139 research outputs found

    Research of Simulation in Character Animation Based on Physics Engine

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    Computer 3D character animation essentially is a product, which is combined with computer graphics and robotics, physics, mathematics, and the arts. It is based on computer hardware and graphics algorithms and related sciences rapidly developed new technologies. At present, the mainstream character animation technology is based on the artificial production of key technologies and capture frames based on the motion capture device technology. 3D character animation is widely used not only in the production of film, animation, and other commercial areas but also in virtual reality, computer-aided education, flight simulation, engineering simulation, military simulation, and other fields. In this paper, we try to study physics based character animation to solve these problems such as poor real-time interaction that appears in the character, low utilization rate, and complex production. The paper deeply studied the kinematics, dynamics technology, and production technology based on the motion data. At the same time, it analyzed ODE, PhysX, Bullet, and other variety of mainstream physics engines and studied OBB hierarchy bounding box tree, AABB hierarchical tree, and other collision detection algorithms. Finally, character animation based on ODE is implemented, which is simulation of the motion and collision process of a tricycle

    Dilation-Erosion for Single-Frame Supervised Temporal Action Localization

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    To balance the annotation labor and the granularity of supervision, single-frame annotation has been introduced in temporal action localization. It provides a rough temporal location for an action but implicitly overstates the supervision from the annotated-frame during training, leading to the confusion between actions and backgrounds, i.e., action incompleteness and background false positives. To tackle the two challenges, in this work, we present the Snippet Classification model and the Dilation-Erosion module. In the Dilation-Erosion module, we expand the potential action segments with a loose criterion to alleviate the problem of action incompleteness and then remove the background from the potential action segments to alleviate the problem of action incompleteness. Relying on the single-frame annotation and the output of the snippet classification, the Dilation-Erosion module mines pseudo snippet-level ground-truth, hard backgrounds and evident backgrounds, which in turn further trains the Snippet Classification model. It forms a cyclic dependency. Furthermore, we propose a new embedding loss to aggregate the features of action instances with the same label and separate the features of actions from backgrounds. Experiments on THUMOS14 and ActivityNet 1.2 validate the effectiveness of the proposed method. Code has been made publicly available (https://github.com/LingJun123/single-frame-TAL).Comment: 28 pages, 8 figure

    Observation of strong attenuation within the photonic band gap of multiconnected networks

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    We theoretically and experimentally study a photonic band gap (PBG) material made of coaxial cables. The coaxial cables are waveguides for the electromagnetic waves and provide paths for direct wave interference within the material. Using multiconnected coaxial cables to form a unit cell, we realize PBGs via (i) direct interference between the waveguides within each cell and (ii) scattering among different cells. We systematically investigate the transmission of EM waves in our PBG materials and discuss the mechanism of band gap formation. We observe experimentally for the first time the wide band gap with strong attenuation caused by direct destructive interference

    Role of OCT4 in cisplatin treatment of testicular embryonal carcinoma

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    Purpose: To determine the role of embryonal transcription factor OCT4 in cisplatin treatment of testicular embryonal carcinoma.Methods: In vitro assays were employed to assess the effect of cisplatin treatment on testicular embryonal carcinoma cell lines under OCT4 silencing. Following treatment with 500 ng/μL cisplatin, MTT assay was used to examine cell proliferation of 2012-EP and 833K-E cells with or without OCT silencing, while wound healing assay was used to examine cell migration ability. Transwell assay and crystal violet staining were employed to measure cell invasive capacity, whereas the distribution pattern of cell cycle was assessed by flow cytometry. The expression levels of several critical components in tumorigenicity related pathways with or without OCT silencing were determined by Western-blot analysis.Results: Cisplatin enhanced OCT4-silenced cell viability at all concentration (p < 0.01) when compared to control cells. Upon treatment with 500 ng/μL cisplatin, OCT4-silenced cells showed 2- to 3-fold enhancement in cell proliferation (p < 0.001), 2-fold increase in cell migration capacity (p < 0.001), and about 1.5-fold enhancement in invasive capacity (p < 0.001) when compared to control cells. In addition, OCT4 silencing upregulated the expression level of the proteins involved in cell proliferation, cell mobility, cancer metastasis and cell cycle control.Conclusion: The results suggest that OCT4 may serve as a therapeutic target for testicular embryonal carcinoma treatment in combination with cisplatin by modulating OCT4 expression level. This physiological evidence indicates that OCT4 downregulation contributes to cisplatin resistance in chemotherapy and subsequent disease relapse.Keywords: OCT4, Cisplatin resistance, Testicular embryonal carcinoma, Chemotherap

    A Liver-Enriched Long Non-Coding RNA, lncLSTR, Regulates Systemic Lipid Metabolism in Mice

