92 research outputs found

    Multidimensionnel Borg-Levinson uniqueness and stability results for the Robin Laplacian with unbounded potential

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    This article deals with the uniqueness and stability issues in the inverse problem of determining the unbounded potential of the Schr\"odinger operator in a bounded domain of dimension 3 or greater, endowed with Robin boundary condition, from knowledge of its boundary spectral data. These data are defined by the pairs formed by the eigenvalues and either full or partial Dirichlet measurement of the eigenfunctions on the boundary of the domain

    Variation of the partition coefficient of phase-partitioning compounds between hydrocarbon and aqueous phases: an experimental study.

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    Many non-ionic chemical compounds will form real solutions in equilibrium between two immiscible phases in contact. The partition coefficient (K) is defined as the quotient between the equilibrium concentration of the substance in the hydrocarbon and the aqueous phase. The reversible partition of a compound between hydrocarbon and aqueous phases is the basis of the partitioning inter-well tracer test (PITT). PITTs are of high interest for the characterization of oil reservoirs, in hydrogeology for assessment of the contamination of soils by non-aqueous phase liquids (NAPLs), and in process technology. The K value of substance is influenced by the actual chemical and physical conditions of the system where it will be used as phase-partitioning tracer. Thus, it is important to evaluate the extent of variation that the K value can exhibit under different relevant conditions. In the present document, we report the methodology and findings from the experimental determination of the K values of 4-methoxybenzyl alcohol, 3,4-dimethoxybenzyl alcohol, 4-chlorobenzyl alcohol, 2,6-dichlorobenzyl alcohol, pyridine, 2,3-dimethylpyrazine and 2,6-dimethylpyrazine between different hydrocarbon and aqueous phases. These 7 compounds were previously identified as interesting PITT tracer candidates. Individual K-values were determined under different temperatures, compositions of the hydrocarbon phase (synthetic mixtures of toluene, isooctane, and 1-octanol and 5 real crude oils), and different ionic strengths (I) and ionic compositions of the aqueous phase. The reversibility of the partitioning phenomena was also evaluated. The composition of the hydrocarbon phase and the ionic strength of the water phase were found to influence the K values of all seven compounds. Results suggest that the substitution of monovalent ions with divalent ions in the aqueous phase, keeping the ionic strength constant, does not influence the K values. Temperature effects on the K-values are always visible for 3,4-dimethoxybenzyl alcohol, 2,6-dichlorobenzyl alcohol, pyridine, 2,3-dimethylpyrazine and 2,6-dimethylpyrazine. Dependent on the hydrocarbon phase composition, temperature also influences the K-values for 4-methoxybenzyl alcohol and 4-chlorobenzyl alcohol.publishedVersio

    First stages of the InP(1 0 0) surfaces nitridation studied by AES, EELS and EPES

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    The nitrides of group III metals: AlN, GaN and InN are very important materials due to their applications for short wavelength opto-electronics (light-emitting diodes and laser diodes). It is essential for the realization of such novel devices to grow high-quality nitride single crystals. In this paper, we report the first stages of the InP(1 0 0) surfaces nitridation in order to grow high-quality nitride films. Indeed, the nitridation process is an important step in the growth of nitrides [J. Vac. Sci. Technol. A 17 (1999) 2194; Phys. Status Solidi A 176 (1999) 595]. Previous works [Synth. Met. 90 (1997) 2233; Appl. Phys. Lett. 63 (1993) 1957] have shown that in situ Ar+ ions bombardment is useful on the one hand to clean the surface, and on the other hand to create droplets of metallic indium in well-controlled quantity. Then the indium metallic enrichment of the surface, monitoring by elastic peak electron spectroscopy (EPES) and Auger electron spectroscopy (AES) allows to prepare the III-V semiconductors surfaces to the nitridation step. The nitridated process has been performed with a high voltage plasma discharge cell and has been studied using quantitative Auger electron spectroscopy, elastic peak electron spectroscopy and electron energy loss spectroscopy (EELS), in order to optimize the conditions of InN layers formation

    EVALUATION OF PHYTOCHEMICALS, ANTIOXIDANT AND CYTOTOXIC ACTIVITIES OF LAVANDULA ANTINEAE MAIRE ENDEMIC MEDICINAL PLANT FROM ALGERIA

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    The present study was designed to investigate the phytochemical screening, total phenolic and flavonoid contents,antioxidant and cytotoxic activities of Lavandula antineae Maire for the first time. Phytochemical screening revealed thepresence of anthraquinones, triterpenes, saponins, flavonoids, tannins, O-heterosides, C-heterosides. Total phenolic andflavonoid contents of the extracts varied between 12.49-262.35 mg GAE/g extract and 1.35-4.03 mg QE/g extract,respectively. The antioxidant activity was investigated using DPPH, reducing power and β-carotene/linoleic acid tests. Theresults indicated that ethyl acetate and diethyl ether fractions exhibited stronger activities than hydromethanolic crude extractand other fractions. In case of cytotoxicity assay, hydromethanolic extract was found to show good toxicity against brineshrimp nauplii (LC50= 13.72 μg/ml)

