1,169 research outputs found

    Increased activity of cell surface peptidases in HeLa cells undergoing UV-induced apoptosis is not mediated by caspase 3

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    We have previously shown that in HeLa cells treated with a variety of agents there is an increase in cell surface peptidase (CSP) activity in those cells undergoing apoptosis. The increase in CSP activity observed in UVB-irradiated cells undergoing apoptosis was unaffected when the cultures were treated with the aminopeptidase inhibitor bestatin, and matrix metalloprotease inhibitor BB3103, but greatly enhanced when treated with the caspase 3 inhibitor-DEVD, and reduced in the presence of the poly(ADP-ribose) polymerase (PARP) inhibitor-3-aminobenzamide (3AB). Neither 3AB nor DEVD had an effect on the gross morphology of the apoptotic cells observed under electron microscopy, nor did they have an effect on phosphatidylserine eversion on the cell membrane, or that of PARP cleavage. All the agents except for DEVD had no effect on the level of caspase 3 activity in the cells. The results suggest that other caspases may cleave PARP in these cells. Both 3AB and DEVD treatment reduced the level of actin cleavage seen in the apoptotic cells. The increase in CSP activity observed in cells undergoing UVB-induced apoptosis appears to involve PARP but not caspase 3

    Possible unconventional superconductivity in substituted BaFe2_{2}As2_{2} revealed by magnetic pair-breaking studies

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    The possible existence of a sign-changing gap symmetry in BaFe2_{2}As2_{2}-derived superconductors (SC) has been an exciting topic of research in the last few years. To further investigate this subject we combine Electron Spin Resonance (ESR) and pressure-dependent transport measurements to investigate magnetic pair-breaking effects on BaFe1.9M0.1_{1.9}M_{0.1}As2_{2} (M=M= Mn, Co, Cu, and Ni) single crystals. An ESR signal, indicative of the presence of localized magnetic moments, is observed only for M=M= Cu and Mn compounds, which display very low SC transition temperature (TcT_{c}) and no SC, respectively. From the ESR analysis assuming the absence of bottleneck effects, the microscopic parameters are extracted to show that this reduction of TcT_{c} cannot be accounted by the Abrikosov-Gorkov pair-breaking expression for a sign-preserving gap function. Our results reveal an unconventional spin- and pressure-dependent pair-breaking effect and impose strong constraints on the pairing symmetry of these materials

    MicroRNA-221 silencing attenuates the degenerated phenotype of intervertebral disc cells.

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    The aim of this study was to investigate the role of an antichondrogenic factor, MIR221 (miR‐221), in intervertebral disc degeneration (IDD), and provide basic information for the development of a therapeutic strategy for the disc repair based on specific nucleic acid based drugs, such as miR‐221 silencing. We established a relatively quick protocol to minimize artifacts from extended in vitro culture, without selecting the different types of cells from intervertebral disc (IVD) or completely disrupting extracellular matrix (ECM), but by using the whole cell population with a part of resident ECM. During the de‐differentiation process miR‐221 expression significantly increased. We demonstrated the effectiveness of miR‐221 silencing in driving the cells towards chondrogenic lineage. AntagomiR‐221 treated cells showed in fact a significant increase of expression of typical chondrogenic markers including COL2A1, ACAN and SOX9, whose loss is associated with IDD. Moreover, antagomiR‐221 treatment restored FOXO3 expression and increased TRPS1 expression levels attenuating the severity grade of degeneration, and demonstrating in a context of tissue degeneration and inflammation not investigated before, that FOXO3 is target of miR‐221. Data of present study are promising in the definition of new molecules useful as potential intradiscal injectable biological agents

    Silicon Atomic Quantum Dots Enable Beyond-CMOS Electronics

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    We review our recent efforts in building atom-scale quantum-dot cellular automata circuits on a silicon surface. Our building block consists of silicon dangling bond on a H-Si(001) surface, which has been shown to act as a quantum dot. First the fabrication, experimental imaging, and charging character of the dangling bond are discussed. We then show how precise assemblies of such dots can be created to form artificial molecules. Such complex structures can be used as systems with custom optical properties, circuit elements for quantum-dot cellular automata, and quantum computing. Considerations on macro-to-atom connections are discussed.Comment: 28 pages, 19 figure
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