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621 results on '"Xia, Lijun"'

1. On-chip generation and collectively coherent control of the superposition of the whole family of Dicke states

Author

Chen, Leizhen, Lu, Liangliang, Xia, Lijun, Lu, Yanqing, Zhu, Shining, and Ma, Xiao-song

Subjects
Quantum Physics
Abstract

Integrated quantum photonics has recently emerged as a powerful platform for generating, manipulating, and detecting entangled photons. Multipartite entangled states lie at the heart of the quantum physics and are the key enabling resources for scalable quantum information processing. Dicke state is an important class of genuinely entangled state, which has been systematically studied in the light-matter interactions, quantum state engineering and quantum metrology. Here, by using a silicon photonic chip, we report the generation and collectively coherent control of the entire family of four-photon Dicke states, i.e. with arbitrary excitations. We generate four entangled photons from two microresonators and coherently control them in a linear-optic quantum circuit, in which the nonlinear and linear processing are achieved in a chip-scale device. The generated photons are in telecom band, which lays the groundwork for large-scale photonic quantum technologies for multiparty networking and metrology., Comment: 19 pages, 4 figures in the main text and 13 figures in the Supplemental Material

Published
2023
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2. Experimental optimal verification of three-dimensional entanglement on a silicon chip

Author

Xia, Lijun, Lu, Liangliang, Wang, Kun, Jiang, Xinhe, Zhu, Shining, and Ma, Xiaosong

Subjects
Quantum Physics, Physics - Optics
Abstract

High-dimensional entanglement is significant for the fundamental studies of quantum physics and offers unique advantages in various quantum information processing (QIP) tasks. Integrated quantum devices have recently emerged as a promising platform for creating, processing, and detecting complex high-dimensional entangled states. A crucial step towards practical quantum technologies is to verify that these devices work reliably with an optimal strategy. In this work, we experimentally implement an optimal quantum verification strategy on a three-dimensional maximally entangled state using local projective measurements on a silicon photonic chip. A 95% confidence is achieved from 1190 copies to verify the target quantum state. The obtained scaling of infidelity as a function of the number of copies is -0.5497+-0.0002, exceeding the standard quantum limit of -0.5 with 248 standard deviations. Our results indicate that quantum state verification could serve as an efficient tool for complex quantum measurement tasks.

Published
2022
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9. Towards the standardization of quantum state verification using optimal strategies

Author

Jiang, Xinhe, Wang, Kun, Qian, Kaiyi, Chen, Zhaozhong, Chen, Zhiyu, Lu, Liangliang, Xia, Lijun, Song, Fangmin, Zhu, Shining, and Ma, Xiaosong

Subjects
Quantum Physics, Physics - Optics
Abstract

Quantum devices for generating entangled states have been extensively studied and widely used. As so, it becomes necessary to verify that these devices truly work reliably and efficiently as they are specified. Here, we experimentally realize the recently proposed two-qubit entangled state verification strategies using both local measurements (nonadaptive) and active feed-forward operations (adaptive) with a photonic platform. About 3283/536 number of copies ($N$) are required to achieve a 99% confidence to verify the target quantum state for nonadaptive/adaptive strategies. These optimal strategies provide the Heisenberg scaling of the infidelity $\epsilon$ as a function of $N$ ($\epsilon$ $\sim$ $N^r$) with the parameter $r=-1$, exceeding the standard quantum limit with $r=-0.5$. We experimentally obtain the scaling parameter of $r=-0.88\pm$0.03 and $-0.78\pm$0.07 for nonadaptive and adaptive strategies, respectively. Our experimental work could serve as a standardized procedure for the verification of quantum states., Comment: 16+19 pages, 6+10 figures

Published
2020
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11. Three-dimensional entanglement on a silicon chip

Author

Lu, Liangliang, Xia, Lijun, Chen, Zhiyu, Chen, Leizhen, Yu, Tonghua, Tao, Tao, Ma, Wenchao, Pan, Ying, Cai, Xinlun, Lu, Yanqing, Zhu, Shining, and Ma, Xiao-Song

Subjects
Quantum Physics, Physics - Optics
Abstract

Entanglement is a counterintuitive feature of quantum physics that is at the heart of quantum technology. High-dimensional quantum states offer unique advantages in various quantum information tasks. Integrated photonic chips have recently emerged as a leading platform for the generation, manipulation and detection of entangled photons. Here, we report a silicon photonic chip that uses novel interferometric resonance-enhanced photon-pair sources, spectral demultiplexers and high-dimensional reconfigurable circuitries to generate, manipulate and analyse path-entangled three-dimensional qutrit states. By minimizing on-chip electrical and thermal cross-talk, we obtain high-quality quantum interference with visibilities above 96.5% and a maximumly entangled qutrit state with a fidelity of 95.5%. We further explore the fundamental properties of entangled qutrits to test quantum nonlocality and contextuality, and to implement quantum simulations of graphs and high-precision optical phase measurements. Our work paves the path for the development of multiphoton high-dimensional quantum technologies., Comment: 36 pages, 14 figures

