Divergence-free approach for obtaining decompositions of quantum-optical processes

Operator-sum representations of quantum channels can be obtained by applying the channel to one subsystem of a maximally entangled state and deploying the channel-state isomorphism. However, for continuous-variable systems, such schemes contain natural divergences since the maximally entangled state is ill-defined. We introduce a method that avoids such divergences by utilizing finitely entangled (squeezed) states and then taking the limit of arbitrary large squeezing. Using this method we derive an operator-sum representation for all single-mode bosonic Gaussian channels where a unique feature is that both quantum-limited and noisy channels are treated on an equal footing. This technique facilitates a proof that the rank-one Kraus decomposition for Gaussian channels at its respective entanglement-breaking thresholds, obtained in the overcomplete coherent state basis, is unique. The methods could have applications to simulation of continuous-variable channels.Comment: 18 pages (8 + appendices), 4 figs. V2: close to published version, dropped Sec.VI of v1 to be expanded elsewher

Direct ultrafast laser written C-band waveguide amplifier in Er-doped chalcogenide glass

This paper reports the fabrication and characterization of an ultrafast laser written Er-doped chalcogenide glass buried waveguide amplifier; Er-doped GeGaS glass has been synthesized by the vacuum sealed melt quenching technique. Waveguides have been fabricated inside the 4 mm long sample by direct ultrafast laser writing. The total passive fiber-to-fiber insertion loss is 2.58 +/- 0.02 dB at 1600 nm, including a propagation loss of 1.6 +/- 0.3 dB. Active characterization shows a relative gain of 2.524 +/- 0.002 dB/cm and 1.359 +/- 0.005 dB/cm at 1541 nm and 1550 nm respectively, for a pump power of 500 mW at a wavelength of 980 nm. (C) 2012 Optical Society of Americ

Regarding High Intensity Interval Training and Left Ventricular Mechanics

The influence of exercise on the mechanical function of the heart has become a topic of considerable interest over recent decades. In a recent issue of Medicine and Science in Sports and Exercise, Huang et al. (2) published a study that investigated the effects of high intensity interval training (HIIT) on echocardiographic-derived indices of left ventricular (LV) mechanical function in young, sedentary but otherwise healthy men. We believe that this study has the potential to further our understanding on how the heart responds to exercise, and it ultimately fits within the current knowledge on exercise-induced cardiac adaptation in health and disease (4). However, given the proposed conclusions, we would appreciate additional details from the authors on the methodology used that may have contributed to some unusual results. Specifically, this letter serves to highlight our concerns regarding the two most notable findings reported in the paper by Huang et al (2), namely 1) the unusually large increase in cardiorespiratory fitness following the HIIT intervention, and 2) the exceptionally low values derived from speckle tracking echocardiography

Physical properties of blood are altered in young and lean women with polycystic ovary syndrome

Classic features of polycystic ovary syndrome (PCOS) include derangement of metabolic and cardiovascular health, and vascular dysfunction is commonly reported. These comorbidities indicate impaired blood flow; however, other than limited reports of increased plasma viscosity, surprisingly little is known regarding the physical properties of blood in PCOS. We aimed to investigate whether haemorheology was impaired in women with PCOS. We thus measured a comprehensive haemorheological profile, in a case-control design, of lean women with PCOS and age-matched healthy controls. A clinical examination determined similar cardiovascular risk for the two groups. Whole blood and plasma viscosity was measured using a cone-plate viscometer. The magnitude and rate of red blood cell (RBC) aggregation was determined using a light-transmission aggregometer, and the degree of RBC deformability was measured via laser-diffraction ektacytometry. Plasma viscosity was significantly increased in women with PCOS. Blood viscosity was also increased for PCOS at lower-to-moderate shear rates in both native and standardised haematocrit samples. The magnitude of RBC aggregation–a primary determinant of low-shear blood viscosity–was significantly increased in PCOS at native and 0.4 L·L(-1) haematocrit. No difference was detected between PCOS and CON groups for RBC deformability measurements. A novel measure indicating the effectiveness of oxygen transport by RBC (i.e., the haematocrit-to-viscosity ratio; HVR) was decreased at all shear rates in women with PCOS. In a group of young and lean women with PCOS with an unremarkable cardiovascular risk profile based on clinical data, significant haemorheological impairment was observed. The degree of haemorheological derangement observed in the present study reflects that of overt chronic disease, and provides an avenue for future therapeutic intervention in PCOS

ERK Phosphorylates p66shcA on Ser36 and Subsequently Regulates p27^kip1 Expression via the Akt-FOXO3a Pathway: Implication of p27^kip1 in Cell Response to Oxidative Stress

Mice deficient for p66shcA represent an animal model to link oxidative stress and aging. p66shcA is implicated in oxidative stress response and mitogenic signaling. Phosphorylation of p66shcA on Ser36 is critical for its function in oxidative stress response. Here we report the identification of ERK as the kinase phosphorylating p66shcA on Ser36. Activation of ERKs was necessary and sufficient for Ser36 phosphorylation. p66shcA interacted with ERK and was demonstrated to be a substrate for ERK, with Ser36 being the major phosphorylation site. Furthermore, in response to H2O2, inhibition of ERK activation repressed p66shcA-dependent phosphorylation of FOXO3a and the down-regulation of its target gene p27kip1. Down-regulation of p27 might promote cell survival, as p27 played a proapoptotic role in oxidative stress response. As a feedback regulation, Ser36 phosphorylated p66shcA attenuated H2O2-induced ERK activation, whereas p52/46shcA facilitated ERK activation, which required tyrosine phosphorylation of CH1 domain. p66shcA formed a complex with p52/46ShcA, which may provide a platform for efficient signal propagation. Taken together, the data suggest there exists an interplay between ERK and ShcA proteins, which modulates the expression of p27 and cell response to oxidative stress