Detection of Tiny Mechanical Motion by Means of the Ratchet Effect

We propose a position detection scheme for a nanoelectromechanical resonator based on the ratchet effect. This scheme has an advantage of being a dc measurement. We consider a three-junction SQUID where a part of the superconducting loop can perform mechanical motion. The response of the ratchet to a dc current is sensitive to the position of the resonator and the effect can be further enhanced by biasing the SQUID with an ac current. We discuss the feasibility of the proposed scheme in existing experimental setups.Comment: 8 pages, 9 figure

Photon production from the vacuum close to the super-radiant transition: When Casimir meets Kibble-Zurek

The dynamical Casimir effect (DCE) predicts the generation of photons from the vacuum due to the parametric amplification of the quantum fluctuation of an electromagnetic field\cite{casimir1,casimir2}. The verification of such effect is still elusive in optical systems due to the very demanding requirements of its experimental implementation. This typically requires very fast changes of the boundary conditions of the problem, such as the high-frequency driving of the positions of the mirrors of a cavity accommodating the field. Here, we show that an ensemble of two-level atoms collectively coupled to the electromagnetic field of a cavity (thus embodying the quantum Dicke model\cite{dicke}), driven at low frequencies and close to a quantum phase transition, stimulates the production of photons from the vacuum. This paves the way to an effective simulation of the DCE through a mechanism that has recently found an outstanding experimental demonstration\cite{esslinger}. The spectral properties of the emitted radiation reflect the critical nature of the system and allow us to link the detection of DCE to the Kibble-Zurek mechanism for the production of defects when crossing a continuous phase transition\cite{KZ1,KZ2}. We illustrate the features of our proposal by addressing a simple cavity quantum-electrodynamics (cQED) setting of immediate experimental realisation.Comment: 4+1 pages, major changes in the second part of the paper. To appear in Physical Review Letter

Long Term Ecological Research (LTER) in the Marine Coastal Environment: Basic Concepts and Keystones from the Plankton Communities.

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Roles for CEP170 in cilia function and dynein-2 assembly

Primary cilia are essential eukaryotic organelles required for signalling and secretion. Dynein-2 is a microtubule-motor protein complex and is required for ciliogenesis via its role in facilitating retrograde intraflagellar transport (IFT) from the cilia tip to the cell body. Dynein-2 must be assembled and loaded onto IFT trains for entry into cilia for this process to occur, but how dynein-2 is assembled and how it is recycled back into a cilium remain poorly understood. Here, we identify centrosomal protein of 170 kDa (CEP170) as a dynein-2-interacting protein in mammalian cells. We show that loss of CEP170 perturbs intraflagellar transport and hedgehog signalling, and alters the stability of dynein-2 holoenzyme complex. Together, our data indicate a role for CEP170 in supporting cilia function and dynein-2 assembly

Long non-coding RNA gas5 and intestinal mmp2 and mmp9 expression: A translational study in pediatric patients with IBD

Background: The long non-coding RNA (lncRNA) growth arrest–specific transcript 5 (GAS5) seems to be involved in the regulation of mediators of tissue injury, in particular matrix metalloproteinases (MMPs), implicated in the pathogenesis of inflammatory bowel disease (IBD). We investigated the role of GAS5 in regulating MMP2 and MMP9 expression in pediatric patients with IBD and in vitro. Methods: In total, 25 IBD patients were enrolled: For each patient paired inflamed and non-inflamed biopsies were collected. RNA was extracted and GAS5, MMP2, and MMP9 were quantified by TaqMan assay. The expression of GAS5 and MMPs was also determined in the human monocytic THP1 cells differentiated into macrophages and stimulated with lipopolysaccharide (LPS). The function of GAS5 was assessed by overexpressing the lncRNA and evaluating the MMPs levels. Results: Real-time PCR results demonstrated a downregulation of GAS5 and an upregulation of both MMPs in inflamed tissues. In vitro data confirmed the trend observed in patients for the three genes: The stimulation with LPS promoted a downregulation of GAS5 while an increase of MMPs was observed. Overexpression experiments showed that higher levels of GAS5 lead to a decrease of both enzymes. Conclusion: These results provide new information about the role of GAS5 in IBD: The lncRNA could mediate tissue damage by modulating the expression of MMPs

Gene expression profiling in white blood cells reveals new insights into the molecular mechanisms of thalidomide in children with inflammatory bowel disease

Thalidomide has emerged as an effective immunomodulator in the treatment of pediatric patients with inflammatory bowel disease (IBD) refractory to standard therapies. Cereblon (CRBN), a component of E3 protein ligase complex that mediates ubiquitination and proteasomal degradation of target proteins, has been identified as the primary target of thalidomide. CRBN plays a crucial role in thalidomide teratogenicity, however it is unclear whether it is also involved in the therapeutic effects in IBD patients. This study aimed at identifying the molecular mechanisms underpinning thalidomide action in pediatric IBD. In this study, ten IBD pediatric patients responsive to thalidomide were prospectively enrolled. RNA-sequencing (RNA-seq) analysis and functional enrichment analysis were carried out on peripheral blood mononuclear cells (PBMC) obtained before and after twelve weeks of treatment with thalidomide. RNA-seq analysis revealed 378 differentially expressed genes before and after treatment with thalidomide. The most deregulated pathways were cytosolic calcium ion concentration, cAMP-mediated signaling, eicosanoid signaling and inhibition of matrix metalloproteinases. Neuronal signaling mechanisms such as CREB signaling in neurons and axonal guidance signaling also emerged. Connectivity Map analysis revealed that thalidomide gene expression changes were similar to those exposed to MLN4924, an inhibitor of NEDD8 activating enzyme, suggesting that thalidomide exerts its immunomodulatory effects by acting on the ubiquitin-proteasome pathway. In vitro experiments on cell lines confirmed the effect of thalidomide on candidate altered pathways observed in patients. These results represent a unique resource for enhanced understanding of thalidomide mechanism in pediatric patients with IBD, providing novel potential targets associated with drug response