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531 results on '"Huang Mo"'

1. The 2-character theory for finite 2-groups

Author

Huang, Mo, Xu, Hao, and Zhang, Zhi-Hao

Subjects
Mathematics - Representation Theory, Mathematics - Category Theory, Mathematics - Quantum Algebra
Abstract

In this work, we generalize the notion of character for 2-representations of finite 2-groups. The properties of 2-characters bear strong similarities to those classical characters of finite groups, including conjugation invariance, additivity, multiplicativity and orthogonality. With a careful analysis using homotopy fixed points and quotients for categories with 2-group actions, we prove that the category of class functors on a 2-group $\mathcal G$ is equivalent to the Drinfeld center of the 2-group algebra $\mathrm{Vec}_{\mathcal G}$, which categorifies the Fourier transform on finite abelian groups. After transferring the canonical nondegenerate braided monoidal structure from $\mathfrak Z_1(\mathrm{Vec}_{\mathcal G})$, we discover that irreducible 2-characters of $\mathcal G$ coincide with full centers of the corresponding 2-representations, which are in a one-to-one correspondence with Lagrangian algebras in the category of class functors on $\mathcal G$. In particular, the fusion rule of $2\mathrm{Rep}(\mathcal G)$ can be calculated from the pointwise product of Lagrangian algebras as class functors. From a topological quantum field theory (TQFT) point of view, the commutative Frobenius algebra structure on a 2-character is induced from a 2D topological sigma-model with target space $\lvert \mathrm{B} \mathcal G \rvert$., Comment: 30 pages. Comments are welcome

Published
2024

3. Tannaka-Krein duality for finite 2-groups

Author

Huang, Mo and Zhang, Zhi-Hao

Subjects
Mathematics - Quantum Algebra, Mathematics - Category Theory, Mathematics - Representation Theory
Abstract

Let $\mathcal{G}$ be a finite 2-group. We show that the 2-category $2\mathrm{Rep}(\mathcal{G})$ of finite semisimple 2-representations is a symmetric fusion 2-category. We also relate the auto-equivalence 2-group of the symmetric monoidal forgetful 2-functor $\omega : 2\mathrm{Rep}(\mathcal{G}) \to 2\mathrm{Vec}$ to the auto-equivalence 2-group of the regular algebra and show that they are equivalent to $\mathcal{G}$. This result categorifies the usual Tannaka-Krein duality for finite groups., Comment: 15 pages. Comments are welcome

Published
2023

5. Systematic transcriptome profiling of hPSC-derived osteoblasts unveils CORIN's mastery in governing osteogenesis through CEBPD modulation

Author

Zhu, Dandan, Huang, Mo-Fan, Xu, An, Gao, Xueqin, Huang, Yu-Wen, Phan, Trinh T.T., Lu, Linchao, Chi, Ting-Yen, Dai, Yulin, Pang, Lon Kai, Gingold, Julian A., Tu, Jian, Huo, Zijun, Bazer, Danielle A., Shoemaker, Rachel, Wang, Jun, Ambrose, Catherine G., Shen, Jingnan, Kameoka, Jun, Zhao, Zhongming, Wang, Lisa L., Zhang, Yang, Zhao, Ruiying, and Lee, Dung-Fang

Published
2024
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7. Individualised neoantigen therapy mRNA-4157 (V940) plus pembrolizumab versus pembrolizumab monotherapy in resected melanoma (KEYNOTE-942): a randomised, phase 2b study

Author

Weber, Jeffrey S, Carlino, Matteo S, Khattak, Adnan, Meniawy, Tarek, Ansstas, George, Taylor, Matthew H, Kim, Kevin B, McKean, Meredith, Long, Georgina V, Sullivan, Ryan J, Faries, Mark, Tran, Thuy T, Cowey, C Lance, Pecora, Andrew, Shaheen, Montaser, Segar, Jennifer, Medina, Theresa, Atkinson, Victoria, Gibney, Geoffrey T, Luke, Jason J, Thomas, Sajeve, Buchbinder, Elizabeth I, Healy, Jane A, Huang, Mo, Morrissey, Manju, Feldman, Igor, Sehgal, Vasudha, Robert-Tissot, Celine, Hou, Peijie, Zhu, Lili, Brown, Michelle, Aanur, Praveen, Meehan, Robert S, and Zaks, Tal

Published
2024
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8. Rewired m6A epitranscriptomic networks link mutant p53 to neoplastic transformation

Author

Xu, An, Liu, Mo, Huang, Mo-Fan, Zhang, Yang, Hu, Ruifeng, Gingold, Julian A., Liu, Ying, Zhu, Dandan, Chien, Chian-Shiu, Wang, Wei-Chen, Liao, Zian, Yuan, Fei, Hsu, Chih-Wei, Tu, Jian, Yu, Yao, Rosen, Taylor, Xiong, Feng, Jia, Peilin, Yang, Yi-Ping, Bazer, Danielle A., Chen, Ya-Wen, Li, Wenbo, Huff, Chad D., Zhu, Jay-Jiguang, Aguilo, Francesca, Chiou, Shih-Hwa, Boles, Nathan C., Lai, Chien-Chen, Hung, Mien-Chie, Zhao, Zhongming, Van Nostrand, Eric L., Zhao, Ruiying, and Lee, Dung-Fang

