Video Coding with Motion Estimation at the Decoder

Predictive video coding is based on motion estimation. In such systems, the temporal correlation is exploited at the encoder, whereas at the decoder, the correlation between the previously decoded frames and the current frame is never exploited. In this chapter, we propose a method for motion estimation at the decoder. Based on the prediction residue and on the already decoded frames, the decoder is able to partially reconstruct the motion field, which therefore can be skipped in the encoded stream. The proposed approach is based on Least Square Estimation (LSE) prediction, and is suitable for low bit-rate video coding, in which the transmission of the motion field has a significant impact on the overall bit-rate. The same technique could also be useful in case of high definition video coding, where a detailed and accurate motion field is required. Preliminary results seem to be very promising

Coherent video reconstruction with motion estimation at the decoder

In traditional predictive video coding the block matching is performed at the encoder. The obtained motion field is then transmitted to the decoder, together with the prediction residue. Nevertheless, if the motion field is not provided it can be reconstructed, as long as the decoder manages to exploit some correlated information. This paper presents an algorithm for the motion estimation at the decoder side, given the prediction residue only. The main novelty of this algorithm relies on the contextual reconstruction of a frame region composed of several blocks. Simulation results show that taking into account a whole row can improve significantly the results obtained with an algorithm that reconstructs each block separately

Error Resilience Performance Evaluation of a Distributed Video Codec

Distributed Video Coding (DVC), one of the most active research field in the video coding community, is based on the combination of Slepian-Wolf coding techniques with the idea of performing the prediction at the decoder side rather than at the encoder side. Besides its main property, which is flexible allocation of computational complexity between encoder and decoder, the distributed approach has other interesting properties. One of the most promising DVC characteristics is its intrinsic robustness to transmission errors. In this work we have evaluated the error resilience performance of a video codec based on the DVC scheme proposed by Stanford, and we have carried out a preliminary comparison with traditional H.264 encoding, showing that at high error probabilities and high bitrates the distributed approach can also outperform the traditional one

Performance of a Distributed Video Codec Behaviours in Presence of Transmission Errors

Distributed Video Coding (DVC) is one of the most important and active research fields in video coding. The basic idea underlying DVC is to exploit the temporal correlation among frames directly in the decoding phase. The main properties of a distributed video coding system is that the computational load could in principle be shifted towards the decoder, with respect to a traditional video coding system. Anyway, the distributed coding approach has other interesting properties. In particular, one of the most promising benefits derived by the use of DVC is its natural error resilience to channel errors. Nevertheless, very few results on the actual error resilience properties of distributed video coding systems have been presented in literature. In this contribution we present a detailed analysis of the error resilience properties of a video coding system based on Stanford architecture. We analyze the behavior of such codec in presence of channel error, first focusing on the effect of such errors on the different parts of the encoded stream, and then making a preliminary comparison with H264

Crystal structure and biochemical characterization of the recombinant ThBgl, a GH1 β-glucosidase overexpressed in Trichoderma harzianum under biomass degradation conditions

Additional file 3: Table S3. Percent identity matrix between the GH3 β-glucosidase. The multiple sequence alignment was performed using the Clustal Omega server ( http://www.ebi.ac.uk/Tools/msa/clustalo/ )

Proteomic profiling reveals the transglutaminase-2 externalization pathway in kidneys after unilateral ureteric obstruction

Increased export of transglutaminase-2 (TG2) by tubular epithelial cells (TECs) into the surrounding interstitium modifies the extracellular homeostatic balance, leading to fibrotic membrane expansion. Although silencing of extracellular TG2 ameliorates progressive kidney scarring in animal models of CKD, the pathway through which TG2 is secreted from TECs and contributes to disease progression has not been elucidated. In this study, we developed a global proteomic approach to identify binding partners of TG2 responsible for TG2 externalization in kidneys subjected to unilateral ureteric obstruction (UUO) using TG2 knockout kidneys as negative controls. We report a robust and unbiased analysis of the membrane interactome of TG2 in fibrotic kidneys relative to the entire proteome after UUO, detected by SWATH mass spectrometry. The data have been deposited to the ProteomeXchange with identifier PXD008173. Clusters of exosomal proteins in the TG2 interactome supported the hypothesis that TG2 is secreted by extracellular membrane vesicles during fibrosis progression. In established TEC lines, we found TG2 in vesicles of both endosomal (exosomes) and plasma membrane origin (microvesicles/ectosomes), and TGF-β1 stimulated TG2 secretion. Knockout of syndecan-4 (SDC4) greatly impaired TG2 exosomal secretion. TG2 coprecipitated with SDC4 from exosome lysate but not ectosome lysate. Ex vivo, EGFP-tagged TG2 accumulated in globular elements (blebs) protruding/retracting from the plasma membrane of primary cortical TECs, and SDC4 knockout impaired bleb formation, affecting TG2 release. Through this combined in vivo and in vitro approach, we have dissected the pathway through which TG2 is secreted from TECs in CKD

