Probabilistic Search for Object Segmentation and Recognition

The problem of searching for a model-based scene interpretation is analyzed within a probabilistic framework. Object models are formulated as generative models for range data of the scene. A new statistical criterion, the truncated object probability, is introduced to infer an optimal sequence of object hypotheses to be evaluated for their match to the data. The truncated probability is partly determined by prior knowledge of the objects and partly learned from data. Some experiments on sequence quality and object segmentation and recognition from stereo data are presented. The article recovers classic concepts from object recognition (grouping, geometric hashing, alignment) from the probabilistic perspective and adds insight into the optimal ordering of object hypotheses for evaluation. Moreover, it introduces point-relation densities, a key component of the truncated probability, as statistical models of local surface shape.Comment: 18 pages, 5 figure

Shape Matching and Object Recognition

We approach recognition in the framework of deformable shape matching, relying on a new algorithm for finding correspondences between feature points. This algorithm sets up correspondence as an integer quadratic programming problem, where the cost function has terms based on similarity of corresponding geometric blur point descriptors as well as the geometric distortion between pairs of corresponding feature points. The algorithm handles outliers, and thus enables matching of exemplars to query images in the presence of occlusion and clutter. Given the correspondences, we estimate an aligning transform, typically a regularized thin plate spline, resulting in a dense correspondence between the two shapes. Object recognition is handled in a nearest neighbor framework where the distance between exemplar and query is the matching cost between corresponding points. We show results on two datasets. One is the Caltech 101 dataset (Li, Fergus and Perona), a challenging dataset with large intraclass variation. Our approach yields a 45 % correct classification rate in addition to localization. We also show results for localizing frontal and profile faces that are comparable to special purpose approaches tuned to faces

Genetic contributions to visuospatial cognition in Williams syndrome: insights from two contrasting partial deletion patients

Background Williams syndrome (WS) is a rare neurodevelopmental disorder arising from a hemizygotic deletion of approximately 27 genes on chromosome 7, at locus 7q11.23. WS is characterised by an uneven cognitive profile, with serious deficits in visuospatial tasks in comparison to relatively proficient performance in some other cognitive domains such as language and face processing. Individuals with partial genetic deletions within the WS critical region (WSCR) have provided insights into the contribution of specific genes to this complex phenotype. However, the combinatorial effects of different genes remain elusive. Methods We report on visuospatial cognition in two individuals with contrasting partial deletions in the WSCR: one female (HR), aged 11 years 9 months, with haploinsufficiency for 24 of the WS genes (up to GTF2IRD1), and one male (JB), aged 14 years 2 months, with the three most telomeric genes within the WSCR deleted, or partially deleted. Results Our in-depth phenotyping of the visuospatial domain from table-top psychometric, and small- and large-scale experimental tasks reveal a profile in HR in line with typically developing controls, albeit with some atypical features. These data are contrasted with patient JB’s atypical profile of strengths and weaknesses across the visuospatial domain, as well as with more substantial visuospatial deficits in individuals with the full WS deletion. Conclusions Our findings point to the contribution of specific genes to spatial processing difficulties associated with WS, highlighting the multifaceted nature of spatial cognition and the divergent effects of genetic deletions within the WSCR on different components of visuospatial ability. The importance of general transcription factors at the telomeric end of the WSCR, and their combinatorial effects on the WS visuospatial phenotype are also discussed

The role of visual similarity and memory in body model distortions

Several studies have shown that the perception of one's own hand size is distorted in proprioceptive localization tasks. It has been suggested that those distortions mirror somatosensory anisotropies. Recent research suggests that non-corporeal items also show some spatial distortions. In order to investigate the psychological processes underlying the localization task, we investigated the influences of visual similarity and memory on distortions observed on corporeal and non-corporeal items. In experiment 1, participants indicated the location of landmarks on: their own hand, a rubber hand (rated as most similar to the real hand), and a rake (rated as least similar to the real hand). Results show no significant differences between rake and rubber hand distortions but both items were significantly less distorted than the hand. Experiment 2 and 3 explored the role of memory in spatial distance judgments of the hand, the rake and the rubber hand. Spatial representations of items measured in experiment 2 and 3 were also distorted but showed the tendency to be smaller than in localization tasks. While memory and visual similarity seem to contribute to explain qualitative similarities in distortions between the hand and non-corporeal items, those factors cannot explain the larger magnitude observed in hand distortions

BART Inhibits Pancreatic Cancer Cell Invasion by PKCα Inactivation through Binding to ANX7

A novel function for the binder of Arl two (BART) molecule in pancreatic cancer cells is reported. BART inhibits invasiveness of pancreatic cancer cells through binding to a Ca2+-dependent, phosphorylated, guanosine triphosphatase (GTPase) membrane fusion protein, annexin7 (ANX7). A tumor suppressor function for ANX7 was previously reported based on its prognostic role in human cancers and the cancer-prone mouse phenotype ANX7(+/−). Further investigation demonstrated that the BART–ANX7 complex is transported toward cell protrusions in migrating cells when BART supports the binding of ANX7 to the protein kinase C (PKC) isoform PKCα. Recent evidence has suggested that phosphorylation of ANX7 by PKC significantly potentiates ANX7-induced fusion of phospholipid vesicles; however, the current data suggest that the BART–ANX7 complex reduces PKCα activity. Knocking down endogenous BART and ANX7 increases activity of PKCα, and specific inhibitors of PKCα significantly abrogate invasiveness induced by BART and ANX7 knockdown. These results imply that BART contributes to regulating PKCα activity through binding to ANX7, thereby affecting the invasiveness of pancreatic cancer cells. Thus, it is possible that BART and ANX7 can distinctly regulate the downstream signaling of PKCα that is potentially relevant to cell invasion by acting as anti-invasive molecules