Biomedical subjects

Jussi Saarinen

Publications and source records attributed to Jussi Saarinen.

3 recordsLinked to original sources

PubMed2006

Detection of irregular spatial structures.

Wilson et al.'s (1997) study on Glass patterns suggested that the integration of stimulus features into a linear shape occurs quite locally, whereas curved structures--such as circular--require global summation. Their conclusion was based on experiments in which they varied the size of the signal area containing a spatial structure. In the present study, we tested the integration of constant-sized linear and curved Glass patterns by varying their global irregularity. If the mechanisms underlying the detection of a Glass pattern pool features globally throughout the stimulus, the irregularity should have a strong effect on detection performance. The irregular Glass patterns were composed of a variable number of sub-areas, each of which contained its own linear or curved structure. The structural irregularity impaired the detection of the curved patterns, whereas the thresholds for the linear patterns were not affected. Thus, our results are in line with the notion that the integration of curved Glass patterns occurs more globally than the integration of linear patterns.

Humans↗

PubMed2004

Perception of mirror symmetry in amblyopic vision.

Mirror symmetry is ubiquitous in natural visual scenes, and detection of mirror symmetry seems to be a global, automatic, effortless and important aspect of visual perception. The perception of mirror symmetry has not been studied in humans with amblyopia. In this paper we measured and quantified the detection of mirror symmetry in adults with naturally occurring amblyopia. Our results show that amblyopia may severely impair the detection of mirror symmetry, and that this impairment is not simply a consequence of reduced stimulus visibility. Rather, we suggest that this loss may reflect, at least in part, a deficit in the integration of local orientation information.

Adult↗

PubMed2002

Identification of p100 as a coactivator for STAT6 that bridges STAT6 with RNA polymerase II.

STAT6 is a central mediator of IL-4-induced gene responses. STAT6-mediated transcription is depend ent on the C-terminal transcription activation domain (TAD), but the mechanisms by which STAT6 activates transcription are poorly understood. Here, we have identified the staphylococcal nuclease (SN)-like domain and tudor domain containing protein p100 as a STAT6 TAD interacting protein. p100 was originally characterized as a transcriptional coactivator for Epstein-Barr virus nuclear antigen 2. STAT6 interacted with p100 in vitro and in vivo. The interaction was mediated by the TAD domain of STAT6 and the SN-like domain of p100. p100 did not affect the immediate activation events of STAT6, but enhanced STAT6-mediated transcriptional activation and the IL-4-induced Igepsilon gene transcription in human B-cell line. Finally, p100 associated with the large subunit of RNA polymerase II and was mediating interaction between STAT6 and RNA polymerase II. These findings identify p100 as a novel coactivator for STAT6 and suggest that p100 functions as a bridging factor between STAT6 and the basal transcription machinery.

Animals↗