Academic literature on the topic 'Duan yu'

We study the problem of distinguishing quantum states using local operations and classical communication (LOCC). A question of fundamental interest is whether there exist sets of $k \leq d$ orthogonal maximally entangled states in $\complex^{d}\otimes\complex^{d}$ that are not perfectly distinguishable by LOCC. A recent result by Yu, Duan, and Ying [Phys. Rev. Lett. 109 020506 (2012)] gives an affirmative answer for the case $k = d$. We give, for the first time, a proof that such sets of states indeed exist even in the case $k < d$. Our result is constructive and holds for an even wider class of operations known as positive-partial-transpose measurements (PPT). The proof uses the characterization of the PPT-distinguishability problem as a semidefinite program.

We have developed a software platform for converting the Chinese classics into a digital format which the original layout is preserved. This method of conversion allows those that are not experts in classical Chinese literature, even those that do not understand Chinese, to partake in the proof-reading process. Since this kind of application involves complicated manipulation of 2D graphics, in the past, we have no choice but writing a native desktop program, with the introduction of CANVAS tag to the HTML 5 standards, we are able to move our code from desktop to browser without any plug-in or JAVA applet. The cost of cross-platform development and maintenance is greatly reduced. In order to clarify the various elements involved in the conversion and proof-reading process, we will use Duan Yu Cai's compilation of the Shuowen Jiezi 1 as an example throughout this paper.

Abstract Bone metastasis is a frequent complication of breast cancer, occurring in about 50-70% of breast cancer patients with late-stage disease. The lack of effective therapy suggests that the precise molecular mechanisms underlying bone metastasis are still unclear. Enhancer of zeste homolog 2 (EZH2) is considered a breast cancer oncogene and its expression is correlated with metastasis of breast cancer, but its function in bone metastasis has not been well explored. Herein we report that EZH2 promotes osteolytic metastasis of breast cancer through regulating transforming growth factor beta (TGFβ) signaling, a key pathway in bone metastasis. Knocking down EZH2 decreases bone metastasis incidence and outgrowth in vivo. EZH2 induces cancer cell proliferation and osteoclast maturation, when breast cancer cells are co-cultured with osteoblasts and osteoclasts together in vitro. Mechanistically, EZH2 increases transcription of ITGB1, which encodes for integrin β1. Integrin β1 activates focal adhesion kinase (FAK), which phosphorylates TGFβ receptor type I (TGFβRI) at tyrosine 182, thus enhances the binding of TGFβRI to TGFβ receptor type II (TGFβRII), therefore activates Smad2 and increases parathyroid hormone-like hormone (PTHLH) expression. Clinically applicable FAK inhibitors but not EZH2 methyltransferase inhibitor effectively inhibits breast cancer bone metastasis in vivo. Overall, our data signify integrin β1-FAK as a new downstream effector of EZH2 in breast cancer cells, and EZH2-integrin β1-FAK axis cooperates with TGFβ signaling pathway to promote bone metastasis of breast cancer. Citation Format: Lin Zhang, Jingkun Qu, Yutao Qi, Yimin Duan, Yu-Wen Huang, Zhifen Zhou, Ping Li, Jun Yao, Beibei Huang, Shuxing Zhang, Dihua Yu. EZH2 engages TGFb signaling to promote breast cancer bone metastasis via Integrin b1-FAK activation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2435.

Abstract Objective Costa Rica has the highest percentage of older adults (65+) of the Central American and Latin American region. In fact, Costa Rica has the highest life expectancy within an advanced healthcare system and socioeconomic infrastructure that differentiates it from neighboring countries in Central America. Previous research has shown that older adults who engage in higher social engagement show overall better cognitive functioning (Chen et al., 2018); however, limited research has examined the impact of socialization on cognition across rural and urban regions and furthermore no research to date has examined these factors in Costa Rican older adults. This study examined the effects of community engagement on cognition in urban and rural older adults residing in Costa Rica. Participants and Method Participants were neurotypical older adults residing in San Jose (urban region, n = 156) and Guanacaste (rural region, n = 69). Those with a history of neurological conditions and major psychiatric disorders were excluded. Results Older adults residing in an urban area (M = 55.43, SD = 23.26) participate more in social engagement within the community compared to those residing in the rural region (M = 46.30, SD = 28.50), p = 0.019. Furthermore, in the urban sample, those with higher social engagement showed better performance on learning and encoding (r = 30), verbal memory (r = 0.26), and executive functioning (r = .20). In older adults residing in the rural region, higher social engagement was only associated with better visuospatial abilities (r = 0.27). Conclusions Findings suggest that social engagement in the community for older adults in Costa Rica may serve as a protective factor for their cognitive health. However, there are significant differences on what cognitive processes serve as a protective factor as a function of location (rural versus urban). This study highlights the importance of examining the quality of social engagement when evaluating the cognition of Costa Rican older adults. References Chen, Ya-Mei, Tu, Yu-Kang, Yu, Hsiao-Wei, Chiu, Tzu-Ying, Chiang, Tung-Liang, Chen, Duan-Rung, & Chang, Ray-E. (2018). Leisure time activities as mediating variables in functional disability progression: An application of parallel latent growth curve modeling. PLoS ONE, 13(10).

