length of preparations for optical microscopy being 13.8±4.3 mm and the mean number of the glomerulus contained being 25.3±15.8 with a range from 7 at the smallest and 66 at the greatest. The value of the utilization of outer trocar of the ascites trocar needle as a guide needle in renal puncture was discussed in detail

Detection and in situ switching of unreversed interfacial antiferromagnetic spins in a perpendicular-exchange-biased system

By using the perpendicular-exchange-biased Pt/Co/α-Cr₂O₃ system, we provide experimental evidence that the unreversed uncompensated Cr spins exist at the Co/α-Cr₂O₃ interface. The unreversed uncompensated Cr spin manifests itself in both the vertical shift of an element-specific magnetization curve and the relative peak intensity of soft-x-ray magnetic circular dichroism spectrum. We also demonstrate an in situ switching of the interfacial Cr spins and correspondingly a reversal of the exchange bias without interfacial atomic diffusion. Such switching shows the direct relationship between the interfacial antiferromagnetic spins and origin of the exchange bias. The demonstrated switching of exchange bias would likely offer a new design of advanced spintronics devices, using the perpendicular-exchange-biased system, with low power consumption and ultrafast operation.Y.Shiratsuchi, H.Noutomi, H.Oikawa, et al. Detection and in situ switching of unreversed interfacial antiferromagnetic spins in a perpendicular-exchange-biased system. Physical Review Letters 109, 077202 (2012); https://doi.org/10.1103/PhysRevLett.109.077202

The clonal relationships between pre-cancer and cancer revealed by ultra-deep sequencing

The study of the relationships between pre-cancer and cancer and identification of early driver mutations is becoming increasingly important as the value of molecular markers of early disease and personalised drug targets is recognized, especially now the extent of clonal heterogeneity in fully invasive disease is being realized. It has been assumed that pre-cancerous lesions exhibit a fairly passive progression to invasive disease; the degree to which they, too, are heterogeneous is unknown. We performed ultra-deep sequencing of thousands of selected mutations, together with copy number analysis, from multiple, matched pre-invasive lesions, primary tumours and metastases from five patients with oral cancer, some with multiple primary tumours presenting either synchronously or metachronously, totalling 75 samples. This allowed the clonal relationships between the samples to be observed for each patient. We expose for the first time the unexpected variety and complexity of the relationships between this group of oral dysplasias and their associated carcinomas and, ultimately, the diversity of processes by which tumours are initiated, spread and metastasize. Instead of a series of genomic precursors of their adjacent invasive disease, we have shown dysplasia to be a distinct dynamic entity, refuting the belief that pre-cancer and invasive tumours with a close spatial relationship always have linearly related genomes. We show that oral pre-cancer exhibits considerable subclonal heterogeneity in its own right, that mutational changes in pre-cancer do not predict the onset of invasion, and that the genomic pathway to invasion is neither unified nor predictable. Sequence data from this study have been deposited in the European Nucleotide Archive, Accession No. PRJEB6588

Breast cancer cell lines carry cell line-specific genomic alterations that are distinct from aberrations in breast cancer tissues: Comparison of the CGH profiles between cancer cell lines and primary cancer tissues

<p>Abstract</p> <p>Background</p> <p>Cell lines are commonly used in various kinds of biomedical research in the world. However, it remains uncertain whether genomic alterations existing in primary tumor tissues are represented in cell lines and whether cell lines carry cell line-specific genomic alterations. This study was performed to answer these questions.</p> <p>Methods</p> <p>Array-based comparative genomic hybridization (CGH) was employed with 4030 bacterial artificial chromosomes (BACs) that cover the genome at 1.0 megabase resolution to analyze DNA copy number aberrations (DCNAs) in 35 primary breast tumors and 24 breast cancer cell lines. DCNAs were compared between these two groups. A tissue microdissection technique was applied to primary tumor tissues to reduce the contamination of samples by normal tissue components.</p> <p>Results</p> <p>The average number of BAC clones with DCNAs was 1832 (45.3% of spotted clones) and 971 (24.9%) for cell lines and primary tumor tissues, respectively. Gains of 1q and 8q and losses of 8p, 11q, 16q and 17p were detected in >50% of primary cancer tissues. These aberrations were also frequently detected in cell lines. In addition to these alterations, the cell lines showed recurrent genomic alterations including gains of 5p14-15, 20q11 and 20q13 and losses of 4p13-p16, 18q12, 18q21, Xq21.1 and Xq26-q28 that were barely detected in tumor tissue specimens. These are considered to be cell line-specific DCNAs. The frequency of the HER2 amplification was high in both cell lines and tumor tissues, but it was statistically different between cell lines and primary tumors (P = 0.012); 41.3 ± 29.9% for the cell lines and 15.9 ± 18.6% for the tissue specimens.</p> <p>Conclusions</p> <p>Established cell lines carry cell lines-specific DCNAs together with recurrent aberrations detected in primary tumor tissues. It must therefore be emphasized that cell lines do not always represent the genotypes of parental tumor tissues.</p

TAK1 Is Required for Survival of Mouse Fibroblasts Treated with TRAIL, and Does So by NF-κB Dependent Induction of cFLIPL

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as a “death ligand”—a member of the TNF superfamily that binds to receptors bearing death domains. As well as causing apoptosis of certain types of tumor cells, TRAIL can activate both NF-κB and JNK signalling pathways. To determine the role of TGF-β-Activated Kinase-1 (TAK1) in TRAIL signalling, we analyzed the effects of adding TRAIL to mouse embryonic fibroblasts (MEFs) derived from TAK1 conditional knockout mice. TAK1−/− MEFs were significantly more sensitive to killing by TRAIL than wild-type MEFs, and failed to activate NF-κB or JNK. Overexpression of IKK2-EE, a constitutive activator of NF-κB, protected TAK1−/− MEFs against TRAIL killing, suggesting that TAK1 activation of NF-κB is critical for the viability of cells treated with TRAIL. Consistent with this model, TRAIL failed to induce the survival genes cIAP2 and cFlipL in the absence of TAK1, whereas activation of NF-κB by IKK2-EE restored the levels of both proteins. Moreover, ectopic expression of cFlipL, but not cIAP2, in TAK1−/− MEFs strongly inhibited TRAIL-induced cell death. These results indicate that cells that survive TRAIL treatment may do so by activation of a TAK1–NF-κB pathway that drives expression of cFlipL, and suggest that TAK1 may be a good target for overcoming TRAIL resistance