Published
2019
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12. Proximal colon–derived O-glycosylated mucus encapsulates and modulates the microbiota

Author

Bergstrom, Kirk, Shan, Xindi, Casero, David, Batushansky, Albert, Lagishetty, Venu, Jacobs, Jonathan P, Hoover, Christopher, Kondo, Yuji, Shao, Bojing, Gao, Liang, Zandberg, Wesley, Noyovitz, Benjamin, McDaniel, J Michael, Gibson, Deanna L, Pakpour, Sepideh, Kazemian, Negin, McGee, Samuel, Houchen, Courtney W, Rao, Chinthalapally V, Griffin, Timothy M, Sonnenburg, Justin L, McEver, Rodger P, Braun, Jonathan, and Xia, Lijun

Subjects
Digestive Diseases, Cancer, Colo-Rectal Cancer, Animals, Colon, Feces, Gastrointestinal Microbiome, Glycosylation, Mice, Mice, Knockout, Mucin-2, Mucus, Transcription, Genetic, General Science & Technology
Abstract

Colon mucus segregates the intestinal microbiota from host tissues, but how it organizes to function throughout the colon is unclear. In mice, we found that colon mucus consists of two distinct O-glycosylated entities of Muc2: a major form produced by the proximal colon, which encapsulates the fecal material including the microbiota, and a minor form derived from the distal colon, which adheres to the major form. The microbiota directs its own encapsulation by inducing Muc2 production from proximal colon goblet cells. In turn, O-glycans on proximal colon-derived Muc2 modulate the structure and function of the microbiota as well as transcription in the colon mucosa. Our work shows how proximal colon control of mucin production is an important element in the regulation of host-microbiota symbiosis.

Published
2020

22. Microbial, metabolomic, and immunologic dynamics in a relapsing genetic mouse model of colitis induced by T-synthase deficiency

Author

Jacobs, Jonathan P, Lin, Lin, Goudarzi, Maryam, Ruegger, Paul, McGovern, Dermot PB, Fornace, Albert J, Borneman, James, Xia, Lijun, and Braun, Jonathan

Subjects
Microbiology, Biological Sciences, Inflammatory Bowel Disease, Human Genome, Clinical Research, Digestive Diseases, Crohn's Disease, Microbiome, Genetics, Autoimmune Disease, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Animals, Bacteria, Cohort Studies, Colitis, Colon, Crohn Disease, Disease Models, Animal, Galactosyltransferases, Gastrointestinal Microbiome, Humans, Mice, Mucins, Polymorphism, Single Nucleotide, T-Lymphocyte Subsets, C1 galt1, core-1 O-glycans, colitis, microbiome, T-synthase, C1galt1
Abstract

Intestinal dysbiosis is thought to confer susceptibility to inflammatory bowel disease (IBD), but it is unknown whether dynamic changes in the microbiome contribute to fluctuations in disease activity. We explored this question using mice with intestine-specific deletion of C1galt1 (also known as T-synthase) (Tsyn mice). These mice develop spontaneous microbiota-dependent colitis with a remitting/relapsing course due to loss of mucin core-1 derived O-glycans. 16S rRNA sequencing and untargeted metabolomics demonstrated age-specific perturbations in the intestinal microbiome and metabolome of Tsyn mice compare with littermate controls at weeks 3 (disease onset), 5 (during remission), and 9 (after relapse). Colitis remission corresponded to increased levels of FoxP3+RORγt+CD4+ T cells in the colonic lamina propria that were positively correlated with operational taxonomic units (OTUs) in the S24-7 family and negatively correlated with OTUs in the Clostridiales order. Relapse was characterized by marked expansion of FoxP3-RORγt+CD4+ T cells expressing IFNγ and IL17A, which were associated with Clostridiales OTUs distinct from those negatively correlated with FoxP3+RORγt+CD4+ T cells. Our findings suggest that colitis remission and relapse in the Tsyn model may reflect alterations in the microbiome due to reduced core-1 O-glycosylation that shift the balance of regulatory and pro-inflammatory T cell subsets. We investigated whether genetic variation in C1galt1 correlated with the microbiome in a cohort of 78 Crohn's disease patients and 101 healthy controls. Polymorphisms near C1galt1 (rs10486157) and its molecular chaperone, Cosmc (rs4825729), were associated with altered composition of the colonic mucosal microbiota, supporting the relevance of core-1 O-glycosylation to host regulation of the microbiome.

