Key enabling technologies for optical communications at 2000 nm.

This paper discusses the potential for opening a new wavelength window at the 2 µm waveband for optical communications, showing current limitations of the system's performance. It focuses on novel results for key enabling technologies, including the analysis of laser injection locking at this waveband, an improved responsivity for bulk and strained InGaAs edge-couple detectors, and also an increased gain profile for thulium-doped fiber amplifiers.

Dense WDM transmission at 2 µm enabled by an arrayed waveguide grating.

We show, for the first time, dense WDM (8×20 Gbit/s) transmission at 2 µm enabled by advanced modulation formats (4-ASK Fast-OFDM) and the development of key components, including a new arrayed waveguide grating (AWGr) at 2 µm. The AWGr shows -12.8±1.78 dB of excess loss with an 18-dB extinction ratio and a thermal tunability of 0.108 nm/°C.

100 Gbit/s WDM transmission at 2 µm: transmission studies in both low-loss hollow core photonic bandgap fiber and solid core fiber.

We show for the first time 100 Gbit/s total capacity at 2 µm waveband, using 4 × 9.3 Gbit/s 4-ASK Fast-OFDM direct modulation and 4 × 15.7 Gbit/s NRZ-OOK external modulation, spanning a 36.3 nm wide wavelength range. WDM transmission was successfully demonstrated over 1.15 km of low-loss hollow core photonic bandgap fiber (HC-PBGF) and over 1 km of solid core fiber (SCF). We conclude that the OSNR penalty associated with the SCF is minimal, while a ~1-2 dB penalty was observed after the HC-PBGF probably due to mode coupling to higher-order modes.

Staphylococcus epidermidis serine--aspartate repeat protein G (SdrG) binds to osteoblast integrin alpha V beta 3.

Staphylococcus epidermidis is the leading etiologic agent of orthopaedic implant infection. Contamination of the implanted device during insertion allows bacteria gain entry into the sterile bone environment leading to condition known as osteomyelitis. Osteomyelitis is characterised by weakened bones associated with progressive bone loss. The mechanism through which S. epidermidis interacts with bone cells to cause osteomyelitis is poorly understood. We demonstrate here that S. epidermidis can bind to osteoblasts in the absence of matrix proteins. S. epidermidis strains lacking the cell wall protein SdrG had a significantly reduced ability to bind to osteoblasts. Consistent with this, expression of SdrG in Lactococcus lactis resulted in significantly increased binding to the osteoblasts. Protein analysis identified that SdrG contains a potential integrin recognition motif. αVß3 is a major integrin expressed on osteoblasts and typically recognises RGD motifs in its ligands. Our results demonstrate that S. epidermidis binds to recombinant purified αVß3, and that a mutant lacking SdrG failed to bind. Blocking αVß3 on osteoblasts significantly reduced binding to S. epidermidis. These studies are the first to identify a mechanism through which S. epidermidis binds to osteoblasts and potentially offers a mechanism through which implant infection caused by S. epidermidis leads to osteomyelitis.

Calcium regulation of oxidative phosphorylation in rat skeletal muscle mitochondria.

Activation of oxidative phosphorylation by physiological levels of calcium in mitochondria from rat skeletal muscle was analysed using top-down elasticity and regulation analysis. Oxidative phosphorylation was conceptually divided into three subsystems (substrate oxidation, proton leak and phosphorylation) connected by the membrane potential or the protonmotive force. Calcium directly activated the phosphorylation subsystem and (with sub-saturating 2-oxoglutarate) the substrate oxidation subsystem but had no effect on the proton leak kinetics. The response of mitochondria respiring on 2-oxoglutarate at two physiological concentrations of free calcium was quantified using control and regulation analysis. The partial integrated response coefficients showed that direct stimulation of substrate oxidation contributed 86% of the effect of calcium on state 3 oxygen consumption, and direct activation of the phosphorylation reactions caused 37% of the increase in phosphorylation flux. Calcium directly activated phosphorylation more strongly than substrate oxidation (78% compared to 45%) to achieve homeostasis of mitochondrial membrane potential during large increases in flux.