Published
2023
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9. Antifungal mechanism of volatile compounds emitted by Actinomycetota Paenarthrobacter ureafaciens from a disease-suppressive soil on Saccharomyces cerevisiae

Author

Tri-Phuong Nguyen, De-Rui Meng, Ching-Han Chang, Pei-Yu Su, Chieh-An Ou, Ping-Fu Hou, Huang-Mo Sung, Chang-Hung Chou, Masaru Ohme-Takagi, and Hao-Jen Huang

Subjects
Paenarthrobacter ureafaciens, phytopathogens, antifungal mechanism, volatile organic compounds, volatile allelochemicals, allelopathy, Microbiology, QR1-502
Abstract

ABSTRACT Increasing evidence suggests that in disease-suppressive soils, microbial volatile compounds (mVCs) released from bacteria may inhibit the growth of plant-pathogenic fungi. However, the antifungal activities and molecular responses of fungi to different mVCs remain largely undescribed. In this study, we first evaluated the responses of pathogenic fungi to treatment with mVCs from Paenarthrobacter ureafaciens. Then, we utilized the well-characterized fungal model organism Saccharomyces cerevisiae to study the potential mechanistic effects of the mVCs. Our data showed that exposure to P. ureafaciens mVCs leads to reduced growth of several pathogenic fungi, and in yeast cells, mVC exposure prompts the accumulation of reactive oxygen species. Further experiments with S. cerevisiae deletion mutants indicated that Slt2/Mpk1 and Hog1 MAPKs play major roles in the yeast response to P. ureafaciens mVCs. Transcriptomic analysis revealed that exposure to mVCs was associated with 1,030 differentially expressed genes (DEGs) in yeast. According to gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses, many of these DEGs are involved in mitochondrial dysfunction, cell integrity, mitophagy, cellular metabolism, and iron uptake. Genes encoding antimicrobial proteins were also significantly altered in the yeast after exposure to mVCs. These findings suggest that oxidative damage and mitochondrial dysfunction are major contributors to the fungal toxicity of mVCs. Furthermore, our data showed that cell wall, antioxidant, and antimicrobial defenses are induced in yeast exposed to mVCs. Thus, our findings expand upon previous research by delineating the transcriptional responses of the fungal model. IMPORTANCE Since the use of bacteria-emitted volatile compounds in phytopathogen control is of considerable interest, it is important to understand the molecular mechanisms by which fungi may adapt to microbial volatile compounds (mVCs). Paenarthrobacter ureafaciens is an isolated bacterium from disease-suppressive soil that belongs to the Actinomycetota phylum. P. ureafaciens mVCs showed a potent antifungal effect on phytopathogens, which may contribute to disease suppression in soil. However, our knowledge about the antifungal mechanism of mVCs is limited. This study has proven that mVCs are toxic to fungi due to oxidative stress and mitochondrial dysfunction. To deal with mVC toxicity, antioxidants and physical defenses are required. Furthermore, iron uptake and CAP proteins are required for antimicrobial defense, which is necessary for fungi to deal with the thread from mVCs. This study provides essential foundational knowledge regarding the molecular responses of fungi to inhibitory mVCs.

Published
2023
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10. Reply to 'Issues arising from benchmarking single-cell RNA sequencing imputation methods'

Author

Huang, Mo and Zhang, Nancy R.

Subjects
Statistics - Applications, Quantitative Biology - Genomics, Quantitative Biology - Quantitative Methods
Abstract

In our Brief Communication (DOI: 10.1038/s41592-018-0033-z), we presented the method SAVER for recovering true gene expression levels in noisy single cell RNA sequencing data. We evaluated the performance of SAVER, along with comparable methods MAGIC and scImpute, in an RNA FISH validation experiment and a data downsampling experiment. In a Comment [arXiv:1908.07084v1], Li & Li were concerned with the use of the downsampled datasets, specifically focusing on clustering results obtained from the Zeisel et al. data. Here, we will address these comments and, furthermore, amend the data downsampling experiment to demonstrate that the findings from the data downsampling experiment in our Brief Communication are valid.

Published
2019

11. Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma.

