MEASURING SULFIDE ACCUMULATION IN DIFFUSIVE GRADIENTS IN THIN FILMS BY MEANS OF PURGE AND TRAP FOLLOWED BY ION-SELECTIVE ELECTRODE

Abstract—A procedure for measuring in situ sulfide concentrations by coupling diffusive gradients in thin films (DGT) to solid-state ion-selective electrodes (ISE) is described and evaluated. Laboratory tests were performed to evaluate the coupling of these techniques, and these results were compared to the previously used methods of computer imaging densitometry (CID) and methylene blue. An average elution efficiency of 89%, as detected by ISE, was determined for a series of solutions containing amounts of sulfide ranging from 0.009 to 2.50 mmol. The validity of the standard mass-transfer equation for sulfide accumulation by DGT probes and subsequent detection by ISE was tested by measuring the mass of sulfide collected over time and with respect to varying diffusive gel thicknesses. Regressions of the sulfide mass accumulation versus the independent variables of time and inverse diffusive thickness proved to be linear. The use of DGT coupled to ISE provides a preconcentration method for sulfide that improves the detection limit (DL) over other techniques. This alternative method provides quantitative measurements of DGT-captured sulfide from solutions with a detection limit of at least 0.1 mmol/L for a 24-h deployment. The DGT technique also provides potential advantages in understanding sulfide speciation over existing methods. Keywords—Sulfide In situ Diffusive gradients Thin films Ion-selective electrod

Phase diagram and influence of defects in the double perovskites

The phase diagram of the double perovskites of the type Sr_{2-x} La_x Fe Mo O_6 is analyzed, with and without disorder due to antisites. In addition to an homogeneous half metallic ferrimagnetic phase in the absence of doping and disorder, we find antiferromagnetic phases at large dopings, and other ferrimagnetic phases with lower saturation magnetization, in the presence of disorder.Comment: 4 pages, 3 postscript figures, some errata correcte

HER4 D-Box Sequences Regulate Mitotic Progression and Degradation of the Nuclear HER4 Cleavage Product s80HER4

Heregulin-mediated activation of HER4 initiates receptor cleavage (releasing an 80-kDa HER4 intracellular domain, s80HER4, containing nuclear localization sequences) and results in G2/M delay by unknown signaling mechanisms. We report herein that s80HER4 contains a functional cyclin B-like sequence known as a D-box, which targets proteins for degradation by APC/C, a multisubunit ubiquitin ligase. s80HER4 ubiquitination and ptoteosomal degradation occurred during mitosis but not during S-phase. Inhibition of an APC subunit (APC2) using siRNA knock-down impaired s80HER4 degradation. Mutation of the s80HER4 D-box sequence stabilized s80HER4 during mitosis, and s80HER4-dependent growth inhibition via G2/M delay was significantly greater with the D-box mutant. Polyomvirus middle-T antigen-transformed HC11 cells expressing s80HER4 resulted in smaller, less proliferative, more differentiated tumors in vivo than those expressing kinase-dead s80HER4 or the empty vector. Cells expressing s80HER4 with a disrupted D-box did not form tumors, instead forming differentiated ductal structures. These results suggest that cell cycle-dependent degradation of s80HER4 limits its growth inhibitory action, and stabilization of s80HER4 enhances tumor suppression, thus providing a link between HER4-mediated growth inhibition and cell cycle control

Evidence for intron length conservation in a set of mammalian genes associated with embryonic development

<p>Abstract</p> <p>Background</p> <p>We carried out an analysis of intron length conservation across a diverse group of nineteen mammalian species. Motivated by recent research suggesting a role for time delays associated with intron transcription in gene expression oscillations required for early embryonic patterning, we searched for examples of genes that showed the most extreme conservation of total intron content in mammals.</p> <p>Results</p> <p>Gene sets annotated as being involved in pattern specification in the early embryo or containing the homeobox DNA-binding domain, were significantly enriched among genes with highly conserved intron content. We used ancestral sequences reconstructed with probabilistic models that account for insertion and deletion mutations to distinguish insertion and deletion events on lineages leading to human and mouse from their last common ancestor. Using a randomization procedure, we show that genes containing the homeobox domain show less change in intron content than expected, given the number of insertion and deletion events within their introns.</p> <p>Conclusions</p> <p>Our results suggest selection for gene expression precision or the existence of additional development-associated genes for which transcriptional delay is functionally significant.</p

