Butcher & Oemler Cluster A2111: A Head-on Merger at z = 0.23

We present ROSAT PSPC and HRI observations of A2111, the richest galaxy cluster photometrically surveyed by Butcher & Oemler (1984). The cluster contains a distinct comet-shaped X-ray subcomponent, which appears hotter than the rest of the cluster. The galaxy and X-ray surface brightness distributions of the cluster show a similarly elongated morphology. These results suggest that the cluster is undergoing a head-on subcluster merger. This merger may also be responsible for the high fraction of gas-rich blue galaxies observed in the cluster. We have further detected a poor cluster along the merging axis and at a projected distance of about 5 Mpc from A2111.Comment: To be published in MNRAS, 16 pages, plus 13 figures in the GIF or jpeg format (uuencoded). Black & white postscript files of the figures are available at http://www.astro.nwu.edu/astro/wqd/paper/a2111

High-dimensional quantum cryptography with twisted light

Quantum key distributions (QKD) systems often rely on polarization of light for encoding, thus limiting the amount of information that can be sent per photon and placing tight bounds on the error that such a system can tolerate. Here we describe a proof-of-principle experiment that indicates the feasibility of high-dimensional QKD based on the transverse structure of the light field, allowing for the transfer of more than 1 bit per photon. Our implementation uses the orbital angular momentum (OAM) of photons and the corresponding mutually unbiased basis of angular position (ANG). Our experiment uses a digital micro-mirror device for the rapid generation of OAM and ANG modes at 4 kHz, and a mode sorter capable of sorting single photons based on their OAM and ANG content with a separation efficiency of 93\%. Through the use of a 7-dimensional alphabet encoded in the OAM and ANG bases, we achieve a channel capacity of 2.05 bits per sifted photon. Our experiment shows that, in addition to having an increased information capacity, QKD systems based on spatial-mode encoding will be more tolerant to errors and thus more robust against eavesdropping attacks

Experimental Analysis of Nonlinear Impairments in Fibre Optic Transmission Systems up to 7.3 THz

An effective way of increasing the overall optical fibre capacity is by expanding the bandwidth used to transmit signals. In this paper, the impact of expanding the transmission bandwidth on the optical communication system is experimentally studied using the achievable rates as a performance metric. The trade-offs between the use of larger bandwidths and higher nonlinear interference (NLI) noise is experimentally and theoretically analysed. The growth of NLI noise is investigated for spectral bandwidths from 40 GHz up to 7.3 THz using 64-QAM and Nyquist pulse-shaping. Experimental results are shown to be in line with the predictions from the Gaussian- Noise model showing a logarithmic growth in NLI noise as the signal bandwidth is extended. A reduction of the information rate of only 10% was found between linear and non-linear transmission across several transmission bandwidths, all the way up to 7.3 THz. Finally, the power transfer between channels due to stimulated Raman scattering effect is analysed showing up to 2 dB power tilt at optimum power for the largest transmitted bandwidth of 7.3 THz

4 X 20 Gbit/s mode division multiplexing over free space using vector modes and a q-plate mode (de)multiplexer

Vector modes are spatial modes that have spatially inhomogeneous states of polarization, such as, radial and azimuthal polarization. They can produce smaller spot sizes and stronger longitudinal polarization components upon focusing. As a result, they are used for many applications, including optical trapping and nanoscale imaging. In this work, vector modes are used to increase the information capacity of free space optical communication via the method of optical communication referred to as mode division multiplexing. A mode (de)multiplexer for vector modes based on a liquid crystal technology referred to as a q-plate is introduced. As a proof of principle, using the mode (de)multiplexer four vector modes each carrying a 20 Gbit/s quadrature phase shift keying signal on a single wavelength channel (~1550nm), comprising an aggregate 80 Gbit/s, were transmitted ~1m over the lab table with <-16.4 dB (<2%) mode crosstalk. Bit error rates for all vector modes were measured at the forward error correction threshold with power penalties < 3.41dB

Abnormal molecular signatures of inflammation, energy metabolism, and vesicle biology in human Huntington disease peripheral tissues

BACKGROUND: A major challenge in neurodegenerative diseases concerns identifying biological disease signatures that track with disease progression or respond to an intervention. Several clinical trials in Huntington disease (HD), an inherited, progressive neurodegenerative disease, are currently ongoing. Therefore, we examine whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in HD patients. RESULTS: We generate large, high-quality human datasets from skeletal muscle, skin and adipose tissue to probe molecular changes in human premanifest and early manifest HD patients—those most likely involved in clinical trials. The analysis of the transcriptomics and proteomics data shows robust, stage-dependent dysregulation. Gene ontology analysis confirms the involvement of inflammation and energy metabolism in peripheral HD pathogenesis. Furthermore, we observe changes in the homeostasis of extracellular vesicles, where we find consistent changes of genes and proteins involved in this process. In-depth single nucleotide polymorphism data across the HTT gene are derived from the generated primary cell lines. CONCLUSIONS: Our ‘omics data document the involvement of inflammation, energy metabolism, and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials. The generated data, complemented by the primary cell lines established from peripheral tissues, and a large panel of iPSC lines that can serve as human models of HD are a valuable and unique resource to advance the current understanding of molecular mechanisms driving HD pathogenesis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13059-022-02752-5

Study protocol : E-freeze-freezing of embryos in assisted conception: A randomised controlled trial evaluating the clinical and cost effectiveness of a policy of freezing embryos followed by thawed frozen embryo transfer compared with a policy of fresh embryo transfer, in women undergoing in vitro fertilisation

Acknowledgements The E-Freeze Collaborators Group contributed to the overall design of the E-Freeze trial. Funding The trial is approved and funded by the National Institute of Health Research (NIHR) Health Technology Assessment (HTA) programme. Availability of data and materials Applications for data sharing should be made to the NPEU CTU, using [email protected], with an accompanying protocol for the intended use of the data. This will be reviewed by the Trial Steering Committee if still operational or Data Sharing Committee/Data Controller. If approved, a Data Sharing Agreement will be compiled laying out the conditions to which the requestor must abide. Protocol E-Freeze Protocol, Version 2.0 (18/01/2017). Author notes All authors contributed equally to this work.Peer reviewedPublisher PD

Prolyl-4-hydroxylase 3 maintains β-cell glucose metabolism during fatty acid excess in mice

The α-ketoglutarate–dependent dioxygenase, prolyl-4-hydroxylase 3 (PHD3), is an HIF target that uses molecular oxygen to hydroxylate peptidyl prolyl residues. Although PHD3 has been reported to influence cancer cell metabolism and liver insulin sensitivity, relatively little is known about the effects of this highly conserved enzyme in insulin-secreting β cells in vivo. Here, we show that the deletion of PHD3 specifically in β cells (βPHD3KO) was associated with impaired glucose homeostasis in mice fed a high-fat diet. In the early stages of dietary fat excess, βPHD3KO islets energetically rewired, leading to defects in the management of pyruvate fate and a shift from glycolysis to increased fatty acid oxidation (FAO). However, under more prolonged metabolic stress, this switch to preferential FAO in βPHD3KO islets was associated with impaired glucose-stimulated ATP/ADP rises, Ca(2+) fluxes, and insulin secretion. Thus, PHD3 might be a pivotal component of the β cell glucose metabolism machinery in mice by suppressing the use of fatty acids as a primary fuel source during the early phases of metabolic stress