72 research outputs found

    Reading in the presence of macular disease: a mini-review.

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    PurposeReading is vital to full participation in modern society. To millions of people suffering from macular disease that results in a central scotoma, reading is difficult and inefficient, rendering reading as the primary goal for most patients seeking low vision rehabilitation. The goals of this review paper are to summarize the dependence of reading speed on several key visual and typographical factors and the current methods or technologies for improving reading performance for people with macular disease.Important findingsIn general, reading speed for people with macular disease depends on print size, text contrast, size of the visual span, temporal processing of letters and oculomotor control. Attempts at improving reading speed by reducing the crowding effect between letters, words or lines; or optimizing properties of typeface such as the presence of serifs or stroke-width thickness proved to be futile, with any improvement being modest at best. Currently, the most promising method to improve reading speed for people with macular disease is training, including perceptual learning or oculomotor training.SummaryThe limitation on reading speed for people with macular disease is likely to be multi-factorial. Future studies should try to understand how different factors interact to limit reading speed, and whether different methods could be combined to produce a much greater benefit

    Suboptimal eye movements for seeing fine details.

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    Human eyes are never stable, even during attempts of maintaining gaze on a visual target. Considering transient response characteristics of retinal ganglion cells, a certain amount of motion of the eyes is required to efficiently encode information and to prevent neural adaptation. However, excessive motion of the eyes leads to insufficient exposure to the stimuli, which creates blur and reduces visual acuity. Normal miniature eye movements fall in between these extremes, but it is unclear if they are optimally tuned for seeing fine spatial details. We used a state-of-the-art retinal imaging technique with eye tracking to address this question. We sought to determine the optimal gain (stimulus/eye motion ratio) that corresponds to maximum performance in an orientation-discrimination task performed at the fovea. We found that miniature eye movements are tuned but may not be optimal for seeing fine spatial details

    Spatial localisation in autism: evidence for differences in early cortical visual processing.

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    BACKGROUND: Vision in people with autism spectrum conditions (ASC) is reported to be different from people without ASC, but the neural level at which the differences begin to occur is not yet known. Here we examine two variants of a vernier acuity task to determine if differences are evident in early visual processing. FINDINGS: Abutting and separated vernier acuity was assessed in 16 people with ASC and 14 matched controls. In controls, abutting and separated thresholds were unrelated (r = 0.13, p = 0.65), suggesting thresholds are determined by two separate mechanisms. In contrast, the abutting and separated thresholds of ASC observers were strongly correlated (r = 0.88, p < 0.0001), with separated thresholds tending towards being superior to those of controls [t(28) = -2.46, p = 0.02]. CONCLUSIONS: The findings suggest the mechanisms employed by ASC observers in separated vernier tasks are different to those of controls. This psychophysical evidence suggests that visual differences in ASC may begin at an early cortical stage of visual processing.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

    Genetic Pathway in Acquisition and Loss of Vancomycin Resistance in a Methicillin Resistant Staphylococcus aureus (MRSA) Strain of Clonal Type USA300

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    An isolate of the methicillin-resistant Staphylococcus aureus (MRSA) clone USA300 with reduced susceptibility to vancomycin (SG-R) (i.e, vancomycin-intermediate S. aureus, VISA) and its susceptible “parental” strain (SG-S) were recovered from a patient at the end and at the beginning of an unsuccessful vancomycin therapy. The VISA phenotype was unstable in vitro generating a susceptible revertant strain (SG-rev). The availability of these 3 isogenic strains allowed us to explore genetic correlates of antibiotic resistance as it emerged in vivo. Compared to the susceptible isolate, both the VISA and revertant strains carried the same point mutations in yycH, vraG, yvqF and lspA genes and a substantial deletion within an intergenic region. The revertant strain carried a single additional frameshift mutation in vraS which is part of two component regulatory system VraSR. VISA isolate SG-R showed complex alterations in phenotype: decreased susceptibility to other antibiotics, slow autolysis, abnormal cell division and increased thickness of cell wall. There was also altered expression of 239 genes including down-regulation of major virulence determinants. All phenotypic properties and gene expression profile returned to parental levels in the revertant strain. Introduction of wild type yvqF on a multicopy plasmid into the VISA strain caused loss of resistance along with loss of all the associated phenotypic changes. Introduction of the wild type vraSR into the revertant strain caused recovery of VISA type resistance. The yvqF/vraSR operon seems to function as an on/off switch: mutation in yvqF in strain SG-R turns on the vraSR system, which leads to increase in vancomycin resistance and down-regulation of virulence determinants. Mutation in vraS in the revertant strain turns off this regulatory system accompanied by loss of resistance and normal expression of virulence genes. Down-regulation of virulence genes may provide VISA strains with a “stealth” strategy to evade detection by the host immune system

    Spatio-temporal properties of letter crowding.

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    Crowding between adjacent letters has been investigated primarily as a spatial effect. The purpose of this study was to investigate the spatio-temporal properties of letter crowding. Specifically, we examined the systematic changes in the degradation effects in letter identification performance when adjacent letters were presented with a temporal asynchrony, as a function of letter separation and between the fovea and the periphery. We measured proportion-correct performance for identifying the middle target letter in strings of three lowercase letters at the fovea and 10° in the inferior visual field, for a range of center-to-center letter separations and a range of stimulus onset asynchronies (SOA) between the target and flanking letters (positive SOAs: target preceded flankers). As expected, the accuracy for identifying the target letters reduces with decreases in letter separation. This crowding effect shows a strong dependency on SOAs, such that crowding is maximal between 0 and ∼100 ms (depending on conditions) and diminishes for larger SOAs (positive or negative). Maximal crowding does not require the target and flanking letters to physically coexist for the entire presentation duration. Most importantly, crowding can be minimized even for closely spaced letters if there is a large temporal asynchrony between the target and flankers. The reliance of letter identification performance on SOAs and how it changes with letter separations imply that the crowding effect can be traded between space and time. Our findings are consistent with the notion that crowding should be considered as a spatio-temporal, and not simply a spatial, effect
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