Saints and lovers: myths of the avant-garde in Michel Georges-Michel's Les Montparnos

This article examines Michel Georges-Michel’s 1924 novel Les Montparnos as a study of the myths circulating around the Montparnasse avant-garde of the 1920s, and their function in relation to art. Key amongst these myths is the idea of art as a religion, according to which avant-garde artists are conceived as secular saints and martyrs. While this notion of artist as saint is strongly present in early-twentieth-century biographies of Van Gogh, Georges-Michel explicitly relates his fictionalized version of Modigliani’s life not to such recent models but rather to the Renaissance masters, and especially to Raphael, a link which is explained in terms of the post-war ‘retour à l’ordre’ in French artistic culture. The novel’s references to Raphael as archetypal painter-lover are also related to its construction of a myth of the artist as virile and sexually prolific, and to its identification of creative and sexual impulses

Sex-specific Trans-regulatory Variation on the Drosophila melanogaster X Chromosome

The X chromosome constitutes a unique genomic environment because it is present in one copy in males, but two copies in females. This simple fact has motivated several theoretical predictions with respect to how standing genetic variation on the X chromosome should differ from the autosomes. Unmasked expression of deleterious mutations in males and a lower census size are expected to reduce variation, while allelic variants with sexually antagonistic effects, and potentially those with a sex-specific effect, could accumulate on the X chromosome and contribute to increased genetic variation. In addition, incomplete dosage compensation of the X chromosome could potentially dampen the male-specific effects of random mutations, and promote the accumulation of X-linked alleles with sexually dimorphic phenotypic effects. Here we test both the amount and the type of genetic variation on the X chromosome within a population of Drosophila melanogaster, by comparing the proportion of X linked and autosomal trans-regulatory SNPs with a sexually concordant and discordant effect on gene expression. We find that the X chromosome is depleted for SNPs with a sexually concordant effect, but hosts comparatively more SNPs with a sexually discordant effect. Interestingly, the contrasting results for SNPs with sexually concordant and discordant effects are driven by SNPs with a larger influence on expression in females than expression in males. Furthermore, the distribution of these SNPs is shifted towards regions where dosage compensation is predicted to be less complete. These results suggest that intrinsic properties of dosage compensation influence either the accumulation of different types of trans-factors and/or their propensity to accumulate mutations. Our findings document a potential mechanistic basis for sex-specific genetic variation, and identify the X as a reservoir for sexually dimorphic phenotypic variation. These results have general implications for X chromosome evolution, as well as the genetic basis of sex-specific evolutionary change

In vitro culturing of ciliary respiratory cells—a model for studies of genetic diseases

Primary ciliary dyskinesia (PCD) is a rare genetic disorder caused by the impaired functioning of ciliated cells. Its diagnosis is based on the analysis of the structure and functioning of cilia present in the respiratory epithelium (RE) of the patient. Abnormalities of cilia caused by hereditary mutations closely resemble and often overlap with defects induced by the environmental factors. As a result, proper diagnosis of PCD is difficult and may require repeated sampling of patients’ tissue, which is not always possible. The culturing of differentiated cells and tissues derived from the human RE seems to be the best way to diagnose PCD, to study genotype–phenotype relations of genes involved in ciliary dysfunction, as well as other aspects related to the functioning of the RE. In this review, different methods of culturing differentiated cells and tissues derived from the human RE, along with their potential and limitations, are summarized. Several considerations with respect to the factors influencing the process of in vitro differentiation (cell-to-cell interactions, medium composition, cell-support substrate) are also discussed