Paired carriers as a way to reduce quantum noise of multi-carrier gravitational-wave detectors

We explore new regimes of laser interferometric gravitational-wave detectors with multiple optical carriers which allow to reduce the quantum noise of these detectors. In particular, we show that using two carriers with the opposite detunings, homodyne angles, and squeezing angles, but identical other parameters (the antisymmetric carriers), one can suppress the quantum noise in such a way that its spectrum follows the Standard Quantum Limit (SQL) at low frequencies. Relaxing this antisymmetry condition, it is also possible to slightly overcome the SQL in broadband. Combining several such pairs in the xylophone configuration, it is possible to shape the quantum noise spectrum flexibly

Quantum back-action in measurements of zero-point mechanical oscillations

Measurement-induced back action, a direct consequence of the Heisenberg Uncertainty Principle, is the defining feature of quantum measurements. We use quantum measurement theory to analyze the recent experiment of Safavi-Naeini et al. [Phys. Rev. Lett. {\bf 108}, 033602 (2012)], and show that results of this experiment not only characterize the zero-point fluctuation of a near-ground-state nanomechanical oscillator, but also demonstrate the existence of quantum back-action noise --- through correlations that exist between sensing noise and back-action noise. These correlations arise from the quantum coherence between the mechanical oscillator and the measuring device, which build up during the measurement process, and are key to improving sensitivities beyond the Standard Quantum Limit.Comment: 11 pages and 4 figure

Advanced quantum techniques for future gravitational-wave detectors

Quantum fluctuation of light limits the sensitivity of advanced laser interferometric gravitational-wave detectors. It is one of the principal obstacles on the way towards the next-generation gravitational-wave observatories. The envisioned significant improvement of the detector sensitivity requires using quantum non-demolition measurement and back-action evasion techniques, which allow us to circumvent the sensitivity limit imposed by the Heisenberg uncertainty principle. In our previous review article (Danilishin and Khalili in Living Rev Relativ 15:5, 2012), we laid down the basic principles of quantum measurement theory and provided the framework for analysing the quantum noise of interferometers. The scope of this paper is to review novel techniques for quantum noise suppression proposed in the recent years and put them in the same framework. Our delineation of interferometry schemes and topologies is intended as an aid in the process of selecting the design for the next-generation gravitational-wave observatories. © 2019, The Author(s)

Endogenous BDNF augments NMDA receptor phosphorylation in the spinal cord via PLCγ, PKC, and PI3K/Akt pathways during colitis

Background Spinal central sensitization is an important process in the generation and maintenance of visceral hypersensitivity. The release of brain-derived neurotrophic factor (BDNF) from the primary afferent neurons to the spinal cord contributes to spinal neuronal plasticity and increases neuronal activity and synaptic efficacy. The N-Methyl-D-aspartic acid (NMDA) receptor possesses ion channel properties, and its activity is modulated by phosphorylation of its subunits including the NMDA receptor 1 (NR1). Methods Colonic inflammation was induced by a single dose of intracolonic instillation of tri-nitrobenzene sulfonic acid (TNBS). NR1 phosphorylation by BDNF in vivo and in culture was examined by western blot and immunohistochemistry. Signal transduction was studied by direct examination and use of specific inhibitors. Results During colitis, the level of NR1 phospho-Ser896 was increased in the dorsal horn region of the L1 and S1 spinal cord; this increase was attenuated by injection of BDNF neutralizing antibody to colitic animals (36 μg/kg, intravenous (i.v.)) and was also reduced in BDNF+/− rat treated with TNBS. Signal transduction examination showed that the extracellular signal-regulated kinase (ERK) activation was not involved in BDNF-induced NR1 phosphorylation. In contrast, the phosphatidylinositol 3-kinase (PI3K)/Akt pathway mediated BDNF-induced NR1 phosphorylation in vivo and in culture; this is an additional pathway to the phospholipase C-gamma (PLCγ) and the protein kinase C (PKC) that was widely considered to phosphorylate NR1 at Ser896. In spinal cord culture, the inhibitors to PLC (U73122), PKC (bisindolylmaleimide I), and PI3K (LY294002), but not MEK (PD98059) blocked BDNF-induced NR1 phosphorylation. In animals with colitis, treatment with LY294002 (50 μg/kg, i.v.) blocked the Akt activity as well as NR1 phosphorylation at Ser896 in the spinal cord. Conclusion BDNF participates in colitis-induced spinal central sensitization by up-regulating NR1 phosphorylation at Ser896. The PI3K/Akt pathway, in addition to PLCγ and PKC, mediates BDNF action in the spinal cord during colitis