Author

Chen, Ye, Xu, Liang, Mayakonda, Anand, Huang, Mo-Li, Kanojia, Deepika, Tan, Tuan Zea, Dakle, Pushkar, Lin, Ruby Yu-Tong, Ke, Xin-Yu, Said, Jonathan W, Chen, Jianxiang, Gery, Sigal, Ding, Ling-Wen, Jiang, Yan-Yi, Pang, Angela, Puhaindran, Mark Edward, Goh, Boon Cher, and Koeffler, H Phillip

Subjects
Cell Line, Tumor, Animals, Mice, Inbred NOD, Humans, Mice, SCID, Liposarcoma, Thalidomide, Azepines, Neoplasm Proteins, Oncogene Proteins, Fusion, Transcription, Genetic, Base Sequence, Genome, Human, Enhancer Elements, Genetic, Carcinogenesis, Cell Line, Tumor, Enhancer Elements, Genetic, Genome, Human, Mice, Inbred NOD, SCID, Oncogene Proteins, Fusion, Transcription
Abstract

Liposarcomas (LPSs) are a group of malignant mesenchymal tumors showing adipocytic differentiation. Here, to gain insight into the enhancer dysregulation and transcriptional addiction in this disease, we chart super-enhancer structures in both LPS tissues and cell lines. We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS. Additionally, SNAI2 is identified as a crucial downstream target that enforces both proliferative and metastatic potentials to de-differentiated LPS cells. Genetic depletion of BET genes, core transcriptional factors, or SNAI2 mitigates consistently LPS malignancy. We also reveal a compelling susceptibility of LPS cells to BET protein degrader ARV-825. BET protein depletion confers additional advantages to circumvent acquired resistance to Trabectedin, a chemotherapy drug for LPS. Moreover, this study provides a framework for discovering and targeting of core oncogenic transcriptional programs in human cancers.

Published
2019

12. Pembrolizumab plus dinaciclib in patients with hematologic malignancies: the phase 1b KEYNOTE-155 study

Author

Gregory, Gareth P., Kumar, Shaji, Wang, Ding, Mahadevan, Daruka, Walker, Patricia, Wagner-Johnston, Nina, Escobar, Carolina, Bannerji, Rajat, Bhutani, Divaya, Chang, Julie, Hernandez-Ilizaliturri, Francisco J., Klein, Andreas, Pagel, John M., Rybka, Witold, Yee, Andrew J., Mohrbacher, Anne, Huang, Mo, Farooqui, Mohammed, Marinello, Patricia, and Quach, Hang

Published
2022
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13. Targetable BET proteins- and E2F1-dependent transcriptional program maintains the malignancy of glioblastoma

Author

Xu, Liang, Chen, Ye, Mayakonda, Anand, Koh, Lynnette, Chong, Yuk Kien, Buckley, Dennis L, Sandanaraj, Edwin, Lim, See Wee, Lin, Ruby Yu-Tong, Ke, Xin-Yu, Huang, Mo-Li, Chen, Jianxiang, Sun, Wendi, Wang, Ling-Zhi, Goh, Boon Cher, Dinh, Huy Q, Kappei, Dennis, Winter, Georg E, Ding, Ling-Wen, Ang, Beng Ti, Berman, Benjamin P, Bradner, James E, Tang, Carol, and Koeffler, H Phillip

Subjects
Brain Disorders, Genetics, Cancer, Neurosciences, Rare Diseases, Brain Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Antineoplastic Agents, Cell Cycle Proteins, Cell Line, Tumor, Drug Delivery Systems, E2F1 Transcription Factor, Gene Expression Regulation, Neoplastic, Glioblastoma, Humans, Nuclear Proteins, Protein Domains, Protein Serine-Threonine Kinases, RNA-Binding Proteins, Transcription Factors, glioma, BRD2, BRD3, BRD4, E2F
Abstract

Competitive BET bromodomain inhibitors (BBIs) targeting BET proteins (BRD2, BRD3, BRD4, and BRDT) show promising preclinical activities against brain cancers. However, the BET protein-dependent glioblastoma (GBM)-promoting transcriptional network remains elusive. Here, with mechanistic exploration of a next-generation chemical degrader of BET proteins (dBET6), we reveal a profound and consistent impact of BET proteins on E2F1- dependent transcriptional program in both differentiated GBM cells and brain tumor-initiating cells. dBET6 treatment drastically reduces BET protein genomic occupancy, RNA-Pol2 activity, and permissive chromatin marks. Subsequently, dBET6 represses the proliferation, self-renewal, and tumorigenic ability of GBM cells. Moreover, dBET6-induced degradation of BET proteins exerts superior antiproliferation effects compared to conventional BBIs and overcomes both intrinsic and acquired resistance to BBIs in GBM cells. Our study reveals crucial functions of BET proteins and provides the rationale and therapeutic merits of targeted degradation of BET proteins in GBM.

