10,777 research outputs found

    FMR Study of Co/Ti Bilayer Thin Films

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    . We focused on the interaction between two ferromagnetic cobalt layers through a non-magnetic titanium layer. The magnetic properties of the structure were characterized by ferromagnetic resonance technique (FMR). The data were collected as a function of non-magnetic titanium layer thickness. Co/Ti multilayer (Ti (50 {\AA})/Co(45 {\AA})/Ti(2-40 {\AA})/Co(40 {\AA})/Ti(100 {\AA}))films were grown onto naturally oxidized p-type single crystal Si (100) substrate at UHV condition with magnetron sputtering system at room temperature. The thickness of Ti spacer layer ranges from 2 to 40 {\AA} with 2 {\AA} steps. We did not observe usual optic and acoustic modes; instead we had two broad overlapped peaks for the films ranged from 6 {\AA} to 40 {\AA}. One interesting result was the high anisotropic resonance field values for these films. Exchange coupling between ferromagnetic layers causes shift on resonance field values but these shifts in our samples were much larger than expected. This large anisotropic behavior is not clear at the moment. Our theoretical model was not able to determine a value for the exchange coupling parameter. One reason can be the close thickness values for Co sublayers. The other reason can be the Ti non-magnetic layer. If titanium did not grow layer by layer on cobalt, the cobalt ferromagnetic layers may behave as a single layer. As a result one cannot observe exchange interaction between ferromagnetic layers through non-magnetic spacer.Comment: 6 pages, 5 figure

    Discrete Cutting Force Model for 5-Axis Milling with Arbitrary Engagement and Feed Direction

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    5-axis machining operations bring new challenges for predicting cutting forces. Complex tool workpiece engagements and tool orientations make it difficult to adapt 3-axis process models for 5-axis operations. A new model is developed to predict cutting forces with arbitrary tool/workpiece engagement and tool feed direction. A discretization approach is used, in which the tool is composed of multiple cutting elements. Each element is processed to determine its effect on cutting forces, and global forces are determined by combining the elemental effects. Cutting tests are conducted to verify force predictions, where the tool/workpiece engagement is provided through a geometric software application

    Application-Specific Heterogeneous Network-on-Chip Design

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    Cataloged from PDF version of article.As a result of increasing communication demands, application-specific and scalable Network-on-Chips (NoCs) have emerged to connect processing cores and subsystems in Multiprocessor System-on-Chips. A challenge in application-specific NoC design is to find the right balance among different tradeoffs, such as communication latency, power consumption and chip area. We propose a novel approach that generates latency-aware heterogeneous NoC topology. Experimental results show that our approach improves the total communication latency up to 27% with modest power consumption. © 2013 The Author 2013. Published by Oxford University Press on behalf of The British Computer Society

    Homozygosity at variant MLH1 can lead to secondary mutation in NF1, neurofibromatosis type I and early onset leukemia

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    Cataloged from PDF version of article.Heterozygous germ-line variants of DNA mismatch repair (MMR) genes predispose individuals to hereditary non-polyposis colorectal cancer. Several independent reports have shown that individuals constitutionally homozygous for MMR allelic variants develop early onset hematological malignancies often associated to features of neurofibromatosis type 1 (NF1) syndrome. The genetic mechanism of NF1 associated to MMR gene deficiency is not fully known. We report here that a child with this form of NF1 displays a heterozygous NF1 gene mutation (c.3721C > T), in addition to a homozygous MLH1 gene mutation (c.676C > T) leading to a truncated MLH1 protein (p.R226X). The parents did not display NF1 features nor the NF1 mutation. This new NF1 gene mutation is recurrent and predicts a truncated neurofibromin (p.R1241X) lacking its GTPase activating function, as well as all C-terminally located functional domains. Our findings suggest that NF1 disease observed in individuals homozygous for deleterious MMR variants may be due to a concomitant NF1 gene mutation. The presence of both homozygous MLH1 and heterozygous NF1 mutation in the child studied here also provides a mechanistic explanation for early onset malignancies that are observed in affected individuals. It also provides a model for cooperation between genetic alterations in human carcinogenesis. © 2007 Elsevier B.V. All rights reserved

    Metalorganic chemical vapor deposition growth and thermal stability of the AllNN/GaN high electron mobility transistor structure

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    Cataloged from PDF version of article.The AlxIn1-xN barrier high electron mobility transistor (HEMT) structure has been optimized with varied barrier composition and thickness grown by metalorganic chemical vapor deposition. After optimization, a transistor structure comprising a 7 nm thick nearly lattice-matched Al0.83In0.17 N barrier exhibits a sheet electron density of 2.0 x 10(13) cm(-2) with a high electron mobility of 1540 cm(2) V-1 s(-1). AnAl(0.83)In(0.17)N barrier HEMT device with 1 mu m gate length provides a current density of 1.0 A mm(-1) at V-GS = 0 V and an extrinsic transconductance of 242 mS mm(-1), which are remarkably improved compared to that of a conventional Al0.3Ga0.7N barrier HEMT. To investigate the thermal stability of the HEMT epi-structures, post-growth annealing experiments up to 800 degrees C have been applied to Al0.83In0.17N and Al0.3Ga0.7N barrier heterostructures. As expected, the electrical properties of an Al0.83In0.17N barrier HEMT structure showed less stability than that of an Al0.3Ga0.7N barrier HEMT to the thermal annealing. The structural properties of Al0.83In0.17N/GaN also showed more evidence for decomposition than that of the Al0.3Ga0.7N/GaN structure after 800 degrees C post-annealing

    Reservoir Computing Approach to Robust Computation using Unreliable Nanoscale Networks

