A video summarisation system for post-production

Post-production facilities deal with large amounts of digital video, which presents difficulties when tracking, managing and searching this material. Recent research work in image and video analysis promises to offer help in these tasks, but there is a gap between what these systems can provide and what users actually need. In particular the popular research models for indexing and retrieving visual data do not fit well with how users actually work. In this thesis we explore how image and video analysis can be applied to an online video collection to assist users in reviewing and searching for material faster, rather than purporting to do it for them. We introduce a framework for automatically generating static 2-dimen- sional storyboards from video sequences. The storyboard consists of a series of frames, one for each shot in the sequence, showing the principal objects and motions of the shot. The storyboards are rendered as vector images in a familiar comic book style, allowing them to be quickly viewed and understood. The process consists of three distinct steps: shot-change detection, object segmentation, and presentation. The nature of the video material encountered in a post-production fa- cility is quite different from other material such as television programmes. Video sequences such as commercials and music videos are highly dy- namic with very short shots, rapid transitions and ambiguous edits. Video is often heavily manipulated, causing difficulties for many video processing techniques. We study the performance of a variety of published shot-change de- tection algorithms on the type of highly dynamic video typically encoun- tered in post-production work. Finding their performance disappointing, we develop a novel algorithm for detecting cuts and fades that operates directly on Motion-JPEG compressed video, exploiting the DCT coeffi- cients to save computation. The algorithm shows superior performance on highly dynamic material while performing comparably to previous algorithms on other material

Modelling and animating cartoon hair

In this paper we present a technique for the modelling and animation of cartoon hair based on its tendency to be drawn and animated in clumps. In our approach the primary shape and motion of the hair is defined by an animated NURBS surface, thus allowing animators greater artistic control. The basis of the hair clumps is formed by key hair curves that are generated along the isocurves of the originating surface and which follow its motion. Profile curves of the hair are then extruded along the length of the key hairs to create the geometry details of the hairdo. A layer of particle dynamics is attached to each individual key hair to achieve some of the animation of the hair automatically. The finished animated hairdo is rendered non-photorealistically in cartoon style shading

Identification of the Sites of Tau Hyperphosphorylation and Activation of Tau Kinases in Synucleinopathies and Alzheimer’s Diseases

<div><p>Objective</p><p>Most neurodegenerative diseases contain hyperphosphorylated Tau [p-Tau]. We examined for the first time epitopes at which Tau is hyperphosphorylated in Parkinson’s disease, dementia with Lewy bodies and Alzheimer’s disease, and also select Tau kinases.</p> <p>Methods</p><p>Postmortem frontal cortex from Parkinson’s disease, dementia with Lewy bodies, Alzheimer’s disease and striata from Parkinson’s disease, were analyzed by immunoblots using commercially available antibodies against 20 different phospho-epitopes of Tau. Major Tau kinases were also screened. Results in diseased tissues were compared to nondiseased controls.</p> <p>Results</p><p>In Alzheimer’s disease, Tau was hyperphosphorylated at all the 20 epitopes of p-Tau. In dementia with Lewy bodies, p-Tau formation occurred at 6 sites sharing 30% overlap with Alzheimer’s disease, while in Parkinson’s frontal cortex, an area which does not degenerate, Tau hyperphosphorylation was seen at just 3 epitopes, indicating 15% overlap with Alzheimer’s disease. In Parkinson’s disease striatum, an area which undergoes considerable neurodegeneration, Tau was hyperphosphorylated at 10 epitopes, sharing 50% overlap with Alzheimer’s disease. Between frontal cortex of Parkinson’s disease and dementia with Lewy bodies, there were only two p-Tau epitopes in common. In striata of Parkinson’s disease, there were 3 clusters of Tau hyperphosphorylated at 3 contiguous sites, while two such clusters were detected in dementia with Lewy bodies; such clusters disrupt axonal transport of mitochondria, cause microtubule remodeling and result in cell death. p-GSK-3β, a major Tau kinase, was activated in all brain regions examined, except in dementia with Lewy bodies. Activation of other Tau kinases was seen in all brain regions, with no clear pattern of activation.</p> <p>Interpretation</p><p>Our studies suggest that the three neurodegenerative diseases each have a signature-specific profile of p-Tau formation which may be useful in understanding the genesis of the diseases and for the development of a panel of specific biomarkers.</p> </div

Schematic of Tau phosphorylation in PD, DLB, and AD.

