23 research outputs found

    Performance Evaluation and Parameter Optimization of SoftCast Wireless Video Broadcast

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    Wireless video broadcast plays an imp ortant role in multimedia communication with the emergence of mobile video applications. However, conventional video broadcast designs suffer from a cliff effect due to separated source and channel encoding. The newly prop osed SoftCast scheme employs a cross-layer design, whose reconstructed video quality is prop ortional to the channel condition. In this pap er, we provide the p erformance evaluation and the parameter optimization of the SoftCast system. Optimization principles on parameter selection are suggested to obtain a b etter video quality, o ccupy less bandwidth and/or utilize lower complexity. In addition, we compare SoftCast with H.264 in the LTE EPA scenario. The simulation results show that SoftCast provides a b etter p erformance in the scalability to channel conditions and the robustness to packet losses

    TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

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    Abstract Background Bladder cancer is one of the most common malignant tumors of the urinary system and is associated with a poor prognosis once invasion and distant metastases occur. Epithelial-mesenchymal transition (EMT) drives metastasis and invasion in bladder cancer. Transforming growth factor β1 (TGF-β1) and stromal fibroblasts, especially cancer-associated fibroblasts (CAFs), are positive regulators of EMT in bladder cancer. However, it remains unclear how TGF-β1 mediates crosstalk between bladder cancer cells and CAFs and how it induces stromal fibroblast-mediated EMT in bladder cancer. We aimed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells. Methods Primary CAFs with high expression of fibroblast activation protein (FAP) were isolated from bladder cancer tissue samples. Subsequently, different conditioned media were used to stimulate the bladder cancer cell line T24 in a co-culture system. Gene set enrichment analysis, a human cytokine antibody array, and cytological assays were performed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells. Results Among the TGF-β family, TGF-β1 was the most highly expressed factor in bladder cancer tissue and primary stromal fibroblast supernatant. In the tumor microenvironment, TGF-β1 was mainly derived from stromal fibroblasts, especially CAFs. In stimulated bladder cells, stromal fibroblast-derived TGF-β1 promoted bladder cancer cell migration, invasion, and EMT. Furthermore, TGF-β1 promoted the activation of stromal fibroblasts, inducing CAF-like features, by upregulating FAP in primary normal fibroblasts and a normal fibroblast cell line. Stromal fibroblast-mediated EMT was induced in bladder cancer cells by TGF-β1/FAP. Versican (VCAN), a downstream molecule of FAP, plays an essential role in TGF-β1/FAP axis-induced EMT in bladder cancer cells. VCAN may also function through the PI3K/AKT1 signaling pathway. Conclusions TGF-β1 is a critical mediator of crosstalk between stromal fibroblasts and bladder cancer cells. We revealed a new mechanism whereby TGF-β1 dominated stromal fibroblast-mediated EMT of bladder cancer cells via the FAP/VCAN axis and identified potential biomarkers (FAP, VCAN, N-cadherin, and Vimentin) of bladder cancer. These results enhance our understanding of bladder cancer invasion and metastasis and provide potential strategies for diagnosis, treatment, and prognosis

    Additional file 6 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

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    Additional file 6:(A) qRT-PCR verifies that the mRNA expression of FAP in OEFAP-HFFs is significantly higher than in NCFAP-HFFs and T24 cells. (B, C) WB indicates that the protein expression of FAP in OEFAP-HFFs is significantly higher than in NCFAP-HFFs and T24 cells. (D, E) WB show that HFF-CM (stimulated or not stimulated) has a pro-EMT effect, with downregulated E-cadherin and upregulated N-cadherin and Vimentin. The pro-EMT effects of HFF-CM were significantly amplified after TGF-β1 induction or overexpression FAP, while the TGF-β1 neutralizing antibody reverses the pro-EMT effects of TGF-β1 induction

    Additional file 10 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

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    Additional file 10: (A) BLCA with lymphovascular invasion expressed more FAP and VCAN than without lymphovascular invasion. In OS (B) and DSS (C) events, FAP, VCAN, N-cadherin, and Vimentin expression in the deceased group is higher than in the alive group. (D) In PFI events, VCAN and N-cadherin are more highly expressed in the deceased group. Immunohistochemistry (E) and dot blot (F) shows that the expression of TGF-β1, FAP, VCAN, N-cadherin, and Vimentin in BLCA tissues is significantly higher than in adjacent normal tissues, while the expression of E-cadherin in BLCA tissues is lower than in adjacent normal tissues. (G) TGF-β1 dominates stromal fibroblast-mediated EMT of bladder cancer cells via the FAP/VCAN axis to promote the invasion and metastasis of BLCA

    Additional file 9 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

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    Additional file 9: qRT-PCR (A, B), WB(C, D), and immunohistochemistry (E, F) showed that TGF-β1/FAP/VCAN axis regulates bladder cancer EMT in vivo. CAF has a stronger EMT-inducing effect than NF. Overexpression of FAP enhanced the EMT-inducing effects of stromal fibroblasts, while knockdown of FAP weakened those effects
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