Spontaneous Conversion from Virtual to Real Photons in the Ultrastrong Coupling Regime

We show that a spontaneous release of virtual photon pairs can occur in a quantum optical system in the ultrastrong coupling regime. In this regime, which is attracting interest both in semiconductor and superconducting systems, the light-matter coupling rate {\Omega}R becomes comparable to the bare resonance frequency of photons {\omega}0. In contrast to the dynamical Casimir effect and other pair creation mechanisms, this phenomenon does not require external forces or time dependent parameters in the Hamiltonian.Comment: To appear on Phys. Rev. Let

A Tactile Sensor Device Exploiting the Tunable Sensitivity of Copper-PDMS Piezoresistive Composite

Abstract A low cost and highly mechanically flexible 8x8 pressure matrix sensor with dedicated electronics has been fabricated with an innovative metal-elastomer composite material. Under the action of a compressive stress the material exhibits a giant piezoresistive effect varying its electrical resistance of several orders of magnitude. This phenomenon can be tuned by changing the material composition parameters, directly modifying the sensitivity of the sensor. The micro casting fabrication technique, used for the preparation of self standing sheet of functional material, gives the possibility of easily fabricating complex-shaped structure suitable for integration on robot surface for tactile sensing. The sensor has been tested with a customized electronic circuit after an exhaustive characterization of the functional properties of the material

Output field-quadrature measurements and squeezing in ultrastrong cavity-QED

We study the squeezing of output quadratures of an electro-magnetic field escaping from a resonator coupled to a general quantum system with arbitrary interaction strengths. The generalized theoretical analysis of output squeezing proposed here is valid for all the interaction regimes of cavity-quantum electrodynamics: from the weak to the strong, ultrastrong, and deep coupling regimes. For coupling rates comparable or larger then the cavity resonance frequency, the standard input\u2013output theory for optical cavities fails to calculate the variance of output field-quadratures and predicts a non-negligible amount of output squeezing, even if the system is in its ground state. Here we show that, for arbitrary interaction strength and for general cavity-embedded quantum systems, no squeezing can be found in the output-field quadratures if the system is in its ground state. We also apply the proposed theoretical approach to study the output squeezing produced by: (i) an artificial two-level atom embedded in a coherently-excited cavity; and (ii) a cascade-type three-level system interacting with a cavity field mode. In the latter case the output squeezing arises from the virtual photons of the atom-cavity dressed states. This work extends the possibility of predicting and analyzing the results of continuous- variable optical quantum-state tomography when optical resonators interact very strongly with other quantum systems

CdO-based nanostructures as novel CO2 gas sensors

Crystalline Cd(OH)2/CdCO3 nanowires, having lengths in the range from 0.3 up to several microns and 5–30 nm in diameter, were synthesized by a microwave-assisted wet chemical route and used as a precursor to obtain CdO nanostructures after a suitable thermal treatment in air. The morphology and microstructure of the as-synthesized and annealed materials have been investigated by scanning electron microscopy, transmission electron microscopy, x-ray diffraction and thermogravimetry–differential scanning calorimetry. The change in morphology and electrical properties with temperature has revealed a wire-to-rod transformation along with a decreases of electrical resistance. Annealed samples were printed on a ceramic substrate with interdigitated contacts to fabricate resistive solid state sensors. Gas sensing properties were explored by monitoring CO2 in synthetic air in the concentration range 0.2–5 v/v% (2000–50 000 ppm). The effect of annealing temperature, working temperature and CO2 concentration on sensing properties (sensitivity, response/recovery time and stability) were investigated. The results obtained demonstrate that CdO-based thick films have good potential as novel CO2 sensors for practical applications

Experimental study of a liquid Xenon PET prototype module

A detector using liquid Xenon in the scintillation mode is studied for Positron Emission Tomography (PET). The specific design aims at taking full advantage of the liquid Xenon properties. It does feature a promising insensitive to any parallax effect. This work reports on the performances of the first LXe prototype module, equipped with a position sensitive PMT operating in the VUV range (178 nm).Comment: Proc. of the 7th International Workshops on Radiation Imaging Detectors (IWORID-7), Grenoble, France 4-7 July 200

cFLIPL Inhibits Tumor Necrosis Factor-related Apoptosis-inducing Ligand-mediated NF-κB Activation at the Death-inducing Signaling Complex in Human Keratinocytes