Statement of the problem. The twentieth century marked an increased interest in polyphonic music. The geography of polyphonic works for piano expanded significantly and a creative development of many Chinese composers, writing polyphonic piano pieces, took place. Today, polyphonic pieces make up a significant part of the piano repertoire in China, but they are little studied by musicologists and performers. The objective of this study – to reveal the contribution of Chinese composers to the creation of polyphonic piano repertoire of the XX – early XXI century. Analysis of the research and publications on the theme. А large number of modern authors study polyphony from the point of physical and mathematical research methods (Igarashi, Yu. & Ito, Masashi & Ito, Akinori, 2013; Weiwei, Zhang & Zhe, Chen, & Fuliang, Yin, 2016; Li, Xiaoquan et al. others, 2018). This approach does not reveal the factual musical component of polyphonic genres. In the 20th century, musicologists explored polyphony in musical folklore (Wiant, 1936; Fan Zuyin, 2004; Li Hong, 2015) and in professional Chinese composing (Sun Wei-bo, 2006, Winzenburg, 2018). The scientific novelty. This article studies the role of Chinese composers in the development of the world polyphonic piano repertoire of the XX – early XXI century. The methodological basis for the analysis of polyphonic works was the theoretical concepts of P. Hindemith, Peng Cheng, Fang Zuin, Li Hong, Sun Wei-bo. The results of the study. The research outcomes demonstrate the evolutionary development of the genre diversity of Chinese piano polyphony as well as those composers who created magnificent musical pieces. Conclusions. Chinese composers have fully mastered the art of modern counterpoint, represented by the genres of polyphonic program pieces (He Lu Ting), invention (Xiao Shu Xian, Du Qian, Sun Yun Yin, Chen Chen Quang), polyphonic suite (Ma Gui), large polyphonic cycle ( He Shao, Chen Hua Do, Xiao Shu Xian), fugue (Li Jun Yong, Yu Su Yan, Chen Gang, Tian Lei Lei, Duan Ping Tai, Zheng Zhong, Xiao Shu Xian) and small cycle “Prelude and Fugue” (Ding Shan Te, Chen Zhi Ming, Wang Li Shan). Creatively assimilating and rethinking the experience of Western polyphonists, Chinese composers have filled their polyphonic works with national features, firmly linking them with the origins of Chinese traditional and folk music. The polyphonic way of transmitting musical material becomes the most expressive at the moments of profound creativity and musical dramatization.

Abstract Among the 300,000 newly diagnosed breast cancer patients every year, 5~20% of them will develop symptomatic brain metastasis, whose 1-year survival rate is lower than 20%. Our group previously reported that brain tumor microenvironment (TME)-mediated PTEN downregulation in brain metastatic tumor cells increases the secretion of the chemokine CCL2, which enhances the infiltration of CCR2+ bone marrow derived myeloid cells, eventually promoting brain metastasis outgrowth. However, the mechanism of CCL2-CCR2 axis promoting brain metastasis is not clear, and the efficacy of targeting either CCR2 or CCL2 remained to be assessed. Here we show that Ccr2 antagonism significantly blocked Ccr2high myeloid cells trafficking in the blood and infiltration into the brain TME. However, Ccr2 antagonism did not sufficiently impede breast cancer brain metastasis in multiple preclinical models. Nevertheless, knocking down CCL2 or targeting CCL2 exhibited significant inhibition of brain metastasis growth. Subsequent analysis of the brain TME through mass cytometry demonstrated dramatically decreased infiltration of both Ccr2high and Ccr2low myeloid cell populations in the CCL2 targeted group, implying that the Ccr2low myeloid cells are also involved in promoting brain metastasis growth. Our data highlights the differential responses between targeting CCR2 or CCL2 in multiple preclinical brain metastasis models, which direct us to explore the function of Ccr2low myeloid cells in regulating brain metastasis progression. Our findings also suggest that carefully choosing between CCR2 or CCL2 as a target to control brain metastasis is important in clinical practice. Citation Format: Yimin Duan, Yutao Qi, Lin Zhang, Xiangliang Yuan, Dihua Yu. Assessing the effect of blocking CCL2-CCR2 axis on breast cancer brain metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6370.