Published
2018

14. Systematic Analysis of Splice-Site-Creating Mutations in Cancer

Author

Jayasinghe, Reyka G, Cao, Song, Gao, Qingsong, Wendl, Michael C, Vo, Nam Sy, Reynolds, Sheila M, Zhao, Yanyan, Climente-González, Héctor, Chai, Shengjie, Wang, Fang, Varghese, Rajees, Huang, Mo, Liang, Wen-Wei, Wyczalkowski, Matthew A, Sengupta, Sohini, Li, Zhi, Payne, Samuel H, Fenyö, David, Miner, Jeffrey H, Walter, Matthew J, Network, The Cancer Genome Atlas Research, Caesar-Johnson, Samantha J, Demchok, John A, Felau, Ina, Kasapi, Melpomeni, Ferguson, Martin L, Hutter, Carolyn M, Sofia, Heidi J, Tarnuzzer, Roy, Wang, Zhining, Yang, Liming, Zenklusen, Jean C, Zhang, Jiashan, Chudamani, Sudha, Liu, Jia, Lolla, Laxmi, Naresh, Rashi, Pihl, Todd, Sun, Qiang, Wan, Yunhu, Wu, Ye, Cho, Juok, DeFreitas, Timothy, Frazer, Scott, Gehlenborg, Nils, Getz, Gad, Heiman, David I, Kim, Jaegil, Lawrence, Michael S, Lin, Pei, Meier, Sam, Noble, Michael S, Saksena, Gordon, Voet, Doug, Zhang, Hailei, Bernard, Brady, Chambwe, Nyasha, Dhankani, Varsha, Knijnenburg, Theo, Kramer, Roger, Leinonen, Kalle, Liu, Yuexin, Miller, Michael, Reynolds, Sheila, Shmulevich, Ilya, Thorsson, Vesteinn, Zhang, Wei, Akbani, Rehan, Broom, Bradley M, Hegde, Apurva M, Ju, Zhenlin, Kanchi, Rupa S, Korkut, Anil, Li, Jun, Liang, Han, Ling, Shiyun, Liu, Wenbin, Lu, Yiling, Mills, Gordon B, Ng, Kwok-Shing, Rao, Arvind, Ryan, Michael, Wang, Jing, Weinstein, John N, Zhang, Jiexin, Abeshouse, Adam, Armenia, Joshua, Chakravarty, Debyani, Chatila, Walid K, de Bruijn, Ino, Gao, Jianjiong, Gross, Benjamin E, Heins, Zachary J, Kundra, Ritika, La, Konnor, Ladanyi, Marc, Luna, Augustin, Nissan, Moriah G, Ochoa, Angelica, and Phillips, Sarah M

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Cancer Genomics, Genetics, Rare Diseases, Immunotherapy, Cancer, Human Genome, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, BRCA1 Protein, GATA3 Transcription Factor, HEK293 Cells, Humans, Mutation, Neoplasms, Poly (ADP-Ribose) Polymerase-1, Programmed Cell Death 1 Receptor, RNA Splice Sites, Tumor Suppressor Protein p53, X-linked Nuclear Protein, Cancer Genome Atlas Research Network, RNA, mutations of clinical relevance, splicing, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

For the past decade, cancer genomic studies have focused on mutations leading to splice-site disruption, overlooking those having splice-creating potential. Here, we applied a bioinformatic tool, MiSplice, for the large-scale discovery of splice-site-creating mutations (SCMs) across 8,656 TCGA tumors. We report 1,964 originally mis-annotated mutations having clear evidence of creating alternative splice junctions. TP53 and GATA3 have 26 and 18 SCMs, respectively, and ATRX has 5 from lower-grade gliomas. Mutations in 11 genes, including PARP1, BRCA1, and BAP1, were experimentally validated for splice-site-creating function. Notably, we found that neoantigens induced by SCMs are likely several folds more immunogenic compared to missense mutations, exemplified by the recurrent GATA3 SCM. Further, high expression of PD-1 and PD-L1 was observed in tumors with SCMs, suggesting candidates for immune blockade therapy. Our work highlights the importance of integrating DNA and RNA data for understanding the functional and the clinical implications of mutations in human diseases.

Published
2018

18. List of contributors

Author

Amaral, Olga, primary, Bertini, Enrico, additional, Bragança, José, additional, Cagavi, Esra, additional, Compagnucci, Claudia, additional, Duarte, Ana, additional, Gingold, Julian A., additional, Giri, Subhajit, additional, Huang, Mo-Fan, additional, Iyer, Shilpa, additional, Jang, Yoon-Young, additional, Lee, Dung-Fang, additional, Lowenthal, Justin, additional, Malgrange, Brigitte, additional, Meshrkey, Fibi, additional, Morizane, Ryuji, additional, Mutlu Burnaz, Ozlem, additional, Pang, Lon Kai, additional, Pena, Mezthly, additional, Rao, Raj R., additional, Ribeiro, Diogo, additional, Santos, Renato, additional, Tartaglia, Marco, additional, Tomaselli, Gordon F., additional, Traitteur, Tamara, additional, Tung, Leslie, additional, Ulrichs, Heidi, additional, Wang, Yichen, additional, West, Franklin D., additional, Wu, Hsueh Fu, additional, Yang, Brenda, additional, Zeltner, Nadja, additional, Zhang, Chengcheng, additional, and Zhao, Ruiying, additional

