Abstract-It is well-known that early integration (also called data fusion) is effective when the modalities are correlated, and late integration (also called decision or opinion fusion) is optimal when modalities are uncorrelated. In this paper, we propose a new multimodal fusion strategy for open-set speaker identification using a combination of early and late integration following canonical correlation analysis (CCA) of speech and lip texture features. We also propose a method for high precision synchronization of the speech and lip features using CCA prior to the proposed fusion. Experimental results show that i) the proposed fusion strategy yields the best equal error rates (EER), which are used to quantify the performance of the fusion strategy for open-set speaker identification, and ii) precise synchronization prior to fusion improves the EER; hence, the best EER is obtained when the proposed synchronization scheme is employed together with the proposed fusion strategy. We note that the proposed fusion strategy outperforms others because the features used in the late integration are truly uncorrelated, since they are output of the CCA analysis.

We have utilized tau-assembled and tau-stabilized microtubules (MTs), in the absence of taxol, to investigate the effects of tau isoforms with three and four MT binding repeats upon kinesin-driven MT gliding. MTs were assembled in the presence of either 3-repeat tau (3R tau) or 4-repeat tau (4R tau) at tau:tubulin dimer molar ratios that approximate those found in neurons. MTs assembled with 3R tau glided at 31.1 lm/min versus 25.8 lm/min for 4R tau, a statistically significant 17% difference. Importantly, the gliding rates for either isoform did not change over a fourfold range of tau concentrations. Further, tau-assembled MTs underwent minimal dynamic instability behavior while gliding and moved with linear trajectories. In contrast, MTs assembled with taxol in the absence of tau displayed curved gliding trajectories. Interestingly, addition of 4R tau to taxol-stabilized MTs restored linear gliding, while addition of 3R tau did not. The data are consistent with the ideas that (i) 3R and 4R tau-assembled MTs possess at least some isoform-specific features that impact upon kinesin translocation, (ii) tau-assembled MTs possess different structural features than do taxol-assembled MTs, and (iii) some features of tau-assembled MTs can be masked by prior assembly by taxol. The differences in kinesin-driven gliding between 3R and 4R tau suggest important features of tau function related to the normal shift in tau isoform composition that occurs during neural development as well as in neurodegeneration caused by altered expression ratios of otherwise normal tau isoforms. V C 2010 Wiley-Liss, Inc.Key Words: neurodegeneration, axonal transport, frontotemporal dementia, motor protein Introduction T au is a neural microtubule (MT)-associated protein (MAP) that binds to MTs, promotes MT assembly, and regulates MT dynamics in the developing and adult nervous systems . Although there is only a single tau gene, alternative RNA splicing produces six tau isoforms, each possessing either three (3R tau) or four (4R tau) imperfect MT binding repeats located in the C-terminal half of the protein, and either zero, one, or two inserts located in the N-terminal portion of the protein (projection domain, Fig. 1), which is believed to extend outward from the MT surface [Hirokawa et al., 1988;Lee et al., 1988;Himmler et al., 1989;Himmler, 1989;Butner and Kirschner, 1991;Chen et al., 1992;Goode and Feinstein, 1994]. Whereas fetal brain expresses only the shortest 3R tau isoform, adult human brain expresses approximately equal amounts of the 3R tau and 4R tau isoforms [Kosik et al., 1989]. 4R tau generally exhibits higher levels of MT assembly promoting and dynamics regulatory activities than 3R tau [Goedert and Jakes, 1990;Trinczek et al., 1995;Goode et al., 2000;Panda et al., 2003;Bunker et al., 2004;Levy et al., 2005]. Qualitative mechanistic differences between 3R and 4R tau action have also been described [Levy et al., 2005]. The fact that 3R and 4R tau differentially regulate MT dynamics has given rise to a functional shift model in ...

In this paper, we present an algorithm for occlusion boundary detection. The main contribution is a probabilistic detection framework defined on spatio-temporal lattices, which enables joint analysis of image frames. For this purpose, we introduce two complementary cost functions for creating the spatio-temporal lattice and for performing global inference of the occlusion boundaries, respectively. In addition, a novel combination of low-level occlusion features is discriminatively learnt in the detection framework. Simulations on the CMU Motion Dataset provide ample evidence that proposed algorithm outperforms the leading existing methods.

Abstract-We propose a new two-stage framework for joint analysis of head gesture and speech prosody patterns of a speaker towards automatic realistic synthesis of head gestures from speech prosody. In the first stage analysis, we perform Hidden Markov Model (HMM) based unsupervised temporal segmentation of head gesture and speech prosody features separately to determine elementary head gesture and speech prosody patterns, respectively, for a particular speaker. In the second stage, joint analysis of correlations between these elementary head gesture and prosody patterns is performed using Multi-Stream HMMs to determine an audio-visual mapping model. The resulting audio-visual mapping model is then employed to synthesize natural head gestures from arbitrary input test speech given a head model for the speaker. In the synthesis stage, the audio-visual mapping model is used to predict a sequence of gesture patterns from the prosody pattern sequence computed for the input test speech. The Euler angles associated with each gesture pattern are then applied to animate the speaker head model. Objective and subjective evaluations indicate that the proposed synthesis by analysis scheme provides natural looking head gestures for the speaker with any input test speech, as well as in "prosody transplant" and "gesture transplant" scenarios.

Tau is a multiply phosphorylated protein that is essential for the development and maintenance of the nervous system. Errors in Tau action are associated with Alzheimer disease and related dementias. A huge literature has led to the widely held notion that aberrant Tau hyperphosphorylation is central to these disorders. Unfortunately, our mechanistic understanding of the functional effects of combinatorial Tau phosphorylation remains minimal. Here, we generated four singly pseudophosphorylated Tau proteins (at Thr 231 , Ser 262 , Ser 396 , and Ser 404 ) and four doubly pseudophosphorylated Tau proteins using the same sites. Each Tau preparation was assayed for its abilities to promote microtubule assembly and to regulate microtubule dynamic instability in vitro. All four singly pseudophosphorylated Tau proteins exhibited loss-of-function effects. In marked contrast to the expectation that doubly pseudophosphorylated Tau would be less functional than either of its corresponding singly pseudophosphorylated forms, all of the doubly pseudophosphorylated Tau proteins possessed enhanced microtubule assembly activity and were more potent at regulating dynamic instability than their compromised singly pseudophosphorylated counterparts. Thus, the effects of multiple pseudophosphorylations were not simply the sum of the effects of the constituent single pseudophosphorylations; rather, they were generally opposite to the effects of singly pseudophosphorylated Tau. Further, despite being pseudophosphorylated at different sites, the four singly pseduophosphorylated Tau proteins often functioned similarly, as did the four doubly pseudophosphorylated proteins. These data lead us to reassess the conventional view of combinatorial phosphorylation in normal and pathological Tau action. They may also be relevant to the issue of combinatorial phosphorylation as a general regulatory mechanism.