Published
2017

23. Core 1– and 3–derived O-glycans collectively maintain the colonic mucus barrier and protect against spontaneous colitis in mice

Author

Bergstrom, Kirk, Fu, Jianxin, Johansson, Malin EV, Liu, Xiaowei, Gao, Nan, Wu, Qian, Song, Jianhua, McDaniel, J Michael, McGee, Samuel, Chen, Weichang, Braun, Jonathan, Hansson, Gunnar C, and Xia, Lijun

Subjects
Biomedical and Clinical Sciences, Immunology, Digestive Diseases, Autoimmune Disease, Nutrition, Inflammatory Bowel Disease, Cancer, Colo-Rectal Cancer, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Animals, Anti-Bacterial Agents, Cells, Cultured, Colitis, Ulcerative, Colon, Disease Models, Animal, Galactosyltransferases, Humans, Immunity, Mucosal, Intestinal Mucosa, Mice, Mice, Inbred C57BL, Mice, Knockout, Mucus, N-Acetylglucosaminyltransferases, Polysaccharides, Proteolysis, Biological Sciences, Medical and Health Sciences
Abstract

Core 1- and 3-derived mucin-type O-glycans are primary components of the mucus layer in the colon. Reduced mucus thickness and impaired O-glycosylation are observed in human ulcerative colitis. However, how both types of O-glycans maintain mucus barrier function in the colon is unclear. We found that C1galt1 expression, which synthesizes core 1 O-glycans, was detected throughout the colon, whereas C3GnT, which controls core 3 O-glycan formation, was most highly expressed in the proximal colon. Consistent with this, mice lacking intestinal core 1-derived O-glycans (IEC C1galt1-/-) developed spontaneous colitis primarily in the distal colon, whereas mice lacking both intestinal core 1- and 3-derived O-glycans (DKO) developed spontaneous colitis in both the distal and proximal colon. DKO mice showed an early onset and more severe colitis than IEC C1galt1-/- mice. Antibiotic treatment restored the mucus layer and attenuated colitis in DKO mice. Mucins from DKO mice were more susceptible to proteolysis than wild-type mucins. This study indicates that core 1- and 3-derived O-glycans collectively contribute to the mucus barrier by protecting it from bacterial protease degradation and suggests new therapeutic targets to promote mucus barrier function in colitis patients.

Published
2017

24. Motif mimetic of epsin perturbs tumor growth and metastasis

Author

Dong, Yunzhou, Wu, Hao, Rahman, HN Ashiqur, Liu, Yanjun, Pasula, Satish, Tessneer, Kandice L, Cai, Xiaofeng, Liu, Xiaolei, Chang, Baojun, McManus, John, Hahn, Scott, Dong, Jiali, Brophy, Megan L, Yu, Lili, Song, Kai, Silasi-Mansat, Robert, Saunders, Debra, Njoku, Charity, Song, Hoogeun, Mehta-D’Souza, Padmaja, Towner, Rheal, Lupu, Florea, McEver, Rodger P, Xia, Lijun, Boerboom, Derek, Srinivasan, R Sathish, and Chen, Hong

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, 2.1 Biological and endogenous factors, Adaptor Proteins, Vesicular Transport, Amino Acid Motifs, Animals, Mice, Mice, Knockout, Neoplasm Metastasis, Neoplasms, Experimental, Neovascularization, Pathologic, Peptides, Protein Structure, Tertiary, Vascular Endothelial Growth Factor Receptor-2, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Tumor angiogenesis is critical for cancer progression. In multiple murine models, endothelium-specific epsin deficiency abrogates tumor progression by shifting the balance of VEGFR2 signaling toward uncontrolled tumor angiogenesis, resulting in dysfunctional tumor vasculature. Here, we designed a tumor endothelium-targeting chimeric peptide (UPI) for the purpose of inhibiting endogenous tumor endothelial epsins by competitively binding activated VEGFR2. We determined that the UPI peptide specifically targets tumor endothelial VEGFR2 through an unconventional binding mechanism that is driven by unique residues present only in the epsin ubiquitin-interacting motif (UIM) and the VEGFR2 kinase domain. In murine models of neoangiogenesis, UPI peptide increased VEGF-driven angiogenesis and neovascularization but spared quiescent vascular beds. Further, in tumor-bearing mice, UPI peptide markedly impaired functional tumor angiogenesis, tumor growth, and metastasis, resulting in a notable increase in survival. Coadministration of UPI peptide with cytotoxic chemotherapeutics further sustained tumor inhibition. Equipped with localized tumor endothelium-specific targeting, our UPI peptide provides potential for an effective and alternative cancer therapy.