Published
2022
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21. Sum Secrecy Rate Maximization in NOMA Downlink SWIPT Systems

Author

Tang, Jie, Dai, Tuwang, Zhang, Xiuyin, Huang, Mo, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Jiming, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Hirche, Sandra, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Liang, Qilian, Series Editor, Martin, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Möller, Sebastian, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zhang, Junjie James, Series Editor, Liu, Xin, editor, Na, Zhenyu, editor, Wang, Wei, editor, Mu, Jiasong, editor, and Zhang, Baoju, editor

Published
2019
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28. A Single-Inductor Multiple-Output DC–DC Converter With Fixed-Frequency Victim-Last Charge Control for Reduced Cross Regulation

Author

Li, Yang, Huang, Mo, Martins, Rui P., and Lu, Yan

Abstract

This paper presents a single-inductor multiple-output (SIMO) DC-DC converter with fixed-frequency victim-last charge control. This scheme switches the load-transient channel (victim) to the last of the charging sequence, addressing the inherent cross-regulation issue in conventional charge control SIMO. We first analyze why the conventional fixed-frequency charge control has such an issue. Then, we present the working principle of the proposed scheme. After that, we propose a charge-error calibration technique that minimizes the side effects caused by victim-last control, ensuring a smooth order switching of the original last channel. We implemented and fabricated the proposed SIMO DC-DC converter in a 0.18- $\mu $ m BCD process. Measurement results show that we are able to reduce the cross-regulation to 0.057mV/mA with a 225-mA load step under fixed switching frequency. The measured peak efficiency is 84.1%.

Published
2024
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29. Therapeutic Strategies for RB1-Deficient Cancers: Intersecting Gene Regulation and Targeted Therapy.

Author

Huang, Mo-Fan, Wang, Yuan-Xin, Chou, Yu-Ting, and Lee, Dung-Fang

Subjects
*GENOMICS, *TRANSCRIPTION factors, *CELLULAR signal transduction, *RETINOBLASTOMA, *GENE expression, *GENETIC mutation, *DISEASE progression, *PSYCHOLOGICAL vulnerability
Abstract

Simple Summary: Addressing RB1-deficient cancers poses substantial challenges. Dysfunctional or deleted RB1 can enhance the proliferation and spread of different cancer types. Scientists strive to grasp the intricate role of RB1 in regulating various biological processes and molecular pathways to devise innovative therapeutic strategies tailored to RB1-deficient cancers. Recent advancements have revealed encouraging tactics for combating these malignancies, heralding a path toward more precise and efficacious treatments. This review underscores the pivotal role of RB1 in cancer research and highlights its potential as a focal point for personalized therapies. The retinoblastoma (RB) transcriptional corepressor 1 (RB1) is a critical tumor suppressor gene, governing diverse cellular processes implicated in cancer biology. Dysregulation or deletion in RB1 contributes to the development and progression of various cancers, making it a prime target for therapeutic intervention. RB1′s canonical function in cell cycle control and DNA repair mechanisms underscores its significance in restraining aberrant cell growth and maintaining genomic stability. Understanding the complex interplay between RB1 and cellular pathways is beneficial to fully elucidate its tumor-suppressive role across different cancer types and for therapeutic development. As a result, investigating vulnerabilities arising from RB1 deletion-associated mechanisms offers promising avenues for targeted therapy. Recently, several findings highlighted multiple methods as a promising strategy for combating tumor growth driven by RB1 loss, offering potential clinical benefits in various cancer types. This review summarizes the multifaceted role of RB1 in cancer biology and its implications for targeted therapy. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Systematic Analysis of Splice-Site-Creating Mutations in Cancer

