The nature of iron-oxygen vacancy defect centers in PbTiO3

The iron(III) center in ferroelectric PbTiO3 together with an oxygen vacancy forms a charged defect associate, oriented along the crystallographic c-axis. Its microscopic structure has been analyzed in detail comparing results from a semi-empirical Newman superposition model analysis based on finestructure data and from calculations using density functional theory. Both methods give evidence for a substitution of Fe3+ for Ti4+ as an acceptor center. The position of the iron ion in the ferroelectric phase is found to be similar to the B-site in the paraelectric phase. Partial charge compensation is locally provided by a directly coordinated oxygen vacancy. Using high-resolution synchrotron powder diffraction, it was verified that lead titanate remains tetragonal down to 12 K, exhibiting a c/a-ratio of 1.0721.Comment: 11 pages, 5 figures, accepted in Phys. Rev.

Clinical and Serologic Manifestations of Autoimmune Disease in MRL-lpr/lpr Mice Lacking Nitric Oxide Synthase Type 2

Nitric oxide (NO) is an important mediator of the inflammatory response. MRL–lpr/lpr mice overexpress inducible nitric oxide synthase (NOS2) and overproduce NO in parallel with the development of an autoimmune syndrome with a variety of inflammatory manifestations. In previous studies, we showed that inhibiting NO production with the nonselective nitric oxide synthase (NOS) inhibitor NG-monomethyl–arginine reduced glomerulonephritis, arthritis, and vasculitis in MRL–lpr/lpr mice. To define further the role of NO and NOS2 in disease in MRL–lpr/lpr mice, mice with targeted disruption of NOS2 were produced by homologous recombination and bred to MRL–lpr/lpr mice to the N4 generation. MRL–lpr/lpr littermates homozygous for disrupted NOS2 (−/−), heterozygous for disrupted NOS2 (+/−), or wildtype (+/+) were derived for this study. Measures of NO production were markedly decreased in the MRL-lpr/lpr (−/−) mice compared with MRL-lpr/lpr (+/+) mice, with intermediate production by the MRL-lpr/lpr (+/−) mice. There was no detectable NOS2 protein by immunoblot analysis of the spleen, liver, kidney, and peritoneal macrophages of the (−/−) animals, whereas that of (+/+) was high and (+/−) intermediate. The (−/−) mice developed glomerular and synovial pathology similar to that of the (+/−) and (+/+) mice. However, (−/−) mice and (+/−) mice had significantly less vasculitis of medium-sized renal vessels than (+/+) mice. IgG rheumatoid factor levels were significantly lower in the (−/−) mice as compared with (+/+) mice, but levels of anti-DNA antibodies were comparable in all groups. Our findings show that NO derived from NOS2 has a variable impact on disease manifestations in MRL-lpr/lpr mice, suggesting heterogeneity in disease mechanisms

Lateral plucking as a mechanism for elongate erosional glacial bedforms : explaining megagrooves in Britain and Canada

Megagrooves are kilometre-scale linear topographic lows carved in bedrock, separated by ridges, typically in areas of largely devoid of till. They have been reported from several areas covered by Pleistocene glaciations, such as Canadian NW Territories, Michigan and NW Scotland. Here we report two previously undocumented megagroove fields from Ungava, Canada, and northern England, and present new analyses of the megagrooves from NW Scotland. This paper seeks to determine the nature of the lithological and structural controls on the occurrence and formation of megagrooves. Analysis of both geomorphological and bedrock properties shows that megagrooves are generally: a) confined to well stratified or layered bedrock, such as (meta)sedimentary rocks with closely spaced joints, and tend not to occur on massive rocks such as gneiss or granite, or thick-bedded sedimentary rocks; b) subparallel to palaeo-ice flow and the strike of the strata; and tend not to occur where palaeo-ice flow is at high angles to the strike of strata; c) produced by significant glacial erosion by sustained unidirectional ice flow. Detailed analysis of megagrooves in NW Scotland shows that neither glacio-fluvial erosion, nor differential abrasion was the dominant mechanism of formation. A mechanism, here termed ‘lateral plucking’, is suggested that involves block plucking on rock steps parallel to ice flow. Removal of joint-bounded blocks from such rock steps involves a component of rotation along a vertical axis. Block removal may be enhanced by a direct component of shear stress onto the vertical stoss sides. The lateral plucking mechanism results in horizontal erosion at right angles to the ice flow, and enhances the groove/ridge topography. Megagrooves are potentially useful as palaeo-ice flow indicators in areas devoid of till, and can thus complement the palaeo-ice stream datasets which are presently largely based on soft-sediment landform studies

Regulation of zinc homeostasis by inducible NO synthase-derived NO: Nuclear metallothionein translocation and intranuclear Zn(2+) release

Zn(2+) is critical for the functional and structural integrity of cells and contributes to a number of important processes including gene expression. It has been shown that NO exogenously applied via NO donors resulting in nitrosative stress leads to cytoplasmic Zn(2+) release from the zinc storing protein metallothionein (MT) and probably other proteins that complex Zn(2+) via cysteine thiols. We show here that, in cytokine-activated murine aortic endothelial cells, NO derived from the inducible NO synthase (iNOS) induces a transient nuclear release of Zn(2+). This nuclear Zn(2+) release depends on the presence of MT as shown by the lack of this effect in activated endothelial cells from MT-deficient mice and temporally correlates with nuclear MT translocation. Data also show that NO is an essential but not sufficient signal for MT-mediated Zn(2+) trafficking from the cytoplasm into the nucleus. In addition, we found that, endogenously via iNOS, synthesized NO increases the constitutive mRNA expression of both MT-1 and MT-2 genes and that nitrosative stress exogenously applied via an NO donor increases constitutive MT mRNA expression via intracellular Zn(2+) release. In conclusion, we here provide evidence for a signaling mechanism based on iNOS-derived NO through the regulation of intracellular Zn(2+) trafficking and homeostasis