High speed electric motors based on high performance novel soft magnets

Novel Co-based soft magnetic materials are presented as a potential substitute for electrical steels in high speed motors for current industry applications. The low losses, high permeabilities, and good mechanical strength of these materials enable application in high rotational speed induction machines. Here, we present a finite element analysis of Parallel Path Magnetic Technology rotating motors constructed with both silicon steel and Co-based nanocomposite. The later achieved a 70% size reduction and an 83% reduction on NdFeB magnet volume with respect to a similar Si-steel design.Fil: Silveyra, Josefina María. Universidad de Buenos Aires. Facultad de Ingenieria. Departamento de Fisica. Laboratorio de Sólidos Amorfos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Tecnologías y Ciencias de la Ingeniería; Argentina; ArgentinaFil: Leary, A. M.. University Of Carnegie Mellon; Estados UnidosFil: DeGeorge, V.. University Of Carnegie Mellon; Estados UnidosFil: Simizu, S.. Advanced Materials Corporation; Estados UnidosFil: McHenry, M. E.. University Of Carnegie Mellon; Estados Unido

Phonon anomalies due to strong electronic correlations in layered organic metals

We show how the coupling between the phonons and electrons in a strongly correlated metal can result in phonon frequencies which have a non-monotonic temperature dependence. Dynamical mean-field theory is used to study the Hubbard-Holstein model that describes the \kappa-(BEDT-TTF)_2 X family of superconducting molecular crystals. The crossover with increasing temperature from a Fermi liquid to a bad metal produces phonon anomalies that are consistent with recent Raman scattering and acoustic experiments.Comment: 6 pages, 3 eps figure

Phenomenological model for the remanent magnetization of dilute quasi-one-dimensional antiferromagnets

We present a phenomenological model for the remanent magnetization at low temperatures in the quasi-one-dimensional dilute antiferromagnets CH_{3}NH_{3}Mn_{1-x}Cd_{x} Cl_{3}\cdot 2H_{2}O and (CH_{3})_{2}NH_{2}Mn_{1-x}Cd_{x}Cl_{3}\cdot 2H_{2}O. The model assumes the existence of uncompensated magnetic moments induced in the odd-sized segments generated along the Mn(^{2+}) chains upon dilution. These moments are further assumed to correlate ferromagnetically after removal of a cooling field. Using a (mean-field) linear-chain approximation and reasonable set of model parameters, we are able to reproduce the approximate linear temperature dependence observed for the remanent magnetization in the real compounds.Comment: 5 pages, 2 figures; final version to appear in Physical Review

Induction of Cytotoxic Oxidative Stress by d-Alanine in Brain Tumor Cells Expressing Rhodotorula gracilis d-Amino Acid Oxidase: A Cancer Gene Therapy Strategy

Overview summary Gene-directed enzyme prodrug therapy (GDEPT) is an antineoplastic treatment strategy designed to overcome the systemic toxicity of chemotherapy by specifically expressing a foreign enzyme in malignant cells that converts a nontoxic prodrug into a cytotoxic metabolite. The relative inefficiency of current in situ gene transfer methodology suggests that enzyme/prodrug combinations that produce membrane permeable metabolites will elicit a more favorable therapeutic response. Ideally, the agent produced by the transduced cell “factories” would be cytotoxic toward both proliferating and quiescent cells. We describe a novel GDEPT approach using d-amino acid oxidase from the red yeast Rhodotorula gracilis and d-alanine as a substrate that generates hydrogen peroxide, a reactive metabolite of oxygen that has both these characteristics. We also demonstrate the ability to sensitize tumor cells to this GDEPT protocol by manipulating cellular antioxidant pathways.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63220/1/hum.1998.9.2-185.pd

Evidence for structural and electronic instabilities at intermediate temperatures in κ\kappa-(BEDT-TTF)2_{2}X for X=Cu[N(CN)2_{2}]Cl, Cu[N(CN)2_{2}]Br and Cu(NCS)2_{2}: Implications for the phase diagram of these quasi-2D organic superconductors

We present high-resolution measurements of the coefficient of thermal expansion $\alpha (T)=\partial \ln l(T)/\partial T$ of the quasi-twodimensional (quasi-2D) salts $\kappa$-(BEDT-TTF)$_2$X with X = Cu(NCS)$_2$, Cu[N(CN)$_2$]Br and Cu[N(CN)$_2$]Cl. At intermediate temperatures (B), distinct anomalies reminiscent of second-order phase transitions have been found at $T^\ast = 38$ K and 45 K for the superconducting X = Cu(NCS)$_2$ and Cu[N(CN)$_2$]Br salts, respectively. Most interestingly, we find that the signs of the uniaxial pressure coefficients of $T^\ast$ are strictly anticorrelated with those of $T_c$. We propose that $T^\ast$ marks the transition to a spin-density-wave (SDW) state forming on minor, quasi-1D parts of the Fermi surface. Our results are compatible with two competing order parameters that form on disjunct portions of the Fermi surface. At elevated temperatures (C), all compounds show $\alpha (T)$ anomalies that can be identified with a kinetic, glass-like transition where, below a characteristic temperature $T_g$, disorder in the orientational degrees of freedom of the terminal ethylene groups becomes frozen in. We argue that the degree of disorder increases on going from the X = Cu(NCS)$_2$ to Cu[N(CN)$_2$]Br and the Cu[N(CN)$_2$]Cl salt. Our results provide a natural explanation for the unusual time- and cooling-rate dependencies of the ground-state properties in the hydrogenated and deuterated Cu[N(CN)$_2$]Br salts reported in the literature.Comment: 22 pages, 7 figure