Author

Caesar-Johnson, Samantha J., Demchok, John A., Felau, Ina, Kasapi, Melpomeni, Ferguson, Martin L., Hutter, Carolyn M., Sofia, Heidi J., Tarnuzzer, Roy, Wang, Zhining, Yang, Liming, Zenklusen, Jean C., Zhang, Jiashan (Julia), Chudamani, Sudha, Liu, Jia, Lolla, Laxmi, Naresh, Rashi, Pihl, Todd, Sun, Qiang, Wan, Yunhu, Wu, Ye, Cho, Juok, DeFreitas, Timothy, Frazer, Scott, Gehlenborg, Nils, Getz, Gad, Heiman, David I., Kim, Jaegil, Lawrence, Michael S., Lin, Pei, Meier, Sam, Noble, Michael S., Saksena, Gordon, Voet, Doug, Zhang, Hailei, Bernard, Brady, Chambwe, Nyasha, Dhankani, Varsha, Knijnenburg, Theo, Kramer, Roger, Leinonen, Kalle, Liu, Yuexin, Miller, Michael, Reynolds, Sheila, Shmulevich, Ilya, Thorsson, Vesteinn, Zhang, Wei, Akbani, Rehan, Broom, Bradley M., Hegde, Apurva M., Ju, Zhenlin, Kanchi, Rupa S., Korkut, Anil, Li, Jun, Liang, Han, Ling, Shiyun, Liu, Wenbin, Lu, Yiling, Mills, Gordon B., Ng, Kwok-Shing, Rao, Arvind, Ryan, Michael, Wang, Jing, Weinstein, John N., Zhang, Jiexin, Abeshouse, Adam, Armenia, Joshua, Chakravarty, Debyani, Chatila, Walid K., de Bruijn, Ino, Gao, Jianjiong, Gross, Benjamin E., Heins, Zachary J., Kundra, Ritika, La, Konnor, Ladanyi, Marc, Luna, Augustin, Nissan, Moriah G., Ochoa, Angelica, Phillips, Sarah M., Reznik, Ed, Sanchez-Vega, Francisco, Sander, Chris, Schultz, Nikolaus, Sheridan, Robert, Sumer, S. Onur, Sun, Yichao, Taylor, Barry S., Wang, Jioajiao, Zhang, Hongxin, Anur, Pavana, Peto, Myron, Spellman, Paul, Benz, Christopher, Stuart, Joshua M., Wong, Christopher K., Yau, Christina, Hayes, D. Neil, Parker, Joel S., Wilkerson, Matthew D., Ally, Adrian, Balasundaram, Miruna, Bowlby, Reanne, Brooks, Denise, Carlsen, Rebecca, Chuah, Eric, Dhalla, Noreen, Holt, Robert, Jones, Steven J.M., Kasaian, Katayoon, Lee, Darlene, Ma, Yussanne, Marra, Marco A., Mayo, Michael, Moore, Richard A., Mungall, Andrew J., Mungall, Karen, Robertson, A. Gordon, Sadeghi, Sara, Schein, Jacqueline E., Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Tse, Kane, Wong, Tina, Berger, Ashton C., Beroukhim, Rameen, Cherniack, Andrew D., Cibulskis, Carrie, Gabriel, Stacey B., Gao, Galen F., Ha, Gavin, Meyerson, Matthew, Schumacher, Steven E., Shih, Juliann, Kucherlapati, Melanie H., Kucherlapati, Raju S., Baylin, Stephen, Cope, Leslie, Danilova, Ludmila, Bootwalla, Moiz S., Lai, Phillip H., Maglinte, Dennis T., Van Den Berg, David J., Weisenberger, Daniel J., Auman, J. Todd, Balu, Saianand, Bodenheimer, Tom, Fan, Cheng, Hoadley, Katherine A., Hoyle, Alan P., Jefferys, Stuart R., Jones, Corbin D., Meng, Shaowu, Mieczkowski, Piotr A., Mose, Lisle E., Perou, Amy H., Perou, Charles M., Roach, Jeffrey, Shi, Yan, Simons, Janae V., Skelly, Tara, Soloway, Matthew G., Tan, Donghui, Veluvolu, Umadevi, Fan, Huihui, Hinoue, Toshinori, Laird, Peter W., Shen, Hui, Zhou, Wanding, Bellair, Michelle, Chang, Kyle, Covington, Kyle, Creighton, Chad J., Dinh, Huyen, Doddapaneni, HarshaVardhan, Donehower, Lawrence A., Drummond, Jennifer, Gibbs, Richard A., Glenn, Robert, Hale, Walker, Han, Yi, Hu, Jianhong, Korchina, Viktoriya, Lee, Sandra, Lewis, Lora, Li, Wei, Liu, Xiuping, Morgan, Margaret, Morton, Donna, Muzny, Donna, Santibanez, Jireh, Sheth, Margi, Shinbrot, Eve, Wang, Linghua, Wang, Min, Wheeler, David A., Xi, Liu, Zhao, Fengmei, Hess, Julian, Appelbaum, Elizabeth L., Bailey, Matthew, Cordes, Matthew G., Ding, Li, Fronick, Catrina C., Fulton, Lucinda A., Fulton, Robert S., Kandoth, Cyriac, Mardis, Elaine