Luminous Intensity for Traffic Signals: A Scientific Basis for Performance Specifications

Humnan factors experiments on visual responses to simulated traffic signals using incandescent lamps and light-emitting diodes are described

Release of dissolved organic carbon from seagrass wrack and its implications for trophic connectivity

ABSTRACT: The export of old leaves and stems (wrack) from seagrass meadows provides a mechanism for trophic connectivity among coastal ecosystems. As little of this wrack is consumed by mesograzers, leached dissolved organic carbon (DOC) may determine the importance of wrack as a trophic subsidy. However, few studies have examined the effect of seagrass type or age on the release of DOC or its bioavailability. We examined the amount and composition of DOC released from different wrack: Posidonia sinuosa, Amphibolis antarctica and the alga Laurencia sp. We then examined the effect of age on DOC leaching from P. sinuosa wrack. The bioavailability of the DOC was also assessed using a bacterial bioassay. The rate of DOC leaching from P. sinuosa leaves decreased exponentially with time. According to that exponential model, ~50% of the total DOC release occurred in the first 14 d and it would require a further 2.94 yr to release the same amount again. Fresh algae Laurencia sp. leached the greatest amount of DOC in the first 16 h (6.7 g kg-1 fresh weight (FW) wrack), followed by fresh P. sinuosa leaves (1.7 g kg-1 FW), A. antarctica leaves (1.1 g kg-1) and stems (0.6 g kg-1), 4 wk old P. sinuosa (67 g kg-1) and fine detritus (74 g kg-1). In all cases, the composition of the DOC was similar and dominated by the hydrophilic component (in P. sinuosa, predominantly sugars and amino acids). Leachates from all fresh wrack supported bacterial growth over 24 h. Leachate from older wrack either failed to support bacterial growth or only supported it for a limited time. Given the exponential decay in DOC release rate, the interacting timescales of transport and leaching will affect the value of wrack as a vector for trophic subsidies

Luminous Intensity for Traffic Signals: A Scientific Basis for Performance Specifications - Appendices

Luminous Intensity for Traffic Signals: A Scientific Basis for Performance Specifications - Appendice

CAG expansion affects the expression of mutant huntingtin in the Huntington's disease brain

AbstractA trinucleotide repeat (CAG) expansion in the huntingtin gene causes Huntington's disease (HD). In brain tissue from HD heterozygotes with adult onset and more clinically severe juvenile onset, where the largest expansions occur, a mutant protein of equivalent intensity to wild-type huntingtin was detected in cortical synaptosomes, indicating that a mutant species is synthesized and transported with the normal protein to nerve endings. The increased size of mutant huntingtin relative to the wild type was highly correlated with CAG repeat expansion, thereby linking an altered electrophoretic mobility of the mutant protein to its abnormal function. Mutant huntingtin appeared in gray and white matter with no difference in expression in affected regions. The mutant protein was broader than the wild type and in 6 of 11 juvenile cases resolved as a complex of bands, consistent with evidence at the DNA level for somatic mosaicism. Thus, HD pathogenesis results from a gain of function by an aberrant protein that is widely expressed in brain and is harmful only to some neurons

The Association of Coloproctology of Great Britain and Ireland consensus guidelines in emergency colorectal surgery

ACKNOWLEDGEMENTS Review and editing: S.R. Brown, Professor of Surgery, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. Email [email protected]. Patient summary: R.G. Arnott, Retired Professor, Patient Liaison Group, Association of Coloproctology of Great Britain and Ireland, Royal College of Surgeons of England, London, UK. Email [email protected]. Delphi review: C.P. Macklin. BMedSci BM BS FRCS DM, Consultant Colorectal Surgeon, Mid Yorkshire Hospitals, UK. Email [email protected] reviewedPublisher PD

Identification and characterization of a novel non-structural protein of bluetongue virus

Bluetongue virus (BTV) is the causative agent of a major disease of livestock (bluetongue). For over two decades, it has been widely accepted that the 10 segments of the dsRNA genome of BTV encode for 7 structural and 3 non-structural proteins. The non-structural proteins (NS1, NS2, NS3/NS3a) play different key roles during the viral replication cycle. In this study we show that BTV expresses a fourth non-structural protein (that we designated NS4) encoded by an open reading frame in segment 9 overlapping the open reading frame encoding VP6. NS4 is 77–79 amino acid residues in length and highly conserved among several BTV serotypes/strains. NS4 was expressed early post-infection and localized in the nucleoli of BTV infected cells. By reverse genetics, we showed that NS4 is dispensable for BTV replication in vitro, both in mammalian and insect cells, and does not affect viral virulence in murine models of bluetongue infection. Interestingly, NS4 conferred a replication advantage to BTV-8, but not to BTV-1, in cells in an interferon (IFN)-induced antiviral state. However, the BTV-1 NS4 conferred a replication advantage both to a BTV-8 reassortant containing the entire segment 9 of BTV-1 and to a BTV-8 mutant with the NS4 identical to the homologous BTV-1 protein. Collectively, this study suggests that NS4 plays an important role in virus-host interaction and is one of the mechanisms played, at least by BTV-8, to counteract the antiviral response of the host. In addition, the distinct nucleolar localization of NS4, being expressed by a virus that replicates exclusively in the cytoplasm, offers new avenues to investigate the multiple roles played by the nucleolus in the biology of the cell

Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington\u27s disease

Neurons in Huntington\u27s disease exhibit selective morphological and subcellular alterations in the striatum and cortex. The link between these neuronal changes and behavioral abnormalities is unclear. We investigated relationships between essential neuronal changes that predict motor impairment and possible involvement of the corticostriatal pathway in developing behavioral phenotypes. We therefore generated heterozygote mice expressing the N-terminal one-third of huntingtin with normal (CT18) or expanded (HD46, HD100) glutamine repeats. The HD mice exhibited motor deficits between 3 and 10 months. The age of onset depended on an expanded polyglutamine length; phenotype severity correlated with increasing age. Neuronal changes in the striatum (nuclear inclusions) preceded the onset of phenotype, whereas cortical changes, especially the accumulation of huntingtin in the nucleus and cytoplasm and the appearance of dysmorphic dendrites, predicted the onset and severity of behavioral deficits. Striatal neurons in the HD mice displayed altered responses to cortical stimulation and to activation by the excitotoxic agent NMDA. Application of NMDA increased intracellular Ca(2+) levels in HD100 neurons compared with wild-type neurons. Results suggest that motor deficits in Huntington\u27s disease arise from cumulative morphological and physiological changes in neurons that impair corticostriatal circuitry

US Cosmic Visions: New Ideas in Dark Matter 2017: Community Report

This white paper summarizes the workshop "U.S. Cosmic Visions: New Ideas in Dark Matter" held at University of Maryland on March 23-25, 2017.Comment: 102 pages + reference