Accurate saccadic programming in natural visual scenes requires a signal designating which of the many potential targets is to be the goal of the saccade. Is this signal controlled by the allocation of perceptual attention, or do saccades have their own independent selective filter? We found evidence for the involvement of perceptual attention, namely: (1) summoning perceptual attention to a target also facilitated saccades; (2) perceptual identification was better at the saccadic goal than elsewhere; and (3) attempts to dissociate the locus of attention from the saccadic goal were unsuccessful, i.e. it was not possible to prepare to look quickly and accurately at one target while at the same time making highly accurate perceptual judgements about targets elsewhere. We also studied the trade-off between saccadic and perceptual performance by means of a novel application of the "attentional operating characteristic" (AOC) to oculomotor performance. This analysis revealed that some attention could be diverted from the saccadic goal with virtually no cost to either saccadic latency or accuracy, showing that there is a ceiling on the attentional demands of saccades. The links we discovered between saccades and attention can be explained by a model in which perceptual attention determines the endpoint of the saccade, while a separate trigger signal initiates the saccade in response to transient changes in the attentional locus. The model will be discussed in the context of current neurophysiological work on saccadic control.

The most deadly phase in cancer progression is attributed to the inappropriate acquisition of molecular machinery leading to metastatic transformation and spread of disease to distant organs. Although it is appreciated that metastasis involves epithelial-mesenchymal interplay, the underlying mechanism defining this process is poorly understood. Specifically, how cancer cells evade immune surveillance and gain the ability to navigate the circulatory system remains a focus. One possible mechanism underlying metastatic conversion is fusion between blood-derived immune cells and cancer cells. While this notion is a century old, in vivo evidence that cell fusion occurs within tumors and imparts genetic or physiologic changes remains controversial. We have previously demonstrated in vivo cell fusion between blood cells and intestinal epithelial cells in an injury setting. Here, we hypothesize that immune cells, such as macrophages, fuse with tumor cells imparting metastatic capabilities by transferring their cellular identity. We used parabiosis to introduce fluorescent-labeled bone marrow-derived cells to mice with intestinal tumors, finding that fusion between circulating blood-derived cells and tumor epithelium occurs during the natural course of tumorigenesis. Moreover, we identify the macrophage as a key cellular partner for this process. Interestingly, cell fusion hybrids retain a transcriptome identity characteristic of both parental derivatives, while also expressing a unique subset of transcripts. Our data supports the novel possibility that tumorigenic cell fusion may impart physical behavior attributed to migratory macrophages, including navigation of circulation and immune evasion. As such, cell fusion may represent a promising novel mechanism underlying the metastatic conversion of cancer cells.

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Objective: To investigate the basis of disturbed moral judgment in patients with frontotemporal dementia (FTD).Background: FTD is characterized by difficulty in modulating so-