R., McLellan, Michael D., Miller, Christopher A., Schmidt, Heather K., Wilson, Richard K., Crain, Daniel, Curley, Erin, Gardner, Johanna, Lau, Kevin, Mallery, David, Morris, Scott, Paulauskis, Joseph, Penny, Robert, Shelton, Candace, Shelton, Troy, Sherman, Mark, Thompson, Eric, Yena, Peggy, Bowen, Jay, Gastier-Foster, Julie M., Gerken, Mark, Leraas, Kristen M., Lichtenberg, Tara M., Ramirez, Nilsa C., Wise, Lisa, Zmuda, Erik, Corcoran, Niall, Costello, Tony, Hovens, Christopher, Carvalho, Andre L., de Carvalho, Ana C., Fregnani, José H., Longatto-Filho, Adhemar, Reis, Rui M., Scapulatempo-Neto, Cristovam, Silveira, Henrique C.S., Vidal, Daniel O., Burnette, Andrew, Eschbacher, Jennifer, Hermes, Beth, Noss, Ardene, Singh, Rosy, Anderson, Matthew L., Castro, Patricia D., Ittmann, Michael, Huntsman, David, Kohl, Bernard, Le, Xuan, Thorp, Richard, Andry, Chris, Duffy, Elizabeth R., Lyadov, Vladimir, Paklina, Oxana, Setdikova, Galiya, Shabunin, Alexey, Tavobilov, Mikhail, McPherson, Christopher, Warnick, Ronald, Berkowitz, Ross, Cramer, Daniel, Feltmate, Colleen, Horowitz, Neil, Kibel, Adam, Muto, Michael, Raut, Chandrajit P., Malykh, Andrei, Barnholtz-Sloan, Jill S., Barrett, Wendi, Devine, Karen, Fulop, Jordonna, Ostrom, Quinn T., Shimmel, Kristen, Wolinsky, Yingli, Sloan, Andrew E., De Rose, Agostino, Giuliante, Felice, Goodman, Marc, Karlan, Beth Y., Hagedorn, Curt H., Eckman, John, Harr, Jodi, Myers, Jerome, Tucker, Kelinda, Zach, Leigh Anne, Deyarmin, Brenda, Hu, Hai, Kvecher, Leonid, Larson, Caroline, Mural, Richard J., Somiari, Stella, Vicha, Ales, Zelinka, Tomas, Bennett, Joseph, Iacocca, Mary, Rabeno, Brenda, Swanson, Patricia, Latour, Mathieu, Lacombe, Louis, Têtu, Bernard, Bergeron, Alain, McGraw, Mary, Staugaitis, Susan M., Chabot, John, Hibshoosh, Hanina, Sepulveda, Antonia, Su, Tao, Wang, Timothy, Potapova, Olga, Voronina, Olga, Desjardins, Laurence, Mariani, Odette, Roman-Roman, Sergio, Sastre, Xavier, Stern, Marc-Henri, Cheng, Feixiong, Signoretti, Sabina, Berchuck, Andrew, Bigner, Darell, Lipp, Eric, Marks, Jeffrey, McCall, Shannon, McLendon, Roger, Secord, Angeles, Sharp, Alexis, Behera, Madhusmita, Brat, Daniel J., Chen, Amy, Delman, Keith, Force, Seth, Khuri, Fadlo, Magliocca, Kelly, Maithel, Shishir, Olson, Jeffrey J., Owonikoko, Taofeek, Pickens, Alan, Ramalingam, Suresh, Shin, Dong M., Sica, Gabriel, Van Meir, Erwin G., Zhang, Hongzheng, Eijckenboom, Wil, Gillis, Ad, Korpershoek, Esther, Looijenga, Leendert, Oosterhuis, Wolter, Stoop, Hans, van Kessel, Kim E., Zwarthoff, Ellen C., Calatozzolo, Chiara, Cuppini, Lucia, Cuzzubbo, Stefania, DiMeco, Francesco, Finocchiaro, Gaetano, Mattei, Luca, Perin, Alessandro, Pollo, Bianca, Chen, Chu, Houck, John, Lohavanichbutr, Pawadee, Hartmann, Arndt, Stoehr, Christine, Stoehr, Robert, Taubert, Helge, Wach, Sven, Wullich, Bernd, Kycler, Witold, Murawa, Dawid, Wiznerowicz, Maciej, Chung, Ki, Edenfield, W. Jeffrey, Martin, Julie, Baudin, Eric, Bubley, Glenn, Bueno, Raphael, De Rienzo, Assunta, Richards, William G., Kalkanis, Steven, Mikkelsen, Tom, Noushmehr, Houtan, Scarpace, Lisa, Girard, Nicolas, Aymerich, Marta, Campo, Elias, Giné, Eva, Guillermo, Armando López, Van Bang, Nguyen, Hanh, Phan Thi, Phu, Bui Duc, Tang, Yufang, Colman, Howard, Evason, Kimberley, Dottino, Peter R., Martignetti, John A., Gabra, Hani, Juhl, Hartmut, Akeredolu, Teniola, Stepa, Serghei, Hoon, Dave, Ahn, Keunsoo, Kang, Koo