Chris Muller | PubMed Health

PubMed2004

Binocular correlation does not improve coherence detection for fronto-parallel motion.

We studied the low-level interactions between motion coherence detection and binocular correlation detection. It is well-established that e.g. depth information from motion parallax and from binocular disparities is effectively integrated. The question we aimed to answer is whether such interactions also exist at the very first correlation level that both mechanisms might have in common. First we quantitatively compared motion coherence detection and binocular correlation detection using similar stimuli (random pixels arrays, RPAs) and the same noise masking paradigm (luminance signal to noise ratio, LSNR). This showed that human observers are much more sensitive to motion than to binocular correlation. Adding noise therefore has a much stronger effect on binocular correlation than on motion detection. Next we manipulated the shape of the stimulus aperture to equalize LSNR thresholds for motion and binocular correlation. Motion sensitivity could be progressively reduced by shortening the length of the motion path, while keeping the aperture area constant. Changing the shape of the aperture did not affect binocular correlation sensitivity. A 'balanced' stimulus, one with equal strengths of motion and binocular correlation signals was then used to study the mutual interactions. In accordance with previous results, motion was found to greatly facilitate binocular correlation. Binocular correlation, however did not facilitate motion detection. We conclude that interactions are asymmetrical; fronto-parallel motion is primarily detected monocularly and this information can then be used to facilitate binocular correlation, but binocular correlation cannot improve motion sensitivity.

Adult↗

PubMed2004

Effects of CFTR, interleukin-10, and Pseudomonas aeruginosa on gene expression profiles in a CF bronchial epithelial cell Line.

Mutations in CFTR lead to a complex phenotype that includes increased susceptibility to Pseudomonas infections, a functional deficiency of IL-10, and an exaggerated proinflammatory cytokine response. We examined the effects of CFTR gene correction on the gene expression profile of a CF bronchial epithelial cell line (IB3-1) and determined which CF-related gene expression changes could be reversed by IL-10 expression. We performed microarray experiments to monitor the gene expression profile of three cell lines over a time course of exposure to Pseudomonas. At baseline, we identified 843 genes with statistically different levels of expression in CFTR-corrected (S9) cells compared to the IB3-1 line or the IL-10-expressing line. K-means clustering and functional group analysis revealed a primary up-regulation of ubiquitination enzymes and TNF pathway components and a primary down-regulation of protease inhibitors and protein glycosylation enzymes in CF. Key gene expression changes were confirmed by real-time RT-PCR. Massive reprogramming of gene expression occurred 3 h after Pseudomonas exposure. Changes specific to CF included exaggerated activation of cytokines, blunted activation of anti-proteases, and repression of protein glycosylation enzymes. In conclusion, the CFTR genotype changes the expression of multiple genes at baseline and in response to bacterial challenge, and only a subset of these changes is secondary to IL-10 deficiency.

Animals↗