The extraordinarily rapid disappearance of entoptic images.

It has been known for more than 40 years that images fade from perception when they are kept at the same position on the retina by abrogating eye movements. Although aspects of this phenomenon were described earlier, the use of close-fitting contact lenses in the 1950s made possible a series of detailed observations on eye movements and visual continuity. In the intervening decades, many investigators have studied the role of image motion on visual perception. Although several controversies remain, it is clear that images deteriorate and in some cases disappear following stabilization; eye movements are, therefore, essential to sustained exoptic vision. The time course of image degradation has generally been reported to be a few seconds to a minute or more, depending upon the conditions. Here we show that images of entoptic vascular shadows can disappear in less than 80 msec. The rapid vanishing of these images implies an active mechanism of image erasure and creation as the basis of normal visual processing.

Separation of the arterial wall from blood contact using hydrogel barriers reduces intimal thickening after balloon injury in the rat: The roles of medial and luminal factors in arterial healing

The objective of this study was to clarify the relative roles of medial versus luminal factors in the induction of thickening of the arterial intima after balloon angioplasty injury. Platelet-derived growth factor (PDGF) and thrombin, both associated with thrombosis, and basic fibroblast growth factor (bFGF), stored in the arterial wall, have been implicated in this process. To unequivocally isolate the media from luminally derived factors, we used a 20-μm thick hydrogel barrier that adhered firmly to the arterial wall to block thrombus deposition after balloon-induced injury of the carotid artery of the rat. Thrombosis, bFGF mobilization, medial repopulation, and intimal thickening were measured. Blockade of postinjury arterial contact with blood prevented thrombosis and dramatically inhibited both intimal thickening and endogenous bFGF mobilization. By blocking blood contact on the two time scales of thrombosis and of intimal thickening, and by using local protein release to probe, by reconstitution, the individual roles of PDGF-BB and thrombin, we were able to conclude that a luminally derived factor other than PDGF or thrombin is required for the initiation of cellular events leading to intimal thickening after balloon injury in the rat. We further conclude that a luminally derived factor is required for mobilization of medial bFGF.