Visual versus phonological abilities in Spanish dyslexic boys and girls.

Phonological and visual theories propose different primary deficits as part of the explanation for dyslexia. Both theories were put to test in a sample of Spanish dyslexic readers. Twenty-one dyslexic and 22 typically-developing children matched on chronological age were administered phonological discrimination and awareness tasks and coherent motion perception tasks. No differences were found between groups on the coherent motion tasks, whereas dyslexic readers were impaired relative to controls on phonological discrimination tasks. Gender differences followed the opposite pattern, with no differences on phonological tasks, and dyslexic girls performing significantly worse than dyslexic boys in coherent motion perception. These results point to the importance of phonological deficits related to speech perception in Spanish, and to possible gender differences in the neurobiological bases for dyslexia.

Telomerase Is Essential for Zebrafish Heart Regeneration.

After myocardial infarction in humans, lost cardiomyocytes are replaced by an irreversible fibrotic scar. In contrast, zebrafish hearts efficiently regenerate after injury. Complete regeneration of the zebrafish heart is driven by the strong proliferation response of its cardiomyocytes to injury. Here we show that, after cardiac injury in zebrafish, telomerase becomes hyperactivated, and telomeres elongate transiently, preceding a peak of cardiomyocyte proliferation and full organ recovery. Using a telomerase-mutant zebrafish model, we found that telomerase loss drastically decreases cardiomyocyte proliferation and fibrotic tissue regression after cryoinjury and that cardiac function does not recover. The impaired cardiomyocyte proliferation response is accompanied by the absence of cardiomyocytes with long telomeres and an increased proportion of cardiomyocytes showing DNA damage and senescence characteristics. These findings demonstrate the importance of telomerase function in heart regeneration and highlight the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction.

Luminance and chromatic contrast sensitivity in dyslexia: the magnocellular deficit hypothesis revisited.

The hypothesis of a magnocellular channel deficit in dyslexia was tested. Subjects were 10-year-old dyslexics and normal readers. Psychophysical thresholds for luminance and chromatic contrasts were estimated using black and white and red and green sinusoidal gratings of various spatial frequencies, presented in static and dynamic conditions (drift and reversal). Significant group differences were found for luminance contrast, with a higher sensitivity in dyslexics. No group differences were obtained for chromatic contrast. High luminance contrast sensitivity correlated with low reading and writing skills. The typical finding of an increase contrast sensitivity to low spatial frequency gratings, due to their dynamic presentations, was absent in dyslexics. The results provide support for the magnocellular deficit hypothesis. The pattern of this deficit, however, is much more complex than that emerging from previous research.

Attentional deficit in dyslexia: a general or specific impairment?

Dyslexic and control children were tested in a visuomotor attentional task, which provides independent measures of the alerting, orienting and conflict components of the attentional system. Our results show that dyslexics are impaired with respect to controls in the attentional conflict component (resolution of conflict of incongruent peripheral information), while the alerting and orienting components remain preserved. It excludes an overall attentional impairment and points to more specific attentional processing difficulty i.e. distributed attention strategy. Generally, results of dyslexic boys are within the range of the control group, while reaction times of dyslexic girls are significantly slower than that of all other groups.

Latencies of stimulus-driven eye movements are shorter in dyslexic subjects.

Eye movements latencies toward peripherally presented stimuli were measured in 10-year-old dyslexic and control children. Dyslexic subjects, previously found to be oversensitive to stimulation of the magnocellular channel, showed reduced latencies as compared to normally reading controls. An attention shifting task was also used which showed no group differences in latencies of eye movements. The data are discussed in terms of the hypothesis of magnocellular system alteration and attention dysfunction in dyslexia. Additionally, sex differences in eye movement latencies were found and are discussed.