Environmental radiation at Izu-Oshima after the Fukushima Daiichi nuclear power plant accident

Environmental radiation at Izu-Oshima Island was observed six months after the accident at the Fukushima Daiichi Nuclear Power Plant (F1-NPP). A car-borne survey of the dose rate in air was conducted over the entire island and the results were compared with measurements performed in 2005 (i.e., before the accident). The activity concentrations of cesium-134 and cesium-137 were also measured using a germanium detector. The dose rate in air was found to be 2.9 ± 1.2 times higher than that in 2005 and cesium-134 was detected on Izu-Oshima Island. These results are attributed to the accident at the F1-NPP

Heparan sulphate synthetic and editing enzymes in ovarian cancer

Several angiogenic growth factors including fibroblast growth factors 1 and 2 (FGF1 and FGF2) depend on heparan sulphate (HS) for biological activity. We previously showed that all cellular elements in ovarian tumour tissue synthesised HS but biologically active HS (i.e. HS capable of binding FGF2 and its receptor) was confined to ovarian tumour endothelium. In this study, we have sought to explain this observation. Heparan sulphate sulphotransferases 1 and 2 (HS6ST1 and HS6ST2) attach sulphate groups to C-6 of glucosamine residues in HS that are critical for FGF2 activation. These enzymes were strongly expressed by tumour cells, but only HS6ST1 was found in endothelial cells. Immunostaining with the 3G10 antibody of tissue sections pretreated with heparinases indicated that HS proteoglycans were produced by tumour and endothelial cells. These results indicated that, in contrast to the endothelium, HS produced by tumour cells may be modified by cell-surface heparanase (HPA1) or endosulphatase (SULF). Protein and RNA analysis revealed that HPA1 was strongly expressed by ovarian tumour cells in eight of ten specimens examined. HSULF-1, which removes specific 6-O-sulphate groups from HS, was abundant in tumour cells but weakly expressed in the endothelium. If this enzyme was responsible for the lack of biologically active HS on the tumour cell surface, we would expect exogenous FGF2 binding to be preserved; we showed previously that this was indeed the case although FGF2 binding was reduced compared to the endothelium and stroma. Thus, the combined effects of heparanase and HSULF could account for the lack of biologically active HS in tumour cells rather than deficiencies in the biosynthetic enzymes

Hsp90 inhibition differentially destabilises MAP kinase and TGF-beta signalling components in cancer cells revealed by kinase-targeted chemoproteomics

<p>Abstract</p> <p>Background</p> <p>The heat shock protein 90 (Hsp90) is required for the stability of many signalling kinases. As a target for cancer therapy it allows the simultaneous inhibition of several signalling pathways. However, its inhibition in healthy cells could also lead to severe side effects. This is the first comprehensive analysis of the response to Hsp90 inhibition at the kinome level.</p> <p>Methods</p> <p>We quantitatively profiled the effects of Hsp90 inhibition by geldanamycin on the kinome of one primary (Hs68) and three tumour cell lines (SW480, U2OS, A549) by affinity proteomics based on immobilized broad spectrum kinase inhibitors ("kinobeads"). To identify affected pathways we used the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway classification. We combined Hsp90 and proteasome inhibition to identify Hsp90 substrates in Hs68 and SW480 cells. The mutational status of kinases from the used cell lines was determined using next-generation sequencing. A mutation of Hsp90 candidate client RIPK2 was mapped onto its structure.</p> <p>Results</p> <p>We measured relative abundances of > 140 protein kinases from the four cell lines in response to geldanamycin treatment and identified many new potential Hsp90 substrates. These kinases represent diverse families and cellular functions, with a strong representation of pathways involved in tumour progression like the BMP, MAPK and TGF-beta signalling cascades. Co-treatment with the proteasome inhibitor MG132 enabled us to classify 64 kinases as true Hsp90 clients. Finally, mutations in 7 kinases correlate with an altered response to Hsp90 inhibition. Structural modelling of the candidate client RIPK2 suggests an impact of the mutation on a proposed Hsp90 binding domain.</p> <p>Conclusions</p> <p>We propose a high confidence list of Hsp90 kinase clients, which provides new opportunities for targeted and combinatorial cancer treatment and diagnostic applications.</p

Cell Survival from Chemotherapy Depends on NF-κB Transcriptional Up-Regulation of Coenzyme Q Biosynthesis

9 pages and 6 figures.[Background] Coenzyme Q (CoQ) is a lipophilic antioxidant that is synthesized by a mitochondrial complex integrated by at least ten nuclear encoded COQ gene products. CoQ increases cell survival under different stress conditions, including mitochondrial DNA (mtDNA) depletion and treatment with cancer drugs such as camptothecin (CPT). We have previously demonstrated that CPT induces CoQ biosynthesis in mammal cells.[Methodology/Principal Findings] CPT activates NF-κB that binds specifically to two κB binding sites present in the 5′-flanking region of the COQ7 gene. This binding is functional and induces both the COQ7 expression and CoQ biosynthesis. The inhibition of NF-κB activation increases cell death and decreases both, CoQ levels and COQ7 expression induced by CPT. In addition, using a cell line expressing very low of NF-κB, we demonstrate that CPT was incapable of enhancing enhance both CoQ biosynthesis and COQ7 expression in these cells.[Conclusions/Significance] We demonstrate here, for the first time, that a transcriptional mechanism mediated by NF-κB regulates CoQ biosynthesis. This finding contributes new data for the understanding of the regulation of the CoQ biosynthesis pathway.This work was supported by spanish Ministerio de Educacion y Ciencia Grant BFU2005-03017.Peer reviewe