    Feedback control of AHR signalling regulates intestinal immunity

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    The aryl hydrocarbon receptor (AHR) recognizes xenobiotics as well as natural compounds such as tryptophan metabolites, dietary components and microbiota-derived factors, and it is important for maintenance of homeostasis at mucosal surfaces. AHR activation induces cytochrome P4501 (CYP1) enzymes, which oxygenate AHR ligands, leading to their metabolic clearance and detoxification. Thus, CYP1 enzymes have an important feedback role that curtails the duration of AHR signalling, but it remains unclear whether they also regulate AHR ligand availability in vivo. Here we show that dysregulated expression of Cyp1a1 in mice depletes the reservoir of natural AHR ligands, generating a quasi AHR-deficient state. Constitutive expression of Cyp1a1 throughout the body or restricted specifically to intestinal epithelial cells resulted in loss of AHR-dependent type 3 innate lymphoid cells and T helper 17 cells and increased susceptibility to enteric infection. The deleterious effects of excessive AHR ligand degradation on intestinal immune functions could be counter-balanced by increasing the intake of AHR ligands in the diet. Thus, our data indicate that intestinal epithelial cells serve as gatekeepers for the supply of AHR ligands to the host and emphasize the importance of feedback control in modulating AHR pathway activation

    Epithelial-Cell-Derived Phospholipase A2 Group 1B Is an Endogenous Anthelmintic.

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    Immunity to intestinal helminth infections has been well studied, but the mechanism of helminth killing prior to expulsion remains unclear. Here we identify epithelial-cell-derived phospholipase A2 group 1B (PLA2g1B) as a host-derived endogenous anthelmintic. PLA2g1B is elevated in resistant mice and is responsible for killing tissue-embedded larvae. Despite comparable activities of other essential type-2-dependent immune mechanisms, Pla2g1b-/- mice failed to expel the intestinal helminths Heligmosomoides polygyrus or Nippostrongylus brasiliensis. Expression of Pla2g1b by epithelial cells was dependent upon intestinal microbiota, adaptive immunity, and common-gamma chain-dependent signaling. Notably, Pla2g1b was downregulated in susceptible mice and inhibited by IL-4R-signaling in vitro, uncoupling parasite killing from expulsion mechanisms. Resistance was restored in Pla2g1b-/- mice by treating infective H. polygyrus L3 larvae with PLA2g1B, which reduced larval phospholipid abundance. These findings uncover epithelial-cell-derived Pla2g1b as an essential mediator of helminth killing, highlighting a previously overlooked mechanism of anti-helminth immunity

    Regulation of human intestinal T-cell responses by type 1 interferon-STAT1 signaling is disrupted in inflammatory bowel disease

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    This work was supported by a research fellowship grant from the Crohn’s and Colitis in Childhood Research Association (CICRA) and a small project grant from Crohn’s and Colitis UK (CCUK). We would like to acknowledge Professor Ian Sanderson, who helped with the initial design of this work, and provided important support throughout. We would also like to thank Dr Gary Warne for his advice and assistance in the use of the sorting by flow cytometry. We would also like to thank Dr Raj Lahiri and Professor Graham Foster for the kind gift of the primers for the ISGs (2’5’ OAS and MxA)

    Loss of Adenomatous polyposis coli function renders intestinal epithelial cells resistant to the cytokine IL-22

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    Interleukin-22 (IL-22) is a critical immune defence cytokine that maintains intestinal homeostasis and promotes wound healing and tissue regeneration, which can support the growth of colorectal tumours. Mutations in the adenomatous polyposis coli gene (Apc) are a major driver of familial colorectal cancers (CRCs). How IL-22 contributes to APC-mediated tumorigenesis is poorly understood. To investigate IL-22 signalling in wild-type (WT) and APC-mutant cells, we performed RNA sequencing (RNAseq) of IL-22-treated murine small intestinal epithelial organoids. In WT epithelia, antimicrobial defence and cellular stress response pathways were most strongly induced by IL-22. Surprisingly, although IL-22 activates signal transducer and activator of transcription 3 (STAT3) in APC-mutant cells, STAT3 target genes were not induced. Our analyses revealed that ApcMin/Min cells are resistant to IL-22 due to reduced expression of the IL-22 receptor, and increased expression of inhibitors of STAT3, particularly histone deacetylases (HDACs). We further show that IL-22 increases DNA damage and genomic instability, which can accelerate cellular transition from heterozygosity (ApcMin/+) to homozygosity (ApcMin/Min) to drive tumour formation. Our data reveal an unexpected role for IL-22 in promoting early tumorigenesis while excluding a function for IL-22 in transformed epithelial cells
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