1,114 research outputs found

    Optimal quantum cloning of orbital angular momentum photon qubits via Hong-Ou-Mandel coalescence

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    The orbital angular momentum (OAM) of light, associated with a helical structure of the wavefunction, has a great potential for quantum photonics, as it allows attaching a higher dimensional quantum space to each photon. Hitherto, however, the use of OAM has been hindered by its difficult manipulation. Here, exploiting the recently demonstrated spin-OAM information transfer tools, we report the first observation of the Hong-Ou-Mandel coalescence of two incoming photons having nonzero OAM into the same outgoing mode of a beam-splitter. The coalescence can be switched on and off by varying the input OAM state of the photons. Such effect has been then exploited to carry out the 1 \rightarrow 2 universal optimal quantum cloning of OAM-encoded qubits, using the symmetrization technique already developed for polarization. These results are finally shown to be scalable to quantum spaces of arbitrary dimension, even combining different degrees of freedom of the photons.Comment: 5 pages, 3 figure

    Health First: An evidence-based alcohol strategy for the UK

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    Alcohol is taken for granted in the UK today. It is easy to get hold of, increasingly affordable, advertised everywhere and accepted by many as an integral part of daily life. Yet, despite this, the great majority of the population recognise the harm that alcohol causes. They believe that drinking damages health, drives anti social behaviour, harms children and families and creates huge costs for the NHS and the Police. They are right. Every year in the UK, there are thousands of deaths and over a million hospital admissions related to drinking. More than two in five (44%) violent crimes are committed under the influence of alcohol, as are 37% of domesti c violence incidents. One fifth of all violent crime occurs in or near pubs and clubs and 45% of adults avoid town centres at night because of drunken behaviour. The personal, social and economic cost of alcohol has been estimated to be up to £55bn for England and £7.5bn for Scotland. None of this should be taken for granted. The impact of drinking on public health and community safety is so great that radical steps are needed to change our relationship with alcohol. We need to imagine a society where low or no alcohol consumpti on is the norm, drunkenness is socially unacceptable and town centres are safe and welcoming places for everyone to use. Our vision is for a safer, healthier and happier world where the harm caused by alcohol is minimised. This vision is achievable. But only if we tackle the primary drivers of alcohol consumption. The evidence is clear: the most effective way to reduce the harm from alcohol is to reduce the affordability, availability and attractiveness of alcohol products. It is not enough to limit the damage once people are drunk, dependent, ill or dying. We need to intervene earlier in order to reduce consumption across the entire population. The tools are available. The ‘four Ps' of the marketing mix - price, product, promotion and place - are used by alcohol producers and retailers to increase their sales of alcohol. They can also be used by government to reduce alcohol sales, alcohol consumption and alcohol-related harm. Alcohol taxes are an effective public health measure as they raise prices and suppress demand. However, if they do not keep pace with both inflation and incomes, alcohol products will become more affordable over time. This has been the case in the UK. Deep discounting by retailers has also driven down the price of alcohol and encouraged heavy drinkers to maintain dangerous levels of consumption. These problems need to be tackled by a combinati on of more effective fiscal policy and controls on pricing and discounting. Alcohol products are an extraordinary anomaly. Unlike most food products, they are both remarkably harmful and excepti onally lightly regulated. As with other toxic products, the product label ought to communicate the content of the product and the risks of its consumpti on. Regulation should drive out products that appeal to young people while also incentivising the development and sale of lower strength products. The pervasive marketing of alcohol products in the UK is indefensible. Current restrictions are woefully inadequate: children and young people are regularly exposed to alcohol adverti sing in both old and new media. Only a complete ban on all alcohol advertising and sponsorship will make a lasting diff erence. Licensing practice in the UK is out of date. The focus on pubs and bars has allowed shops and supermarkets to become the dominant players in alcohol sales. Consequently, alcohol is now more available than it has ever been. This has driven pre-loading: getting drunk on cheap, shop-bought alcohol before heading out to late-opening night life. Licensing must focus on public health and seek to control the overall availability of alcohol as well as the effects of drunkenness. Beyond these populati on-level approaches, many more targeted measures are needed to reduce alcohol-related harm. Early interventi on by health and social care professionals is an important and underexploited opportunity to prevent problems developing. Stronger drink driving measures are also required. All these measures are needed. Together, they provide a template for an integrated and comprehensive strategy to tackle the harm from alcohol in the UK.Additional co-authors: Gerry McElwee, Dr Kieran Moriarty CBE, Dr Robin Purshouse, Dr Peter Rice, Alison Rogers, George Roycroft , Chit Selvarajah, Don Shenker, Eric Appleby, Dr Nick Sheron, and Colin Shevill

    Uridine Metabolism in the Goldfish Retina During Optic Nerve Regeneration: Whole Retina Studies

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    Accumulation of radioactivity from [ 3 H]uridine in incubations of whole goldfish retinas is increased in the ipsilateral retina during a period of regeneration that follows unilateral optic nerve crush. Brief incubations to investigate the nature of enhanced labeling of the acid-soluble fraction showed a peak uptake 4 days following crush, with a gradual decrease to control levels by 21 days following crush. That nucleoside uptake may not mediate the effect is supported by the observation that the rate of uptake of 5′-deoxyadenosine, a nonmetabolizable nucleoside analog, is the same in post-crush (PC) and normal (N) retinal incubations. Following brief incubations of PC and N retinas with [ 3 H]uridine, there is enhanced labeling in PC retinas relative to N retinas of recovered UMP, UDP, UTP, and uridine nucleotide sugars, whereas recovery of labeled uridine itself is slightly decreased. The results suggest that the increased accumulation of radioactivity in PC retinas following incubation with uridine reflects an increase in the activities of retinal uridine kinase and uridine nucleotide kinases.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65630/1/j.1471-4159.1981.tb01713.x.pd

    A genome-wide association study of anorexia nervosa.

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    Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countries (15 sites) and 14 860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery data sets. Seventy-six (72 independent) single nucleotide polymorphisms were taken forward for in silico (two data sets) or de novo (13 data sets) replication genotyping in 2677 independent AN cases and 8629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication data sets comprised 5551 AN cases and 21 080 controls. AN subtype analyses (1606 AN restricting; 1445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01 × 10(-7)) in SOX2OT and rs17030795 (P=5.84 × 10(-6)) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76 × 10(-)(6)) between CUL3 and FAM124B and rs1886797 (P=8.05 × 10(-)(6)) near SPATA13. Comparing discovery with replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P=4 × 10(-6)), strongly suggesting that true findings exist but our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field

    New genetic loci link adipose and insulin biology to body fat distribution.

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    Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead
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