Human keratinocytes undergo apoptosis following treatment with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via surface-expressed TRAIL receptors 1 and 2. In addition, TRAIL triggers nonapoptotic signaling pathways including activation of the transcription factor NF-kappaB, in particular when TRAIL-induced apoptosis is blocked. The intracellular protein cFLIP(L) interferes with TRAIL-induced apoptosis at the death-inducing signaling complex (DISC) in many cell types. To study the role of cFLIP(L) in TRAIL signaling, we established stable HaCaT keratinocyte cell lines expressing varying levels of cFLIP(L). Functional analysis revealed that relative cFLIP(L) levels correlated with apoptosis resistance to TRAIL. Surprisingly, cFLIP(L) specifically blocked TRAIL-induced NF-kappaB activation and TRAIL-dependent induction of the proinflammatory target gene interleukin-8. Biochemical characterization of the signaling pathways involved showed that apoptosis signaling was inhibited at the DISC in cFLIP(L)-overexpressing keratinocytes, although cFLIP(L) did not significantly impair enzymatic activity of the receptor complex. In contrast, recruitment and modification of receptor-interacting protein was blocked in cFLIP(L)-overexpressing cells. Taken together, our data demonstrate that cFLIP(L) is not only a central antiapoptotic modulator of TRAIL-mediated apoptosis but also an inhibitor of TRAIL-induced NF-kappaB activation and subsequent proinflammatory target gene expression. Hence, cFLIP(L) modulation in keratinocytes may not only influence apoptosis sensitivity but may also lead to altered death receptor-dependent skin inflammation

Dual targeting of HER3 and MEK may overcome HER3-dependent drug-resistance of colon cancers

Although the medical treatment of colorectal cancer has evolved greatly in the last years, a significant portion of early-stage patients develops recurrence after therapies. The current clinical trials are directed to evaluate new drug combinations and treatment schedules. By the use of patient-derived or established colon cancer cell lines, we found that the tyrosine kinase receptor HER3 is involved in the mechanisms of resistance to therapies. In agreement, the immunohistochemical analysis of total and phospho-HER3 expression in 185 colorectal cancer specimens revealed a significant correlation with lower disease-free survival. Targeting HER3 by the use of the monoclonal antibody patritumab we found induction of growth arrest in all cell lines. Despite the high efficiency of patritumab in abrogating the HER3-dependent activation of PI3K pathway, the HER2 and EGFR-dependent MAPK pathway is activated as a compensatory mechanism. Interestingly, we found that the MEK-inhibitor trametinib inhibits, as expected, the MAPK pathway but induces the HER3-dependent activation of PI3K pathway. The combined treatment results in the abrogation of both PI3K and MAPK pathways and in a significant reduction of cell proliferation and survival. These data suggest a new strategy of therapy for HER3-overexpressing colon cancers

Targeting Phosphatases and Kinases: How to Checkmate Cancer

Metastatic disease represents the major cause of death in oncologic patients worldwide. Accumulating evidence have highlighted the relevance of a small population of cancer cells, named cancer stem cells (CSCs), in the resistance to therapies, as well as cancer recurrence and metastasis. Standard anti-cancer treatments are not always conclusively curative, posing an urgent need to discover new targets for an effective therapy. Kinases and phosphatases are implicated in many cellular processes, such as proliferation, differentiation and oncogenic transformation. These proteins are crucial regulators of intracellular signaling pathways mediating multiple cellular activities. Therefore, alterations in kinases and phosphatases functionality is a hallmark of cancer. Notwithstanding the role of kinases and phosphatases in cancer has been widely investigated, their aberrant activation in the compartment of CSCs is nowadays being explored as new potential Achille’s heel to strike. Here, we provide a comprehensive overview of the major protein kinases and phosphatases pathways by which CSCs can evade normal physiological constraints on survival, growth, and invasion. Moreover, we discuss the potential of inhibitors of these proteins in counteracting CSCs expansion during cancer development and progression