Perception of biological motion from size-invariant body representations

The visual recognition of action is one of the socially most important and computationally demanding capacities of the human visual system. It combines visual shape recognition with complex non-rigid motion perception. Action presented as a point-light animation is a striking visual experience for anyone who sees it for the first time. Information about the shape and posture of the human body is sparse in point-light animations, but it is essential for action recognition. In the posturo-temporal filter model of biological motion perception posture information is picked up by visual neurons tuned to the form of the human body before body motion is calculated. We tested whether point-light stimuli are processed through posture recognition of the human body form by using a typical feature of form recognition, namely size invariance. We constructed a point-light stimulus that can only be perceived through a size-invariant mechanism. This stimulus changes rapidly in size from one image to the next. It thus disrupts continuity of early visuo-spatial properties but maintains continuity of the body posture representation. Despite this massive manipulation at the visuo-spatial level, size-changing point-light figures are spontaneously recognized by naive observers, and support discrimination of human body motion

Trans-saccadic adaptation of perceived size independent of saccadic adaptation

Systematic shortening or lengthening of target objects during saccades modifies saccade amplitudes and perceived size of the objects. These two events are concomitant when size change during the saccade occurs asymmetrically, thereby shifting the center of mass of the object. In the present study, we asked whether or not the two are necessarily linked. We tested human participants in symmetrical systematic shortening and lengthening of a vertical bar during a horizontal saccade, aiming to not modify the saccade amplitude. Before and after a phase of trans-saccadic changes of the target bar, participants manually indicated the sizes of various vertically oriented bars by open-loop grip aperture. We evaluated the effect of trans-saccadic changes of bar length on manual perceptual reports and whether this change depended on saccade amplitude. As expected, we did not induce any change in horizontal or vertical components of saccade amplitude, but we found a significant difference in perceived size after the lengthening experiment compared to after the shortening experiment. Moreover, after the lengthening experiment, perceived size differed significantly from pre-lengthening baseline. These findings suggest that a change of size perception can be induced trans-saccadically, and its mechanism does not depend on saccadic amplitude change

Homogeneity and Heterogeneity as Situational Properties: Producing – and Moving Beyond? – Race in Post-Genomic Science

In this article, we explore current thinking and practices around the logics of difference in gene–environment interaction research in the post-genomic era. We find that scientists conducting gene–environment interaction research continue to invoke well-worn notions of racial difference and diversity, but use them strategically to try to examine other kinds of etiologically significant differences among populations. Scientists do this by seeing populations not as inherently homogeneous or heterogeneous, but rather by actively working to produce homogeneity along some dimensions and heterogeneity along others in their study populations. Thus we argue that homogeneity and heterogeneity are situational properties – properties that scientists seek to achieve in their study populations, the available data, and other aspects of the research situation they are confronting, and then leverage to advance post-genomic science. Pointing to the situatedness of homogeneity and heterogeneity in gene–environment interaction research underscores the work that these properties do and the contingencies that shape decisions about research procedures. Through a focus on the situational production of homogeneity and heterogeneity more broadly, we find that gene–environment interaction research attempts to shift the logic of difference from solely racial terms as explanatory ends unto themselves, to racial and other dimensions of difference that may be important clues to the causes of complex diseases

A demonstration of 'broken' visual space

It has long been assumed that there is a distorted mapping between real and ‘perceived’ space, based on demonstrations of systematic errors in judgements of slant, curvature, direction and separation. Here, we have applied a direct test to the notion of a coherent visual space. In an immersive virtual environment, participants judged the relative distance of two squares displayed in separate intervals. On some trials, the virtual scene expanded by a factor of four between intervals although, in line with recent results, participants did not report any noticeable change in the scene. We found that there was no consistent depth ordering of objects that can explain the distance matches participants made in this environment (e.g. A > B > D yet also A < C < D) and hence no single one-to-one mapping between participants’ perceived space and any real 3D environment. Instead, factors that affect pairwise comparisons of distances dictate participants’ performance. These data contradict, more directly than previous experiments, the idea that the visual system builds and uses a coherent 3D internal representation of a scene

Axon Myelin Transfer of a Non-Enveloped Virus

We showed previously that Theiler's virus, a neurotropic non-enveloped picornavirus of mouse, traffics from the axon of infected neurons into the surrounding myelin. When this traffic is interrupted, as in the shiverer mouse which bears a mutation in the myelin basic protein gene, the virus is unable to persist in the central nervous system. In the present work, we used the Wlds mutant mouse, a strain in which axonal degeneration is considerably slowed down, to show that axon to myelin traffic takes place in the absence of axon degeneration. Our results suggest the existence of a mechanism of transfer of axonal cytoplasm into the myelin which Theiler's virus might exploit to ensure its persistence