Nanoscale phase separation in the iron chalcogenide superconductor K0.8Fe1.6Se2 as seen via scanning nanofocused x-ray diffraction

Advanced synchrotron radiation focusing down to a size of 300 nm has been used to visualize nanoscale phase separation in the K0.8Fe1.6Se2 superconducting system using scanning nanofocus single-crystal X-ray diffraction. The results show an intrinsic phase separation in K0.8Fe1.6Se2 single crystals at T< 520 K, revealing coexistence of i) a magnetic phase characterized by an expanded lattice with superstructures due to Fe vacancy ordering and ii) a non-magnetic phase with an in-plane compressed lattice. The spatial distribution of the two phases at 300 K shows a frustrated or arrested nature of the phase separation. The space-resolved imaging of the phase separation permitted us to provide a direct evidence of nanophase domains smaller than 300 nm and different micrometer-sized regions with percolating magnetic or nonmagnetic domains forming a multiscale complex network of the two phases.Comment: 5 pages, 4 figure

Inhomogeneity of charge density wave order and quenched disorder in a high Tc superconductor

It has recently been established that the high temperature (high-Tc) superconducting state coexists with short-range charge-density-wave order and quenched disorder arising from dopants and strain. This complex, multiscale phase separation invites the development of theories of high temperature superconductivity that include complexity. The nature of the spatial interplay between charge and dopant order that provides a basis for nanoscale phase separation remains a key open question, because experiments have yet to probe the unknown spatial distribution at both the nanoscale and mescoscale (between atomic and macroscopic scale). Here we report micro X-ray diffraction imaging of the spatial distribution of both the charge-density-wave puddles (domains with only a few wavelengths) and quenched disorder in HgBa2CuO4+y, the single layer cuprate with the highest Tc, 95 kelvin. We found that the charge-density-wave puddles, like the steam bubbles in boiling water, have a fat-tailed size distribution that is typical of self-organization near a critical point. However, the quenched disorder, which arises from oxygen interstitials, has a distribution that is contrary to the usual assumed random, uncorrelated distribution. The interstitials-oxygen-rich domains are spatially anti-correlated with the charge-density-wave domains, leading to a complex emergent geometry of the spatial landscape for superconductivity.Comment: 11 pages, 3 figure

Anionic glycolipids related to glucuronosyldiacylglycerol inhibit protein kinase Akt

New glucuronosyldiacylglycerol (GlcADG) analogues based on a 2-O-\u3b2-D-glucopyranosyl-sn-glycerol scaffold and carrying one or two acyl chains of different lengths have been synthesized as phosphatidylinositol 3-phosphate (PI3P) mimics targeting the protein kinase Akt. Akt inhibitory effect of prepared compounds, was assayed using an in vitro kinase assay. The antiproliferative activity of the compounds was tested in the human ovarian carcinoma IGROV-1 cell line in which we found that two of them could inhibit proliferation, in keeping with the target inhibitory effect

Sperm morphology of two marine neogastropods from the southwestern Atlantic Ocean (Caenogastropoda: Volutidae and Olividae)

Volume: 123Start Page: 166End Page: 17

PKC-alpha modulation by miR-483-3p in platinum-resistant ovarian carcinoma cells

The occurrence of drug resistance limits the efficacy of platinum compounds in the cure of ovarian carcinoma. Since microRNAs (miRNAs) may contribute to this phenomenon by regulating different aspects of tumor cell response, the aim of this study was to exploit the analysis of expression of miRNAs in platinum sensitive/resistant cells in an attempt to identify potential regulators of drug response. MiR-483-3p, which may participate in apoptosis and cell proliferation regulation, was found up-regulated in 4 platinum resistant variants, particularly in the IGROV-1/Pt1 subline, versus parental cells. Transfection of a synthetic precursor of miR-483-3p in IGROV-1 parental cells elicited a marked up-regulation of the miRNA levels. Growth-inhibition and colony-forming assays indicated that miR-483-3p over-expression reduced cell growth and conferred mild levels of cisplatin resistance in IGROV-1 cells, by interference with their proliferative potential. Predicted targets of miR-483-3p included PRKCA (encoding PKC-alpha), previously reported to be associated to platinum-resistance in ovarian carcinoma. We found that miR-483-3p directly targeted PRKCA in IGROV-1 cells. In keeping with this finding, cisplatin sensitivity of IGROV-1 cells decreased upon molecular/pharmacological inhibition of PKC-alpha. Overall, our results suggest that overexpression of miR-483-3p by ovarian carcinoma platinum-resistant cells may interfere with their proliferation, thus protecting them from DNA damage induced by platinum compounds and ultimately representing a drug-resistance mechanism. The impairment of cell growth may account for low levels of drug resistance that could be relevant in the clinical setting

miR-875-5p counteracts epithelial-to-mesenchymal transition and enhances radiation response in prostate cancer through repression of the EGFR-ZEB1 axis

Radiotherapy is one of the main treatment choices for non-metastatic prostate cancer (PCa), although development of radioresistance limits its effectiveness. Mounting evidence supports the ability of microRNAs to interfere with different radioresistance-associated pathways, suggesting their potential as radiosensitizers. Here, we demonstrate that reconstitution of miR-875-5p, whose expression is down-regulated in PCa clinical samples and directly correlates with that of E-cadherin, was able to enhance radiation response in PCa cell lines and xenografts through EGFR direct targeting. Consistent with the established role of EGFR in sustaining epithelial-to-mesenchymal transition (EMT) and promoting DNA repair following radiation-induced nuclear translocation, we found that miR-875-5p reconstitution in PCa cells counteracted EMT and impaired DNA lesion clearance. Down-regulation of the EMT-inducing transcription factor ZEB1, which also plays a role in homologous recombination-mediated repair of DNA lesions by regulating CHK1 expression, was found to be a major determinant of miR-875-5p-induced radiosensitization, as confirmed by phenocopy experiments showing that siRNA-mediated ZEB1 knock-down was able to reproduce the microRNA radiosensitizing effect. Overall, our data support the clinical interest in developing a novel therapeutic approach based on miR-875-5p reconstitution to increase PCa response to radiotherapy