Experimental demonstration of adaptive digital monitoring and compensation of chromatic dispersion for coherent DP-QPSK receiver

We experimentally demonstrate a digital signal processing (DSP)-based optical performance monitoring (OPM) algorithm for inservice monitoring of chromatic dispersion (CD) in coherent transport networks. Dispersion accumulated in 40 Gbit/s QPSK signal after 80 km of fiber transmission is successfully monitored and automatically compensated without prior knowledge of fiber dispersion coefficient. Four different metrics for assessing CD mitigation are implemented and simultaneously verified proving to have high estimation accuracy. No observable penalty is measured when the monitoring module drives an adaptive digital CD equalizer. © 2011 Optical Society of America

High phase noise tolerant pilot-tone-aided DP-QPSK optical communication systems

In this paper we experimentally demonstrate a novel, high phase-noise tolerant, optical dual polarization (DP) quadrature phase-shift keying (QPSK) communication system based on pilot-tone-aided phase noise cancellation (PNC) algorithm. Vertical cavity surface emitting lasers (VCSELs) with approximate 300 MHz linewidth are used as transmitters and local oscillators for coherent detection of optical DP-QPSK signals. The proposed system, with central wavelength at 1540.68 nm, operates at 40 Gb/s over 80 km single mode fiber (SMF) as part of a passive optical network (PON). The deployment of pilot-tone-aided PNC algorithm guarantees a bit error rate (BER) performance below the forward error correction (FEC) threshold. Moreover, we also evaluate a novel digital signal processing (DSP) algorithm for adaptive pilot tone detection

Mycobacterium tuberculosis Eis Regulates Autophagy, Inflammation, and Cell Death through Redox-dependent Signaling

The “enhanced intracellular survival” (eis) gene of Mycobacterium tuberculosis (Mtb) is involved in the intracellular survival of M. smegmatis. However, its exact effects on host cell function remain elusive. We herein report that Mtb Eis plays essential roles in modulating macrophage autophagy, inflammatory responses, and cell death via a reactive oxygen species (ROS)-dependent pathway. Macrophages infected with an Mtb eis-deletion mutant H37Rv (Mtb-Δeis) displayed markedly increased accumulation of massive autophagic vacuoles and formation of autophagosomes in vitro and in vivo. Infection of macrophages with Mtb-Δeis increased the production of tumor necrosis factor-α and interleukin-6 over the levels produced by infection with wild-type or complemented strains. Elevated ROS generation in macrophages infected with Mtb-Δeis (for which NADPH oxidase and mitochondria were largely responsible) rendered the cells highly sensitive to autophagy activation and cytokine production. Despite considerable activation of autophagy and proinflammatory responses, macrophages infected with Mtb-Δeis underwent caspase-independent cell death. This cell death was significantly inhibited by blockade of autophagy and c-Jun N-terminal kinase-ROS signaling, suggesting that excessive autophagy and oxidative stress are detrimental to cell survival. Finally, artificial over-expression of Eis or pretreatment with recombinant Eis abrogated production of both ROS and proinflammatory cytokines, which depends on the N-acetyltransferase domain of the Eis protein. Collectively, these data indicate that Mtb Eis suppresses host innate immune defenses by modulating autophagy, inflammation, and cell death in a redox-dependent manner

Loneliness and biological responses to acute stress in people with Type 2 diabetes

Loneliness is linked with all-cause mortality and coronary heart disease. Altered neuroendocrine and inflammatory responses to stress constitute potential pathways linking loneliness and ill-health. Stress responsivity is modified in people with Type 2 diabetes, but it is unclear whether loneliness influences biological stress responses in this population. We assessed interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1RA), monocyte chemoattractant protein-1 (MCP-1), and cortisol responses to acute stress in 135 people with Type 2 diabetes. Loneliness was measured used the Revised UCLA Loneliness Scale. Loneliness was inversely associated with cortisol output poststress (B = -4.429, p = 0.019) independent of age, sex, education, marital status, body mass index, and smoking. Lonelier individuals had raised MCP-1 concentrations 75 min poststress independent of covariates (B = 0.713, p = 0.022). No associations between loneliness and IL-6 or IL-1RA concentrations were detected. These results suggest that loneliness is associated with disturbances in stress responsivity in people with diabetes, and the impact of loneliness on health in people with diabetes may be mediated in part through dysregulation of inflammatory and neuroendocrine systems. Future research is required to understand if such changes increase the risk of poorer outcomes in this population

Diabetes, oxidative stress and therapeutic strategies

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