Biomedical subjects
N Brady
Publications and source records attributed to N Brady.
What's constant in contrast constancy? The effects of scaling on the perceived contrast of bandpass patterns.
"Contrast constancy" refers to the ability to perceive objects as maintaining a constant contrast independent of size or distance. When tested with high contrast sinusoidal gratings, contrast constancy has been shown to hold for a wide range of spatial frequencies, suggesting that sensitivity is constant across the spectrum at suprathreshold. In this study, we show that contrast constancy also holds for relatively broadband patterns. We describe how the frequency spectra of such functions change as the patterns scale in size. In particular, we emphasize how these changes in the spectra depend on whether the functions are localized (coherent phase) or spatially distributed (incoherent phase). In Fourier terms, the scaling properties depend on the phase spectra of the patterns. Contrast constancy is shown to hold for both localized Gabor patches (coherent phase spectra) and bandpass noise patterns (incoherent phase spectra). Constancy holds over a wide range of suprathreshold contrasts; in fact, matching is quite accurate as soon as the pattern is suprathreshold. These results are explained with a model in which mechanism bandwidths increase with frequency (constant in octaves) and peak spectral sensitivity is equal across frequency out to around 16 c/deg. In the case of the Gabor stimuli, perceived contrast is assumed to be mediated by a mechanism centered on the patch. For the bandpass noise, contrast is determined by the average response of units distributed across the stimulus. This model can account for the matching data without assuming that the contrast-response gain of the underlying channels changes with spatial frequency. Neither does the model assume "response pooling". In addition to explaining the experimental results, the model also predicts that perceived contrast will be approximately constant across scale for scenes whose spectra fall as 1/f, as is typical of natural scenes.
Molecular basis of essential fructosuria: molecular cloning and mutational analysis of human ketohexokinase (fructokinase).
Essential fructosuria is one of the oldest known inborn errors of metabolism. It is a benign condition which is believed to result from deficiency of hepatic fructokinase (ketohexokinase, KHK, E.C.2.7.1.3). This enzyme catalyses the first step of metabolism of dietary fructose, conversion of fructose to fructose-1-phosphate. Despite the early recognition of this disorder, the primary structure of human KHK and the molecular basis of essential fructosuria have not been previously defined. In this report, the isolation and sequencing of full-length cDNA clones encoding human ketohexokinase are described. Alternative mRNA species and alternative KHK isozymes are produced by alternative polyadenylation and splicing of the KHK gene. The KHK proteins show a high level of sequence conservation relative to rat KHK. Direct evidence that mutation of the KHK structural gene is the cause of essential fructosuria was also obtained. In a well-characterized family, in which three of eight siblings have fructosuria, all affected individuals are compound heterozygotes for two mutations Gly40Arg and Ala43Thr. Both mutations result from G-->A transitions, and each alters the same conserved region of the KHK protein. Neither mutation was seen in a sample of 52 unrelated control individuals. An additional conservative amino acid change (Val49IIe) was present on the KHK allele bearing Ala43Thr.
Assessing nursing systems relationships.
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Oxidation of DL-3-phenylalanine-1- 14 C, DL-leucine-1- 14 C, and D-glucose-1- 14 C-6-phosphate to 14 CO 2 in human placenta.
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