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    As we approach the physical limits of CMOS technology, advances in materials science and nanotechnology are making available a variety of unconventional computing substrates that can potentially replace top-down-designed silicon-based computing devices. Inherent stochasticity in the fabrication process and nanometer scale of these substrates inevitably lead to design variations, defects, faults, and noise in the resulting devices. A key challenge is how to harness such devices to perform robust computation. We propose reservoir computing as a solution. In reservoir computing, computation takes place by translating the dynamics of an excited medium, called a reservoir, into a desired output. This approach eliminates the need for external control and redundancy, and the programming is done using a closed-form regression problem on the output, which also allows concurrent programming using a single device. Using a theoretical model, we show that both regular and irregular reservoirs are intrinsically robust to structural noise as they perform computation

    Genome-Wide Transcriptional Reorganization Associated with Senescence-to-Immortality Switch during Human Hepatocellular Carcinogenesis

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    Cataloged from PDF version of article.Senescence is a permanent proliferation arrest in response to cell stress such as DNA damage. It contributes strongly to tissue aging and serves as a major barrier against tumor development. Most tumor cells are believed to bypass the senescence barrier (become "immortal") by inactivating growth control genes such as TP53 and CDKN2A. They also reactivate telomerase reverse transcriptase. Senescence-to-immortality transition is accompanied by major phenotypic and biochemical changes mediated by genome-wide transcriptional modifications. This appears to happen during hepatocellular carcinoma (HCC) development in patients with liver cirrhosis, however, the accompanying transcriptional changes are virtually unknown. We investigated genome-wide transcriptional changes related to the senescence-to-immortality switch during hepatocellular carcinogenesis. Initially, we performed transcriptome analysis of senescent and immortal clones of Huh7 HCC cell line, and identified genes with significant differential expression to establish a senescence-related gene list. Through the analysis of senescence-related gene expression in different liver tissues we showed that cirrhosis and HCC display expression patterns compatible with senescent and immortal phenotypes, respectively; dysplasia being a transitional state. Gene set enrichment analysis revealed that cirrhosis/senescence-associated genes were preferentially expressed in non-tumor tissues, less malignant tumors, and differentiated or senescent cells. In contrast, HCC/immortality genes were up-regulated in tumor tissues, or more malignant tumors and progenitor cells. In HCC tumors and immortal cells genes involved in DNA repair, cell cycle, telomere extension and branched chain amino acid metabolism were up-regulated, whereas genes involved in cell signaling, as well as in drug, lipid, retinoid and glycolytic metabolism were down-regulated. Based on these distinctive gene expression features we developed a 15-gene hepatocellular immortality signature test that discriminated HCC from cirrhosis with high accuracy. Our findings demonstrate that senescence bypass plays a central role in hepatocellular carcinogenesis engendering systematic changes in the transcription of genes regulating DNA repair, proliferation, differentiation and metabolism

    Interface modification of clay and graphene platelets reinforced epoxy nanocomposites: a comparative study

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    The interface between the matrix phase and dispersed phase of a composite plays a critical role in influencing its properties. However, the intricate mecha-nisms of interface are not fully understood, and polymer nanocomposites are no exception. This study compares the fabrication, morphology, and mechanical and thermal properties of epoxy nanocomposites tuned by clay layers (denoted as m-clay) and graphene platelets (denoted as m-GP). It was found that a chemical modification, layer expansion and dispersion of filler within the epoxy matrix resulted in an improved interface between the filler mate-rial and epoxy matrix. This was confirmed by Fourier transform infrared spectroscopy and transmission electron microscope. The enhanced interface led to improved mechanical properties (i.e. stiffness modulus, fracture toughness) and higher glass transition temperatures (Tg) compared with neat epoxy. At 4 wt% m-GP, the critical strain energy release rate G1c of neat epoxy improved by 240 % from 179.1 to 608.6 J/m2 and Tg increased from 93.7 to 106.4 �C. In contrast to m-clay, which at 4 wt%, only improved the G1c by 45 % and Tg by 7.1 %. The higher level of improvement offered by m-GP is attributed to the strong interaction of graphene sheets with epoxy because the covalent bonds between the carbon atoms of graphene sheets are much stronger than silicon-based clay

    Inhibition of Akt signaling in hepatoma cells induces apoptotic cell death independent of Akt activation status

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    Cataloged from PDF version of article.The serine/threonine kinase Akt, a downstream effector of phosphatidylinositol 3-kinase (PI3K), is involved in cell survival and anti-apoptotic signaling. Akt has been shown to be constitutively expressed in a variety of human tumors including hepatocellular carcinoma (HCC). In this report we analyzed the status of Akt pathway in three HCC cell lines, and tested cytotoxic effects of Akt pathway inhibitors LY294002, Wortmannin and Inhibitor VIII. In Mahlavu human hepatoma cells Akt was constitutively activated, as demonstrated by its Ser473 phosphorylation, downstream hyperphosphorylation of BAD on Ser136, and by a specific cell-free kinase assay. In contrast, Huh7 and HepG2 did not show hyperactivation when tested by the same criteria. Akt enzyme hyperactivation in Mahlavu was associated with a loss of PTEN protein expression. Akt signaling was inhibited by the upstream kinase inhibitors, LY294002, Wortmannin, as well as by the specific Akt Inhibitor VIII in all three hepatoma cell lines. Cytotoxicity assays with Akt inhibitors in the same cell lines indicated that they were all sensitive, but with different IC50 values as assayed by RT-CES. We also demonstrated that the cytotoxic effect was through apoptotic cell death. Our findings provide evidence for its constitutive activation in one HCC cell line, and that HCC cell lines, independent of their Akt activation status respond to Akt inhibitors by apoptotic cell death. Thus, Akt inhibition may be considered as an attractive therapeutic intervention in liver cancer. © Springer Science+Business Media, LLC 2010
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