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    SummaryLong non-coding RNAs (lncRNAs) constitute a significant portion of mammalian genome, yet the physiological importance of lncRNAs is largely unknown. Here, we identify a liver-enriched lncRNA in mouse that we term liver-specific triglyceride regulator (lncLSTR). Mice with a liver-specific depletion of lncLSTR exhibit a marked reduction in plasma triglyceride levels. We show that lncLSTR depletion enhances apoC2 expression, leading to robust lipoprotein lipase activation and increased plasma triglyceride clearance. We further demonstrate that the regulation of apoC2 expression occurs through an FXR-mediated pathway. LncLSTR forms a molecular complex with TDP-43 to regulate expression of Cyp8b1, a key enzyme in the bile acid synthesis pathway, and engenders an in vivo bile pool that induces apoC2 expression through FXR. Finally, we demonstrate that lncLSTR depletion can reduce triglyceride levels in a hyperlipidemia mouse model. Taken together, these data support a model in which lncLSTR regulates a TDP-43/FXR/apoC2-dependent pathway to maintain systemic lipid homeostasis

    Terlipressin May Decrease In-Hospital Mortality of Cirrhotic Patients with Acute Gastrointestinal Bleeding and Renal Dysfunction: A Retrospective Multicenter Observational Study

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    Acute gastrointestinal bleeding (GIB) rapidly reduces effective blood volume, thereby precipitating acute kidney injury (AKI). Terlipressin, which can induce splanchnic vasoconstriction and increase renal perfusion, has been recommended for acute GIB and hepatorenal syndrome in liver cirrhosis. Thus, we hypothesized that terlipressin might be beneficial for cirrhotic patients with acute GIB and renal impairment. In this Chinese multi-center study, 1644 cirrhotic patients with acute GIB were retrospectively enrolled. AKI was defined according to the International Club of Ascites (ICA) criteria. Renal dysfunction was defined as serum creatinine (sCr) > 133 μmol/L at admission and/or any time point during hospitalization. Incidence of renal impairment and in-hospital mortality were the primary end-points. The incidence of any stage ICA-AKI, ICA-AKI stages 1B, 2, and 3, and renal dysfunction in cirrhotic patients with acute GIB was 7.1%, 1.8%, and 5.0%, respectively. The in-hospital mortality was significantly increased by renal dysfunction (14.5% vs. 2.2%, P < 0.001) and ICA-AKI stages 1B, 2, and 3 (11.1% vs. 2.8%, P = 0.011), but not any stage ICA-AKI (5.7% vs. 2.7%, P = 0.083). The in-hospital mortality was significantly decreased by terlipressin in patients with renal dysfunction (3.6% vs. 20.0%, P = 0.044), but not in those with any stage ICA-AKI (4.5% vs. 6.0%, P = 0.799) or ICA-AKI stages 1B, 2, and 3 (0.0% vs. 14.3%, P = 0.326). Renal dysfunction increased the in-hospital mortality of cirrhotic patients with acute GIB. Terlipressin might decrease the in-hospital mortality of cirrhotic patients with acute GIB and renal dysfunction. NCT03846180 ( https://clinicaltrials.gov )

    Identification of a Novel UT-B Urea Transporter in Human Urothelial Cancer

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    The urea transporter UT-B is widely expressed and has been studied in erythrocyte, kidney, brain and intestines. Interestingly, UT-B gene has been found more abundant in bladder than any other tissue. Recently, gene analyses demonstrate that SLC14A1 (UT-B) gene mutations are associated with bladder cancer, suggesting that urea transporter UT-B may play an important role in bladder carcinogenesis. In this study, we examined UT-B expression in bladder cancer with human primary bladder cancer tissues and cancer derived cell lines. Human UT-B has two isoforms. We found that normal bladder expresses long form of UT-B2 but was lost in 8 of 24 (33%) or significantly downregulated in 16 of 24 (67%) of primary bladder cancer patients. In contrast, the short form of UT-B1 lacking exon 3 was detected in 20 bladder cancer samples. Surprisingly, a 24-nt in-frame deletion in exon 4 in UT-B1 (UT-B1Δ24) was identified in 11 of 20 (55%) bladder tumors. This deletion caused a functional defect of UT-B1. Immunohistochemistry revealed that UT-B protein levels were significantly decreased in bladder cancers. Western blot analysis showed a weak UT-B band of 40 kDa in some tumors, consistent with UT-B1 gene expression detected by RT-PCR. Interestingly, bladder cancer associate UT-B1Δ24 was barely sialylated, reflecting impaired glycosylation of UT-B1 in bladder tumors. In conclusion, SLC14A1 gene and UT-B protein expression are significantly changed in bladder cancers. The aberrant UT-B expression may promote bladder cancer development or facilitate carcinogenesis induced by other carcinogens
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