Published
2015

27. Clearance of VWF by hepatic macrophages is critical for the protective effect of ADAMTS13 in sickle cell anemia mice

Author

Shi, Huiping, primary, Gao, Liang, additional, Kirby, Nicole, additional, Shao, Bojing, additional, Shan, Xindi, additional, Kudo, Mariko, additional, Silasi, Robert, additional, McDaniel, Michael J., additional, Zhou, Meixiang, additional, McGee, Samuel, additional, Jing, Wei, additional, Lupu, Florea, additional, Cleuren, Audrey, additional, George, James N, additional, and Xia, Lijun, additional

Published
2023
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34. PROX1 Inhibits PDGF-B Expression to Prevent Myxomatous Degeneration of Heart Valves

Author

Ho, Yen-Chun, primary, Geng, Xin, additional, O’Donnell, Anna, additional, Ibarrola, Jaime, additional, Fernandez-Celis, Amaya, additional, Varshney, Rohan, additional, Subramani, Kumar, additional, Azartash-Namin, Zheila J., additional, Kim, Jang, additional, Silasi, Robert, additional, Wylie-Sears, Jill, additional, Alvandi, Zahra, additional, Chen, Lijuan, additional, Cha, Boksik, additional, Chen, Hong, additional, Xia, Lijun, additional, Zhou, Bin, additional, Lupu, Florea, additional, Burkhart, Harold M., additional, Aikawa, Elena, additional, Olson, Lorin E., additional, Ahamed, Jasimuddin, additional, López-Andrés, Natalia, additional, Bischoff, Joyce, additional, Yutzey, Katherine E., additional, and Srinivasan, R. Sathish, additional

Published
2023
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49. Epsins 1 and 2 promote NEMO linear ubiquitination via LUBAC to drive breast cancer development

Author

Song, Kai, Cai, Xiaofeng, Dong, Yunzhou, Wu, Hao, Wei, Yong, Shankavaram, Uma T., Cui, Kui, Lee, Yang, Zhu, Bo, Bhattacharjee, Sudarshan, Wang, Beibei, Zhang, Kun, Wen, Aiyun, Wong, Scott, Yu, Lili, Xia, Lijun, Welm, Alana L., Bielenberg, Diane R., Camphausen, Kevin A., Kang, Yibin, and Chen, Hong

Subjects
Care and treatment, Development and progression, Genetic aspects, Health aspects, Estrogen receptors -- Health aspects, Ubiquitin-proteasome system -- Health aspects, Breast cancer -- Genetic aspects -- Development and progression -- Care and treatment, Estrogen -- Receptors
Abstract

Introduction NF-[kappa]B is a crucial oncogenic transcription factor that is frequently activated in estrogen receptor-negative (ER-negative) breast tumor subtypes (1, 2) and plays an obligatory role in breast cancer tumorigenesis [...], Estrogen receptor-negative (ER-negative) breast cancer is thought to be more malignant and devastating than ER-positive breast cancer. ER-negative breast cancer exhibits elevated NF-[kappa]B activity, but how this abnormally high NF-[kappa]B activity is maintained is poorly understood. The importance of linear ubiquitination, which is generated by the linear ubiquitin chain assembly complex (LUBAC), is increasingly appreciated in NF-[kappa]B signaling, which regulates cell activation and death. Here, we showed that epsin proteins, a family of ubiquitin-binding endocytic adaptors, interacted with LUBAC via its ubiquitininteracting motif and bound LUBAC's bona fide substrate NEMO via its N-terminal homolog (ENTH) domain. Furthermore, epsins promoted NF-[kappa]B essential modulator (NEMO) linear ubiquitination and served as scaffolds for recruiting other components of the I[kappa]B kinase (IKK) complex, resulting in the heightened IKK activation and sustained NF-[kappa]B signaling essential for the development of ER-negative breast cancer. Heightened epsin levels in ER-negative human breast cancer are associated with poor relapse-free survival. We showed that transgenic and pharmacological approaches eliminating epsins potently impeded breast cancer development in both spontaneous and patient-derived xenograft breast cancer mouse models. Our findings established the pivotal role epsins played in promoting breast cancer. Thus, targeting epsins may represent a strategy to restrain NF-[kappa]B signaling and provide an important perspective into ER-negative breast cancer treatment.

Published
2021
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