<p>Full length Tau [2N4R] contains ~45 known Thr/Ser sites known to be hyperphosphorylated in AD. These sites are spread throughout several regions of Tau, including the E2/E3 domains, the proline-rich domain, the MT-binding domain, and the C-terminal of the Tau protein. Phosphorylation at 20 sites [Table S1 in File S1] was analyzed in PD striata [bottom] and DLB FC [top]. Sites with elevated phosphorylation are indicated in red, while sites where phosphorylation was similar to controls are indicated in blue. A decrease in phosphorylation at T231 was identified in DLB tissues [green]. Sites in orange represent hyperphosphorylated sites present in DLB FC. Sites in black denote epitopes not tested in PD or DLB or AC. All sites shown, regardless of color, are hyperphosphorylated in AD.</p

Expression of synuclein proteins in FC of PD, DLB, AD and PD striata.

<p>[A] Postmortem PD FC from [N = 7-9] diseased and [N = 7] non-diseased controls, [B] FC from DLB cases [N = 7-10] and non-diseased controls [N = 7-10], [C] FC from AD cases [N = 5-6] and non-diseased controls [N = 4-6], and [D] Striata from PD cases [N = 7-9] and non-diseased controls [N = 7-10]; were analyzed using immunoblots for expression of α-Syn, β-Syn, and γ-Syn, using antibodies listed in Table S1 in File S1. OD of each protein relative to GAPDH is presented as percent of corresponding non-diseased control cases [mean ± SEM]. Data for each Syn protein were analyzed by t-test for difference from corresponding control group [*p<0.05; **p<0.01].</p

Identification of Tau phosphorylation sites in postmortem human FC from PD, DLB AD and PD striata.

<p>Western blot analyses of p-Tau levels were conducted using specific p-Tau antibodies as described in Materials [see Table S1 in File S1]. [A] postmortem FC of human PD cases [N = 7-9] and non-diseased controls [N = 7]; [B] FC from human DLB cases [N = 7-10] and non-diseased controls [N = 7-10]; [C] postmortem FC from human AD cases [N = 5-6] and non-diseased controls [N = 4-6], [D] postmortem striata from human PD cases [N = 7-9] and non-diseased controls [N = 7-10]; Summary of quantitation for opticzal density [OD] of each p-Tau site relative to total Tau is presented as percent of age-matched control. Due to large variation in human tissues, scatter plots were drawn to show variations within each individual control sample [blue squares] or diseased sample [red circles]. Bars show group means ± SEM. Data for each p-Tau site were analyzed by t-test for difference from the control group [*p<0.05].</p

Immunohistochemical analyses of α-Syn and p-Tau.

<p>IHC of paraffin embedded tissue from AD FC, PD substantia nigra and DLB FC with appropriate aged matched non-diseased controls, were conducted as described in Methods of File S1. [A] Analysis of α-Syn associated pathology in PD [uppermost horizontal panel], DLB [middle horizontal panel] and AD [lower horizontal panel] comparing age matched control tissue [left vertical panel] with diseased tissue [middle and right-magnified vertical panels]. Lewy bodies increased in intensity and density as follows: PD > DLB > AZ. * denotes Lewy bodies and were present only in PD and DLB tissues. [B] Analysis of p-Ser396/404 associated pathology in AD [uppermost horizontal panel], PD substantia nigra [middle horizontal panel] and DLB [bottom horizontal panel], compared age matched control tissue [left vertical panel] with diseased tissue [middle and right-magnified]. * Aggregates, ** Tangles.</p