4 resultados para Daniel 1-6

em Aston University Research Archive


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Binocular vision is traditionally treated as two processes: the fusion of similar images, and the interocular suppression of dissimilar images (e.g. binocular rivalry). Recent work has demonstrated that interocular suppression is phase-insensitive, whereas binocular summation occurs only when stimuli are in phase. But how do these processes affect our perception of binocular contrast? We measured perceived contrast using a matching paradigm for a wide range of interocular phase offsets (0–180°) and matching contrasts (2–32%). Our results revealed a complex interaction between contrast and interocular phase. At low contrasts, perceived contrast reduced monotonically with increasing phase offset, by up to a factor of 1.6. At higher contrasts the pattern was non-monotonic: perceived contrast was veridical for in-phase and antiphase conditions, and monocular presentation, but increased a little at intermediate phase angles. These findings challenge a recent model in which contrast perception is phase-invariant. The results were predicted by a binocular contrast gain control model. The model involves monocular gain controls with interocular suppression from positive and negative phase channels, followed by summation across eyes and then across space. Importantly, this model—applied to conditions with vertical disparity—has only a single (zero) disparity channel and embodies both fusion and suppression processes within a single framework.

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We propose and experimentally realize a composite Raman converter based on P-doped and Gedoped fibers. The converter has an emission wavelength of 1.649 μm and an output power of 1.2 W. Numerical simulation of the configuration suggested was performed. A similar converter scheme can be used to build sources with any emission wavelength in the range from 1.6 to 1.75 μm.

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This study evaluates the antidiabetic potential of an enzyme-resistant analog, (Val8)GLP-1. The effects of daily administration of a novel dipeptidyl peptidase IV-resistant glucagon-like peptide-1 (GLP-1) analog, (Val8)GLP-1, on glucose tolerance and pancreatic β-cell function were examined in obese-diabetic (ob/ob) mice. Acute intraperitoneal administration of (Val8)GLP-1 (6.25-25 nmol/kg) with glucose increased the insulin response and reduced the glycemic excursion in a dose-dependent manner. The effects of (Val8)GLP-1 were greater and longer lasting than native GLP-1. Once-daily subcutaneous administration of (Val8)GLP-1 (25 nmol/kg) for 21 days reduced plasma glucose concentrations, increased plasma insulin, and reduced body weight more than native GLP-1 without a significant change in daily food intake. Furthermore, (Val8)GLP-1 improved glucose tolerance, reduced the glycemic excursion after feeding, increased the plasma insulin response to glucose and feeding, and improved insulin sensitivity. These effects were consistently greater with (Val8)GLP-1 than with native GLP-1, and both peptides retained or increased their acute efficacy compared with initial administration. (Val8)GLP-1 treatment increased average islet area 1.2-fold without changing the number of islets, resulting in an increased number of larger islets. These data demonstrate that (Val8)GLP-1 is more effective and longer acting than native GLP-1 in obese-diabetic ob/ob mice.

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Examining complete gene knockouts within a viable organism can inform on gene function. We sequenced the exomes of 3222 British Pakistani-heritage adults with high parental relatedness, discovering 1111 rare-variant homozygous genotypes with predicted loss of gene function (knockouts) in 781 genes. We observed 13.7% fewer than expected homozygous knockout genotypes, implying an average load of 1.6 recessive-lethal-equivalent LOF variants per adult. Linking genetic data to lifelong health records, knockouts were not associated with clinical consultation or prescription rate. In this dataset we identified a healthy PRDM9 knockout mother, and performed phased genome sequencing on her, her child and controls, which showed meiotic recombination sites localized away from PRDM9-dependent hotspots. Thus, natural LOF variants inform upon essential genetic loci, and demonstrate PRDM9 redundancy in humans.