Guided Vortex Motion Control in Superconducting Thin Films by Sawtooth Ion Surface Modification.

Design of flux profile and guided motion of magnetic flux quanta (also known as vortices) are central issues for functionality of superconducting devices. Anchoring vortex movement by trapping flux lines through the use of defects and preventing vortex entry by shielding magnetic field have been broadly explored, which can also enable reduction of noise for optimal device operation. Removing vortices entirely via the so-called ratchet effect (employing an asymmetric energy potential) is another alternative. This ratcheting potential is also used in DNA splitting, particle separation, surface atom electromigration, and electrophoresis. Utilizing a superconductor with the ratchet vortex pinning potential induces a dominant motion direction, which can be used to pump flux out from device functional zones. In this work, a varying thickness superconductor with its tailored intrinsic pinning mechanism has been simulated and proven to provide this preferential vortex motion. We demonstrate both theoretically and experimentally that a varying thickness superconducting ratchet is indeed possible. Furthermore, the sawtooth shape of the bridge provides a tunability to the preferred vortex motion direction, dependent on the ramp gradient and intrinsic pinning strength.

Field dependence of the ferromagnetic/superconducting proximity effect in a YBCO/STO/LCMO multilayer.

The interaction between superconductivity and magnetism in spatially confined heterostructures of thin film multilayers is investigated in the ferromagnetic manganite La2/3Ca1/3MnO3 (LCMO) and the high-temperature superconductor YBa2Cu3O7-δ (YBCO) mediated by an intermediate insulating SrTiO3 (STO) layer. The STO layer is used to mediate and tune the range of interactions between the ferromagnet and superconductor. A magnetically depleted layer with zero-magnetisation within the LCMO layer is shown by polarised neutron reflectometry measurements. This zero-magnetisation layer is caused by the onset of superconductivity in YBCO despite being separated by an insulating layer with a thickness much larger than the superconducting coherence length. The magnetic field dependence of this interaction is also explored. We show that the magnetism of the depleted layer can be restored by applying a magnetic field that partially destroys the superconductivity in YBCO, restricting the electronic interaction between the materials.

The influence of in situ chemical oxidation on microbial community composition in groundwater contaminated with chlorinated solvents.

In situ chemical oxidation with permanganate has become an accepted remedial treatment for groundwater contaminated with chlorinated solvents. This study focuses on the immediate and short-term effects of sodium permanganate (NaMnO(4)) on the indigenous subsurface microbial community composition in groundwater impacted by trichloroethylene (TCE). Planktonic and biofilm microbial communities were studied using groundwater grab samples and reticulated vitreous carbon passive samplers, respectively. Microbial community composition was analyzed by terminal restriction fragment length polymorphism and a high-density phylogenetic microarray (PhyloChip). Significant reductions in microbial diversity and biomass were shown during NaMnO(4) exposure, followed by recovery within several weeks after the oxidant concentrations decreased to <1 mg/L. Bray-Curtis similarities and nonmetric multidimensional scaling showed that microbial community composition before and after NaMnO(4) was similar, when taking into account the natural variation of the microbial communities. Also, 16S rRNA genes of two reductive dechlorinators (Desulfuromonas spp. and Sulfurospirillum spp.) and diverse taxa capable of cometabolic TCE oxidation were detected in similar quantities by PhyloChip across all monitoring wells, irrespective of NaMnO(4) exposure and TCE concentrations. However, minimal biodegradation of TCE was observed in this study, based on oxidized conditions, concentration patterns of chlorinated and nonchlorinated hydrocarbons, geochemistry, and spatiotemporal distribution of TCE-degrading bacteria.

Regulators encoded in the Escherichia coli type III secretion system 2 gene cluster influence expression of genes within the locus for enterocyte effacement in enterohemorrhagic E. coli O157:H7.

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 subverts host cells through a type III secretion system encoded by the locus for enterocyte effacement (LEE). Genome sequencing of this pathotype revealed the existence of a gene cluster encoding components of a second cryptic type III secretion system, E. coli type III secretion system 2 (ETT2). Recently, we showed that the ETT2 gene cluster is present in whole or in part in the majority of E. coli strains but is unable to encode a functional secretion system in most strains, including EHEC O157:H7. However, here we show that mutational inhibition of two regulatory genes (ECs3720 or etrA and ECs3734 or eivF) from the ETT2 cluster in EHEC O157:H7 leads to greatly increased secretion of proteins encoded by the LEE and to increased adhesion to human intestinal cells. Studies in which transcriptional fusions and microarrays were used indicated that EtrA and EivF exert profound negative effects on gene transcription within the LEE. Consistent with these observations, expression of these regulators in an EHEC O26:H- strain led to suppression of protein secretion under LEE-inducing conditions. These findings provide fresh examples of the influence of mobile genetic elements on regulation of the LEE and of cross talk between type III secretion system gene clusters. In addition, they provide a cautionary tale because they show that the effects of regulatory genes can outlive widespread decay of other genes in a functionally coherent gene cluster, a phenomenon that we have named the "Cheshire cat effect." It also seems likely that variations in the ETT2 regulator repertoire might account for strain-to-strain variation in secretion of LEE-encoded proteins.