In a conventional optical motion capture (MoCap) workflow, two processes are needed to turn captured raw marker sequences into correct skeletal animation sequences. Firstly, various tracking errors present in the markers must be fixed ( cleaning or refining ). Secondly, an agent skeletal mesh must be prepared for the actor/actress, and used to determine skeleton information from the markers ( re-targeting or solving ). The whole process, normally referred to as solving MoCap data, is extremely time-consuming, labor-intensive, and usually the most costly part of animation production. Hence, there is a great demand for automated tools in industry. In this work, we present MoCap-Solver, a production-ready neural solver for optical MoCap data. It can directly produce skeleton sequences and clean marker sequences from raw MoCap markers, without any tedious manual operations. To achieve this goal, our key idea is to make use of neural encoders concerning three key intrinsic components: the template skeleton, marker configuration and motion, and to learn to predict these latent vectors from imperfect marker sequences containing noise and errors. By decoding these components from latent vectors, sequences of clean markers and skeletons can be directly recovered. Moreover, we also provide a novel normalization strategy based on learning a pose-dependent marker reliability function, which greatly improves system robustness. Experimental results demonstrate that our algorithm consistently outperforms the state-of-the-art on both synthetic and real-world datasets.

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The thermal and mechanical properties of two types of polyester nanofiber, poly (1,4-cyclohexanedimethylene isosorbide terephthalate) (PICT) copolymers and the terpolyester of isosorbide, ethylene glycol, 1,4-cyclohexane dimethanol, and terephthalic acid (PEICT), were investigated. This is the first attempt to fabricate PICT nanofiber via the electrospinning method; comparison with PEICT nanofiber could give greater understanding of eco-friendly nanofibers containing biomass monomers. The nanofibers fabricated from each polymer show similar smooth and thin-and-long morphologies. On the other hand, the polymers exhibited significantly different mechanical and thermal properties; in particular, a higher tensile strength was observed for PICT nanofiber mat than for that of PEICT. We hypothesized that PICT has more trans-configuration than PEICT, resulting in enhancement of its tensile strength, and demonstrated this by Fourier transform infrared spectroscopy. In addition, PICT nanofibers showed clear crystallization behavior upon increased temperature, while PEICT nanofibers showed completely amorphous structure. Both nanofibers have better tensile properties and thermal stability than the typical polyester polymer, implying that they can be utilized in various industrial applications.

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Excessive amyloid beta (Aβ) deposition in brain is mainly responsible for cell damage and blood-brain barrier (BBB) disruption in Alzheimer's disease (AD). Catalpol, an iridoid glucoside extracted from the root of Rehmannia glutinosa Libosch, has neuroprotective effect against AD. It is unclear whether catalpol has a protective effect on Aβ-induced BBB leakage. We employed an immortalized endothelial cell line (bEnd.3) and astrocytes co-culture to mimic a BBB model in vitro and investigated the effect of catalpol on BBB. We found that treatment with catalpol decreased BBB hyperpermeability induced by fibrillar Aβ . Data from western blotting showed that catalpol prevented fibrillar Aβ -induced bEnd.3 cell apoptosis through mitochondria-dependent and death receptor pathways; decreased the levels of matrix metalloproteinases (MMPs), MMP-2, MMP-9, and the receptor for advanced glycation end products; and increased the levels of tight junction proteins (ZO-1, occludin, and claudin-5), low-density lipoprotein receptor-related protein 1, and P-glycoprotein in fibrillar Aβ -treated bEnd.3 cells. Moreover, catalpol also enhanced soluble Aβ efflux across the fibrillar Aβ -treated bEnd.3 cells BBB monolayer model. Altogether, our results suggest that catalpol alleviate fibrillar Aβ -induced BBB disruption, enhance soluble Aβ clearance, and offer a feasible therapeutic application in AD treatment.

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Type I interferon (IFN)‐induced Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signaling drives the expression of IFN‐stimulated genes (ISGs) to mediate antiviral response. The strength and duration of JAK‐STAT signaling are tightly regulated to ensure effective antiviral defense while avoiding pathological inflammation and autoimmunity. Here, we report that cTAZ, an isoform of the Hippo pathway effector TAZ, is transcribed by an alternative promoter. Although majority of C‐terminal sequences of TAZ is retained, cTAZ is not regulated by the Hippo signaling and does not mediate its growth‐inhibitory functions. Instead, cTAZ negatively regulates JAK‐STAT signaling by inhibiting STAT1/2 nuclear localization and ISG expression, and its expression is induced by type I IFN. Thus, cTAZ functions as a modulator of JAK‐STAT signaling and may play a role in fine‐tuning cellular antiviral response.