Abstract In the multicenter, dose-escalation and dose-expansion phase 1 clinical trial (NCT05767866), we evaluated safety and tolerability of YK-029A in various EGFR mutated non-small-cell lung cancer (NSCLC). We have reported efficacy of YK-029A in untreated NSCLC with EGFR ex20ins mutation[1]. This time we report efficacy of YK-029A in patients with acquired EGFR T790M mutation after failure of first or second generation EGFR tyrosine kinase inhibitors (TKIs). Method: This dose-escalation and dose-expansion phase 1 trial recruited previously treated NSCLC patients with EGFR T790M mutation or patients with EGFR ex20ins or EGFR rare mutations. In dose-escalation phase, patients with EGFR T790M mutation were enrolled. YK-029A was given at doses of 50, 100, 150, 200 to 250 mg/day (3+3 design). In dose-expansion phase, patients with EGFR T790M, EGFR ex20ins, or EGFR rare mutations were enrolled. The primary objective was safety. Dose-limiting toxicity (DLT) and maximum tolerated dose (MTD) were explored. Efficacy of YK-029A in EGFR T790M mutated NSCLC was assessed by the investigators. Results: A total of 114 patients were recruited into the study. Safety profile of the first 108 patients was reported previously[1]. By the cut-off date on Sep 12, 2023, 38 patients harbored EGFR T790M mutation were included in efficacy analysis. All these patients were previously treated with first or second generation EGFR-TKIs. The objective response rate (ORR; RECIST 1.1) was 65.8% (95%CI: 48.6%-80.4%) and disease control rate (DCR) was 84.2% (95%CI: 68.7%-94.0%). With a median follow-up time of 8.2 months,the median progression free survival (PFS) was 11.0 months (95%CI: 7.75-NR). The median overall survival (OS) was not reached. Among the 8 patients with measurable brain metastases, intracranial ORR was 75% (95%CI: 35.6%-95.6%) . Conclusions: YK-029A has promising activity in previously treated NSCLC patients harboring EGFR T790M mutation. Reference[1] DUAN J, WU L, YANG K, et al. Safety, Tolerability, Pharmacokinetics, and Preliminary Efficacy of YK-029A in Treatment-Naive Patients With Advanced NSCLC Harboring EGFR Exon 20 Insertion Mutations: A Phase 1 Trial [J]. J Thorac Oncol, 2023. Citation Format: Rui Wan, Yi Fung Chau, Jun Zhao, Zhe Liu, Mingfang Zhao, Yanqiu Zhao, Xiumei Dai, Yueyin Pan, Zhihong Zhang, Yu Yao, Kunyu Yang, Lin Wu, Yanyan Xie, Bi Chen, Yixuan Yang, Yongqi Guo, Jie Wang, Jianchun Duan. Efficacy of YK-029A, a novel EGFR TKI, in advanced NSCLC patients with acquired T790M mutation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr CT055.

Abstract Regulatory T Cells (Treg) inhibit effector T cell (Teff) activity in the tumor microenvironment (TME). Therefore, depletion of regulatory T cells (Treg cells) is a promising therapeutic strategy for tumor immunotherapy. Tumor necrosis factor receptor-2 (TNFR2) is highly expressed on Treg cells and is a potential target for anti-tumor therapy. A TNFR2 non-blocking antibody (1C3) was generated from humanized IgG mice (RenMice), which is an effective platform for human antibody generation. 1C3 was selected from a large panel of antibody candidates through an unbiased, high-throughput in vivo efficacy screen in syngeneic tumor mouse models in humanized TNFR2 mice. Compared with other TNFR2 antagonistic antibodies, 1C3 effectively promoted the proliferation of CD8+ cytotoxic T cells in vitro, a population that is inhibited by Treg cells. To evaluate 1C3 efficacy and safety in vivo, syngeneic mouse tumor models were established. 1C3 monotherapy significantly inhibited tumor growth in a dose-dependent manner in syngeneic tumor mouse models in TNFR2 humanized mice. In combination with anti-human PD-1 or PD-L1 antibody, 1C3 also greatly increased antitumor activity compared to the monotherapy of each therapeutic agent. Mechanistically, 1C3 treatment significantly increased the ratio of Teff/Treg in the TME. In addition, 1C3 was well tolerated in TNFR2 humanized mice, and no side effects were observed even when the dose was increased to 100 mg/kg. Taken together, our data demonstrates that 1C3 is a novel anti-TNFR2 antibody for anti-tumor therapy and provides a great potential for the next generation of immunotherapy. Citation Format: Yongfei Yang, Shuzhen Cao, Jing Zhang, Zhe Shao, Xueyuan Jiang, Qingya Duan, Maopeng Tian, Sen Mei, Luke (Zhaoxue) Yu. 1C3, a Novel non-blocking anti-human TNFR2 antibody generated from RenMice, exhibits promising anti-tumor activity and safety in syngeneic tumor models in humanized TNFR2 mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2907.