Coexistance of giant tunneling electroresistance and magnetoresistance in an all-oxide magnetic tunnel junction

We demonstrate with first-principles electron transport calculations that large tunneling magnetoresistance (TMR) and tunneling electroresistance (TER) effects can coexist in an all-oxide device. The TMR originates from the symmetry-driven spin filtering provided by the insulating BaTiO3 barrier to the electrons injected from SrRuO3. In contrast the TER is possible only when a thin SrTiO3 layer is intercalated at one of the SrRuO3/BaTiO3 interfaces. As the complex band-structure of SrTiO3 has the same symmetry than that of BaTiO3, the inclusion of such an intercalated layer does not negatively alter the TMR and in fact increases it. Crucially, the magnitude of the TER also scales with the thickness of the SrTiO3 layer. The SrTiO3 thickness becomes then a single control parameter for both the TMR and the TER effect. This protocol offers a practical way to the fabrication of four-state memory cells

Large bias-dependent magnetoresistance in all-oxide magnetic tunnel junctions with a ferroelectric barrier

All-oxide magnetic tunnel junctions (MTJs) incorporating functional materials as insulating barriers have the potential of becoming the founding technology for novel multi-functional devices. We investigate, by first-principles density functional theory, the bias-dependent transport properties of an all-oxide SrRuO3/BaTiO3/SrRuO3 MTJ. This incorporates a BaTiO3 barrier which can be found either in a non-ferroic or in a ferroelectric state. In such an MTJ not only can the tunneling magnetoresistance reach enormous values, but also, for certain voltages, its sign can be changed by altering the barrier electric state. These findings pave the way for a new generation of electrically-controlled magnetic sensors.Comment: 4 pages, 5 figure

Materials Degradation in the Jovian Radiation Environment

The radiation environment of Jupiter represents a significant hazard for Europa Lander deorbit stage components, and presents a significant potential mission risk. The radiolytic degradation of ammonium perchlorate (AP) oxidizer in solid propellants may affect its properties and performance. The Monte Carlo code MONSOL was used for modeling of laboratory experiments on the electron irradiation of propellant samples. An approach for flattening dose profiles along the depth of irradiated samples is proposed. Depth-dose distributions produced by Jovian electrons in multi-layer slabs of materials are calculated. It is found that the absorbed dose in a particular slab is significantly affected by backscattered electrons and photons from neighboring slabs. The dose and radiolytic decomposition of AP crystals are investigated and radiation-induced chemical yields and weight percent of radical products are reported

Vancomycin plus piperacillin/tazobactam and acute kidney injury in adults: a systematic review and meta-analysis

Objectives: The objective of this systematic review and meta-analysis was to assess acute kidney injury with combination therapy of vancomycin plus piperacillin-tazobactam, in general, adult patients and in critically ill adults. Rates of acute kidney injury, time to acute kidney injury, and odds of acute kidney injury were compared with vancomycin monotherapy, vancomycin plus cefepime or carbapenem, or piperacillin-tazobactam monotherapy. Data Sources: Studies were identified by searching Pubmed, Embase, Web of Science, and Cochrane from inception to April 2017. Abstracts from selected conference proceedings were manually searched. Study Selection: Articles not in English, pediatric studies, and case reports were excluded. Data Extraction: Two authors independently extracted data on study methods, rates of acute kidney injury, and time to acute kidney injury. Effect estimates and 95% CIs were calculated using the random effects model in RevMan 5.3. Data Synthesis: Literature search identified 15 published studies and 17 conference abstracts with at least 24,799 patients. The overall occurrence rate of acute kidney injury was 16.7%, with 22.2% for vancomycin plus piperacillin-tazobactam and 12.9% for comparators. This yielded an overall number needed to harm of 11. Time to acute kidney injury was faster for vancomycin plus piperacillin-tazobactam than vancomycin plus cefepime or carbapenem, but not significantly (mean difference, –1.30; 95% CI, –3.00 to 0.41 d). The odds of acute kidney injury with vancomycin plus piperacillin-tazobactam were increased versus vancomycin monotherapy (odds ratio, 3.40; 95% CI, 2.57–4.50), versus vancomycin plus cefepime or carbapenem (odds ratio, 2.68; 95% CI, 1.83–3.91), and versus piperacillin-tazobactam monotherapy (odds ratio, 2.70; 95% CI, 1.97–3.69). In a small subanalysis of 968 critically ill patients, the odds of acute kidney injury were increased versus vancomycin monotherapy (odds ratio, 9.62; 95% CI, 4.48–20.68), but not significantly different for vancomycin plus cefepime or carbapenem (odds ratio, 1.43; 95% CI, 0.83–2.47) or piperacillin-tazobactam monotherapy (odds ratio, 1.35; 95% CI, 0.86–2.11). Conclusions: The combination of vancomycin plus piperacillin-tazobactam increased the odds of acute kidney injury over vancomycin monotherapy, vancomycin plus cefepime or carbapenem, and piperacillin-tazobactam monotherapy. Limited data in critically ill patients suggest the odds of acute kidney injury are increased versus vancomycin monotherapy, and mitigated versus the other comparators. Further research in the critically ill population is needed

MUC1 Regulates Cyclin D1 Gene Expression Through p120 Catenin and β-catenin

MUC1 interacts with β-catenin and p120 catenin to modulate WNT signaling. We investigated the effect of overexpressing MUC1 on the regulation of cyclin D1, a downstream target for the WNT/β-catenin signaling pathway, in two human pancreatic cancer cell lines, Panc-1 and S2-013. We observed a significant enhancement in the activation of cyclin D1 promoter-reporter activity in poorly differentiated Panc1.MUC1F cells that overexpress recombinant MUC1 relative to Panc-1.NEO cells, which express very low levels of endogenous MUC1. In stark contrast, cyclin D1 promoter activity was not affected in moderately differentiated S2-013.MUC1F cells that overexpressed recombinant MUC1 relative to S2-013.NEO cells that expressed low levels of endogenous MUC1. The S2-013 cell line was recently shown to be deficient in p120 catenin. MUC1 is known to interact with P120 catenin. We show here that re-expression of different isoforms of p120 catenin restored cyclin D1 promoter activity. Further, MUC1 affected subcellular localization of p120 catenin in association with one of the main effectors of P120 catenin, the transcriptional repressor Kaiso, supporting the hypothesis that p120 catenin relieved transcriptional repression by Kaiso. Thus, full activation of cyclin D1 promoter activity requires β-catenin activation of TCF-lef and stabilization of specific p120 catenin isoforms to relieve the repression of KAISO. Our data show MUC1 enhances the activities of both β-catenin and p120 catenin