Proximity effect in planar superconducting tunnel junctions containing Nb/NiCu superconductor/ferromagnet bilayers

We present experimental results concerning both the fabrication and characterization of superconducting tunnel junctions containing superconductor/ferromagnet (S/F) bilayers made by niobium (S) and a weak ferromagnetic Ni0.50Cu0.50 alloy. Josephson junctions have been characterized down to T=1.4 K in terms of current-voltage I-V characteristics and Josephson critical current versus magnetic field. By means of a numerical deconvolution of the I-V data the electronic density of states on both sides of the S/F bilayer has been evaluated at low temperatures. Results have been compared with theoretical predictions from a proximity model for S/F bilayers in the dirty limit in the framework of Usadel equations for the S and F layers, respectively. The main physical parameters characterizing the proximity effect in the Nb/NiCu bilayer, such as the coherence length and the exchange field energy of the F metal, and the S/F interface parameters have been also estimated

Mechanistic insights on the mode of action of an antiproliferative thiosemicarbazone-nickel complex revealed by an integrated chemogenomic profiling study

Thiosemicarbazones (TSC) and their metal complexes display diverse biological activities and are active against multiple pathological conditions ranging from microbial infections to abnormal cell proliferation. Ribonucleotide reductase (RNR) is considered one of the main targets of TSCs, yet, the existence of additional targets, differently responsible for the multifaceted activities of TSCs and their metal complexes has been proposed. To set the basis for a more comprehensive delineation of their mode of action, we chemogenomically profiled the cellular effects of bis(citronellalthiosemicarbazonato)nickel(II) [Ni(S-tcitr)2] using the unicellular eukaryote Saccharomyces cerevisiae as a model organism. Two complementary genomic phenotyping screens led to the identification of 269 sensitive and 56 tolerant deletion mutant strains and of 14 genes that when overexpressed make yeast cells resistant to an otherwise lethal concentration of Ni(S-tcitr)2. Chromatin remodeling, cytoskeleton organization, mitochondrial function and iron metabolism were identified as lead cellular processes responsible for Ni(S-tcitr)2 toxicity. The latter process, and particularly glutaredoxin-mediated iron loading of RNR, was found to be affected by Ni(S-tcitr)2. Given the multiple pathways regulated by glutaredoxins, targeting of these proteins by Ni(S-tcitr)2 can negatively affect various core cellular processes that may critically contribute to Ni(S-tcitr)2 cytotoxicity

Cobalt oxide nanoparticles induce oxidative stress and alter electromechanical function in rat ventricular myocytes

Background: Nanotoxicology is an increasingly relevant field and sound paradigms on how inhaled nanoparticles (NPs) interact with organs at the cellular level, causing harmful conditions, have yet to be established. This is particularly true in the case of the cardiovascular system, where experimental and clinical evidence shows morphological and functional damage associated with NP exposure. Giving the increasing interest on cobalt oxide (Co3O4) NPs applications in industrial and bio-medical fields, a detailed knowledge of the involved toxicological effects is required, in view of assessing health risk for subjects/workers daily exposed to nanomaterials. Specifically, it is of interest to evaluate whether NPs enter cardiac cells and interact with cell function. We addressed this issue by investigating the effect of acute exposure to Co3O4-NPs on excitation-contraction coupling in freshly isolated rat ventricular myocytes. Results: Patch clamp analysis showed instability of resting membrane potential, decrease in membrane electrical capacitance, and dose-dependent decrease in action potential duration in cardiomyocytes acutely exposed to Co3O4-NPs. Motion detection and intracellular calcium fluorescence highlighted a parallel impairment of cell contractility in comparison with controls. Specifically, NP-treated cardiomyocytes exhibited a dose-dependent decrease in the fraction of shortening and in the maximal rate of shortening and re-lengthening, as well as a less efficient cytosolic calcium clearing and an increased tendency to develop spontaneous twitches. In addition, treatment with Co3O4-NPs strongly increased ROS accumulation and induced nuclear DNA damage in a dose dependent manner. Finally, transmission electron microscopy analysis demonstrated that acute exposure did lead to cellular internalization of NPs. Conclusions: Taken together, our observations indicate that Co3O4-NPs alter cardiomyocyte electromechanical efficiency and intracellular calcium handling, and induce ROS production resulting in oxidative stress that can be related to DNA damage and adverse effects on cardiomyocyte functionality

Changes in CD4+ cells’ miRNA expression following exposure to HIV-1

Background: MiRNAs inhibit HIV-1 expression by either modulating host innate immunity or by directly interfering with viral mRNAs. Here, we investigated the miRNA profile that discriminates different classes of HIV-1 infected patients from multiple exposed uninfected individuals. Methods: The expression levels of 377 miRNAs were selectively analyzed in CD4+ cells isolated from whole blood of HIV-1 \ue9lite LTNP (\ue9LTNP), naive, and multiply exposed uninfected individuals (MEU). MiRNA extraction was performed by the mirVana miRNA Isolation Kit (Ambion) and their expression was subsequently examined by real-time PCR-based arrays. The expression of miRNAs was also determined in primary culture of CD4+T cells and monocyte-macrophages infected in vitro by R5 strains. Expression of Dicer and Drosha was evaluated by real-time PCR. Results: We only considered miRNAs that were expressed in the 70% of patients of at least one class and varied by at least 1 log10 from healthy controls. Out of 377 miRNAs, 26 were up-regulated, while 88 were down-regulated. Statistical analysis showed that 21 miRNAs significantly differentiated \ue9LTNP from MEU and 23 miRNAs distinguished naive from MEU, while only 1 (miR-155) discriminated \ue9LTNP from naive. By hierarchical clustering of the miRNAs according to patient class, \ue9LTNP clustered with naive whereas all MEU subjects grouped together. The Dicer and Drosha expression in the patient classes correlated with miRNA profile changes. Among miRNAs differentially expressed in patient classes, 32 were detected in in vitro infection model: the most of the up-regulated miRNAs were expressed in monocyte-macrophages, whereas the most of the down-regulated miRNAs were expressed in T lymphocytes. Conclusions: These findings support that miRNA profile could be the result not only of a productive infection, but also of the exposure to HIV products that leave a signature in immune cells. These data provide some intriguing issues relative to the development of HIV vaccines targeting viral proteins

Effect of the magnetic order on the room-temperature band-gap of Mn-doped ZnO thin films

Author name used in this publication: Ruotolo A.2012-2013 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe