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Conway, B. R.

Publications and source records attributed to Conway, B. R..

2 recordsLinked to original sources

Uncovering the geometry of color space with magnetoencephalography (MEG)

The geometry that describes the relationship among colors is unsettled despite centuries of study. Here we present a new approach, using multivariate analyses of direct measurements of brain activity obtained with magnetoencephalography to reverse-engineer the geometry of the neural representation of color space. The analyses depend upon determining similarity relationships among the neural responses to different colors and assessing how these relationships change in time. To evaluate the approach, we relate patterns of neural activity to universal patterns in color naming. Control experiments showed that responses to color words could not decode activity elicited by color stimuli. The results suggest that three patterns of color naming can be accounted for by decoding the similarity relationships in the neural representation of color: the association of warm colors such as reds and oranges with "light" and cool colors such as blues and greens with "dark"; the greater precision among all languages in naming warm colors compared to cool colors; and the preeminence of red.

neuroscience

Kidney single-cell atlas reveals myeloid heterogeneity in progression and regression of kidney disease.

The kidney has a limited capacity to repair following injury, however, the endogenous reparative pathways are not well understood. Here we employ integrated droplet- and plate-based scRNA-seq in the murine reversible unilateral ureteric obstruction model to dissect the transcriptomic landscape at the single cell level during renal injury and resolution of fibrosis. We generate a comprehensive catalogue of the changes induced during injury and repair, revealing significant myeloid cell heterogeneity, which would not have been identifiable by conventional flow cytometry. We identify new markers for the myeloid populations within the kidney as well as identification of novel subsets including an Arg1+ monocyte population specific to early injury and a Mmp12+ macrophage subset exclusive to repair. Finally, using paired blood exchange to track circulating immune cells, we confirm that monocytes are recruited to the kidney early after injury and are the source of Ccr2+ macrophages that accumulate in late injury. Our data demonstrate the utility of complementary technologies to identify novel myeloid subtypes that may represent therapeutic targets to inhibit progression or promote regression of kidney disease.

immunology