Mid-infrared quantum optics in silicon

Applied quantum optics stands to revolutionise many aspects of information technology, provided performance can be maintained when scaled up. Silicon quantum photonics satisfies the scaling requirements of miniaturisation and manufacturability, but at 1.55 $\mu$m it suffers from unacceptable linear and nonlinear loss. Here we show that, by translating silicon quantum photonics to the mid-infrared, a new quantum optics platform is created which can simultaneously maximise manufacturability and miniaturisation, while minimising loss. We demonstrate the necessary platform components: photon-pair generation, single-photon detection, and high-visibility quantum interference, all at wavelengths beyond 2 $\mu$m. Across various regimes, we observe a maximum net coincidence rate of 448 $\pm$ 12 Hz, a coincidence-to-accidental ratio of 25.7 $\pm$ 1.1, and, a net two photon quantum interference visibility of 0.993 $\pm$ 0.017. Mid-infrared silicon quantum photonics will bring new quantum applications within reach.Comment: 8 pages, 4 figures; revised figures, updated discussion in section 3, typos corrected, added referenc

High-performance, adiabatically nanotapered fibre-chip couplers in silicon at 2 microns wavelength

Fibre optic technology connects the world through the Internet, enables remote sensing, and connects disparate functional optical devices. Highly confined silicon photonics promises extreme scale and functional integration. However, the optical modes of silicon nanowire waveguides and optical fibres are very different, making efficient fibre-chip coupling a challenge. Vertical grating couplers, the dominant coupling method today, have limited optical bandwidth and are naturally out-of-plane. Here we demonstrate a new method that is low-loss, broadband, easily manufacturable, and naturally planar. We adiabatically couple a tapering silicon nanowire waveguide to a conic nanotapered optical fibre, measuring transmission between 2.0 and 2.2 micron wavelength. The silicon chip is fabricated at a commercial foundry and then post-processed to release the tapering nanowires. We estimate an optimal per-coupler transmission of -0.48 dB (maximum; 95% confidence interval [+0.46, -1.68] dB) and a 1-dB bandwidth of 295 nm . With automated measurements, we quantify the device tolerance to lateral misalignment, measuring a flat response within +/- 0.968 micron. This design can enable low-loss modular systems of integrated photonics irrespective of material and waveband.Comment: 6 pages, 3 figure

Safety outcomes during pediatric GH therapy: final results from the prospective GeNeSIS observational program

CONTEXT: Safety concerns regarding premature mortality, diabetes, neoplasia and cerebrovascular disease in association with growth hormone (GH) therapy have been raised. OBJECTIVE: To assess incidence of key safety outcomes. DESIGN: Prospective, multinational, observational study (1999-2015). SETTING: 22,311 GH-treated children from 827 investigative sites in 30 countries. PATIENTS: Children with growth disorders. INTERVENTIONS: GH treatment. MAIN OUTCOME MEASURES: Standardized mortality (SMR) and incidence (SIR) ratios with 95% confidence intervals (CI) for mortality, diabetes, and primary cancer, using general population registries. RESULTS: Predominant short stature diagnoses were GH deficiency (63%), idiopathic short stature (13%), and Turner syndrome (8%), with mean±SD follow-up of 4.2±3.2 years (∼92,000 person-years [PY]). Forty-two deaths occurred in patients with follow-up, with SMR (95% CI) of 0.61 (0.44-0.82); the SMR was elevated for patients with cancer-related organic GH deficiency (5.87 [3.21-9.85]). Based on 18 cases, Type 2 diabetes (T2DM) risk was elevated (SIR 3.77 [2.24-5.96]), but 72% had risk factors. In patients without cancer history, 14 primary cancers were observed (SIR 0.71 [0.39-1.20]). Second neoplasms occurred in 31/622 (5.0%) cancer survivors (10.7 [7.5-15.2] cases/1000 PY), and intracranial tumor recurrences in 67/823 (8.1%) tumor survivors (16.9 [13.3-21.5] cases/1000 PY). All 3 hemorrhagic stroke cases had risk factors. CONCLUSIONS: GeNeSIS data support the favourable safety profile of pediatric GH treatment. Overall risk for death or primary cancer was not elevated in GH-treated children, and no hemorrhagic strokes occurred in patients without risk factors. T2DM incidence was elevated compared to the general population, but most cases had diabetes risk factors

Complement C3 Inhibitor Pegcetacoplan for Geographic Atrophy Secondary to Age-Related Macular Degeneration : A Randomized Phase 2 Trial

Copyright © 2019 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.Peer reviewedPublisher PD

Prime movers : mechanochemistry of mitotic kinesins

Mitotic spindles are self-organizing protein machines that harness teams of multiple force generators to drive chromosome segregation. Kinesins are key members of these force-generating teams. Different kinesins walk directionally along dynamic microtubules, anchor, crosslink, align and sort microtubules into polarized bundles, and influence microtubule dynamics by interacting with microtubule tips. The mechanochemical mechanisms of these kinesins are specialized to enable each type to make a specific contribution to spindle self-organization and chromosome segregation

Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents

<p>Abstract</p> <p>Background</p> <p>Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency. These levels in rats increase sigmoidally with increasing dietary Se and reach defined plateaus at the Se requirement, making them sensitive biomarkers for Se deficiency. These levels, however, do not further increase with super-nutritional or toxic Se status, making them ineffective for detection of high Se status. Biomarkers for high Se status are needed as super-nutritional Se intakes are associated with beneficial as well as adverse health outcomes. To characterize Se regulation of the transcriptome, we conducted 3 microarray experiments in weanling mice and rats fed Se-deficient diets supplemented with up to 5 μg Se/g diet.</p> <p>Results</p> <p>There was no effect of Se status on growth of mice fed 0 to 0.2 μg Se/g diet or rats fed 0 to 2 μg Se/g diet, but rats fed 5 μg Se/g diet showed a 23% decrease in growth and elevated plasma alanine aminotransferase activity, indicating Se toxicity. Rats fed 5 μg Se/g diet had significantly altered expression of 1193 liver transcripts, whereas mice or rats fed ≤ 2 μg Se/g diet had < 10 transcripts significantly altered relative to Se-adequate animals within an experiment. Functional analysis of genes altered by Se toxicity showed enrichment in cell movement/morphogenesis, extracellular matrix, and development/angiogenesis processes. Genes up-regulated by Se deficiency were targets of the stress response transcription factor, Nrf2. Multiple regression analysis of transcripts significantly altered by 2 μg Se/g and Se-deficient diets identified an 11-transcript biomarker panel that accounted for 99% of the variation in liver Se concentration over the full range from 0 to 5 μg Se/g diet.</p> <p>Conclusion</p> <p>This study shows that Se toxicity (5 μg Se/g diet) in rats vastly alters the liver transcriptome whereas Se-deficiency or high but non-toxic Se intake elicits relatively few changes. This is the first evidence that a vastly expanded number of transcriptional changes itself can be a biomarker of Se toxicity, and that identified transcripts can be used to develop molecular biomarker panels that accurately predict super-nutritional and toxic Se status.</p