Reduction of sulfenic acids by ascorbate in proteins, connecting thiol-dependent to alternative redox pathways

Sulfenic acids are the primary product of thiol oxidation by hydrogen peroxide and other oxidants. Several aspects of sulfenic acid formation through thiol oxidation were established recently. In contrast, the reduction of sulfenic acids is still scarcely investigated. Here, we characterized the kinetics of the reduction of sulfenic acids by ascorbate in several proteins. Initially, we described the crystal structure of our model protein (Tsa2-C170S). There are other Tsa2 structures in distinct redox states in public databases and all of them are decamers, with the peroxidatic cysteine very accessible to reductants, convenient features to investigate kinetics. We determined that the reaction between Tsa2-C170S-Cys-SOH and ascorbate proceeded with a rate constant of 1.40 ± 0.08 × 103 M−1 s−1 through a competition assay developed here, employing 2,6–dichlorophenol-indophenol (DCPIP). A series of peroxiredoxin enzymes (Prx6 sub family) were also analyzed by this competition assay and we observed that the reduction of sulfenic acids by ascorbate was in the 0.4–2.2 × 103 M−1 s−1 range. We also evaluated the same reaction on glyceraldehyde 3-phosphate dehydrogenase and papain, as the reduction of their sulfenic acids by ascorbate were reported previously. Once again, the rate constants are in the 0.4–2.2 × 103 M−1 s−1 range. We also analyzed the reduction of Tsa2-C170S-SOH by ascorbate by a second, independent method, following hydrogen peroxide reduction through a specific electrode (ISO-HPO-2, World Precision Instruments) and employing a bi-substrate, steady state approach. The was 7.4 ± 0.07 × 103 M−1 s−1, which was in the same order of magnitude as the value obtained by the DCPIP competition assay. In conclusion, our data indicates that reduction of sulfenic acid in various proteins proceed at moderate rate and probably this reaction is more relevant in biological systems where ascorbate concentrations are high

Emx2 is a dose-dependent negative regulator of Sox2 telencephalic enhancers.

The transcription factor Sox2 is essential for neural stem cells (NSC) maintenance in the hippocampus and in vitro. The transcription factor Emx2 is also critical for hippocampal development and NSC self-renewal. Searching for 'modifier' genes affecting the Sox2 deficiency phenotype in mouse, we observed that loss of one Emx2 allele substantially increased the telencephalic β-geo (LacZ) expression of a transgene driven by the 5' or 3' Sox2 enhancer. Reciprocally, Emx2 overexpression in NSC cultures inhibited the activity of the same transgene. In vivo, loss of one Emx2 allele increased Sox2 levels in the medial telencephalic wall, including the hippocampal primordium. In hypomorphic Sox2 mutants, retaining a single 'weak' Sox2 allele, Emx2 deficiency substantially rescued hippocampal radial glia stem cells and neurogenesis, indicating that Emx2 functionally interacts with Sox2 at the stem cell level. Electrophoresis mobility shift assays and transfection indicated that Emx2 represses the activities of both Sox2 enhancers. Emx2 bound to overlapping Emx2/POU-binding sites, preventing binding of the POU transcriptional activator Brn2. Additionally, Emx2 directly interacted with Brn2 without binding to DNA. These data imply that Emx2 may perform part of its functions by negatively modulating Sox2 in specific brain areas, thus controlling important aspects of NSC function in development