University of Glasgow

About: University of Glasgow is a education organization based out in Glasgow, United Kingdom. It is known for research contribution in the topics: Population & Context (language use). The organization has 40355 authors who have published 98254 publications receiving 3815419 citations. The organization is also known as: Glasgow University & Glasgow Uni.

100 Tbit/s free-space data link enabled by three-dimensional multiplexing of orbital angular momentum, polarization, and wavelength

Abstract: We investigate the orthogonality of orbital angular momentum (OAM) with other multiplexing domains and present a free-space data link that uniquely combines OAM-, polarization-, and wavelength-division multiplexing. Specifically, we demonstrate the multiplexing/demultiplexing of 1008 data channels carried on 12 OAM beams, 2 polarizations, and 42 wavelengths. Each channel is encoded with 100 Gbit/s quadrature phase-shift keying data, providing an aggregate capacity of 100.8 Tbit/s (12×2×42×100 Gbit/s).

Evolution in Economic Geography: Institutions, Political Economy, and Adaptation

Abstract: Economic geography has, over the past decade or so, drawn upon ideas from evolutionary economics in trying to understand processes of regional growth and change. Recently, some researchers have sought to delimit and develop an “evolutionary economic geography” (EEG), aiming to create a more systematic theoretical framework for research. This article provides a sympathetic critique and elaboration of this emergent EEG but takes issue with some aspects of its characterization in recent programmatic statements. While acknowledging that EEG is an evolving and pluralist project, we are concerned that the reliance on certain theoretical frameworks that are imported from evolutionary economics and complexity science threatens to isolate it from other approaches in economic geography, limiting the opportunities for cross-fertilization. In response, the article seeks to develop a social and pluralist conception of institutions and social agency in EEG, drawing upon the writings of leading institutional eco...

A short cut to deforestation

Abstract: Lists are often used as “glue” to connect separate parts of a program together. We propose an automatic technique for improving the efficiency of such programs, by removing many of these intermediate lists, based on a single, simple, local transformation. We have implemented the method in the Glasgow Haskell compiler.

Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape

Abstract: Senescence is a stable proliferation arrest, associated with an altered secretory pathway, thought to promote tumor suppression and tissue aging. While chromatin regulation and lamin B1 down-regulation have been implicated as senescence effectors, functional interactions between them are poorly understood. We compared genome-wide Lys4 trimethylation on histone H3 (H3K4me3) and H3K27me3 distributions between proliferating and senescent human cells and found dramatic differences in senescence, including large-scale domains of H3K4me3- and H3K27me3-enriched “mesas” and H3K27me3-depleted “canyons.” Mesas form at lamin B1-associated domains (LADs) in replicative senescence and oncogene-induced senescence and overlap DNA hypomethylation regions in cancer, suggesting that pre-malignant senescent chromatin changes foreshadow epigenetic cancer changes. Hutchinson-Gilford progeria syndrome fibroblasts (mutant lamin A) also show evidence of H3K4me3 mesas, suggesting a link between premature chromatin changes and accelerated cell senescence. Canyons mostly form between LADs and are enriched in genes and enhancers. H3K27me3 loss is correlated with up-regulation of key senescence genes, indicating a link between global chromatin changes and local gene expression regulation. Lamin B1 reduction in proliferating cells triggers senescence and formation of mesas and canyons. Our data illustrate profound chromatin reorganization during senescence and suggest that lamin B1 down-regulation in senescence is a key trigger of global and local chromatin changes that impact gene expression, aging, and cancer.