Jeong, Beuschlein, Felix, Breggia, Anne, Birrer, Michael, Bell, Debra, Borad, Mitesh, Bryce, Alan H., Castle, Erik, Chandan, Vishal, Cheville, John, Copland, John A., Farnell, Michael, Flotte, Thomas, Giama, Nasra, Ho, Thai, Kendrick, Michael, Kocher, Jean-Pierre, Kopp, Karla, Moser, Catherine, Nagorney, David, O’Brien, Daniel, O’Neill, Brian Patrick, Patel, Tushar, Petersen, Gloria, Que, Florencia, Rivera, Michael, Roberts, Lewis, Smallridge, Robert, Smyrk, Thomas, Stanton, Melissa, Thompson, R. Houston, Torbenson, Michael, Yang, Ju Dong, Zhang, Lizhi, Brimo, Fadi, Ajani, Jaffer A., Gonzalez, Ana Maria Angulo, Behrens, Carmen, Bondaruk, Jolanta, Broaddus, Russell, Czerniak, Bogdan, Esmaeli, Bita, Fujimoto, Junya, Gershenwald, Jeffrey, Guo, Charles, Lazar, Alexander J., Logothetis, Christopher, Meric-Bernstam, Funda, Moran, Cesar, Ramondetta, Lois, Rice, David, Sood, Anil, Tamboli, Pheroze, Thompson, Timothy, Troncoso, Patricia, Tsao, Anne, Wistuba, Ignacio, Carter, Candace, Haydu, Lauren, Hersey, Peter, Jakrot, Valerie, Kakavand, Hojabr, Kefford, Richard, Lee, Kenneth, Long, Georgina, Mann, Graham, Quinn, Michael, Saw, Robyn, Scolyer, Richard, Shannon, Kerwin, Spillane, Andrew, Stretch, Jonathan, Synott, Maria, Thompson, John, Wilmott, James, Al-Ahmadie, Hikmat, Chan, Timothy A., Ghossein, Ronald, Gopalan, Anuradha, Levine, Douglas A., Reuter, Victor, Singer, Samuel, Singh, Bhuvanesh, Tien, Nguyen Viet, Broudy, Thomas, Mirsaidi, Cyrus, Nair, Praveen, Drwiega, Paul, Miller, Judy, Smith, Jennifer, Zaren, Howard, Park, Joong-Won, Hung, Nguyen Phi, Kebebew, Electron, Linehan, W. Marston, Metwalli, Adam R., Pacak, Karel, Pinto, Peter A., Schiffman, Mark, Schmidt, Laura S., Vocke, Cathy D., Wentzensen, Nicolas, Worrell, Robert, Yang, Hannah, Moncrieff, Marc, Goparaju, Chandra, Melamed, Jonathan, Pass, Harvey, Botnariuc, Natalia, Caraman, Irina, Cernat, Mircea, Chemencedji, Inga, Clipca, Adrian, Doruc, Serghei, Gorincioi, Ghenadie, Mura, Sergiu, Pirtac, Maria, Stancul, Irina, Tcaciuc, Diana, Albert, Monique, Alexopoulou, Iakovina, Arnaout, Angel, Bartlett, John, Engel, Jay, Gilbert, Sebastien, Parfitt, Jeremy, Sekhon, Harman, Thomas, George, Rassl, Doris M., Rintoul, Robert C., Bifulco, Carlo, Tamakawa, Raina, Urba, Walter, Hayward, Nicholas, Timmers, Henri, Antenucci, Anna, Facciolo, Francesco, Grazi, Gianluca, Marino, Mirella, Merola, Roberta, de Krijger, Ronald, Gimenez-Roqueplo, Anne-Paule, Piché, Alain, Chevalier, Simone, McKercher, Ginette, Birsoy, Kivanc, Barnett, Gene, Brewer, Cathy, Farver, Carol, Naska, Theresa, Pennell, Nathan A., Raymond, Daniel, Schilero, Cathy, Smolenski, Kathy, Williams, Felicia, Morrison, Carl, Borgia, Jeffrey A., Liptay, Michael J., Pool, Mark, Seder, Christopher W., Junker, Kerstin, Omberg, Larsson, Dinkin, Mikhail, Manikhas, George, Alvaro, Domenico, Bragazzi, Maria Consiglia, Cardinale, Vincenzo, Carpino, Guido, Gaudio, Eugenio, Chesla, David, Cottingham, Sandra, Dubina, Michael, Moiseenko, Fedor, Dhanasekaran, Renumathy, Becker, Karl-Friedrich, Janssen, Klaus-Peter, Slotta-Huspenina, Julia, Abdel-Rahman, Mohamed H., Aziz, Dina, Bell, Sue, Cebulla, Colleen M., Davis, Amy, Duell, Rebecca, Elder, J. Bradley, Hilty, Joe, Kumar, Bahavna, Lang, James, Lehman, Norman L., Mandt, Randy, Nguyen, Phuong, Pilarski, Robert, Rai, Karan, Schoenfield, Lynn, Senecal, Kelly, Wakely, Paul, Hansen, Paul, Lechan, Ronald, Powers, James, Tischler, Arthur, Grizzle, William E., Sexton, Katherine C., Kastl, Alison, Henderson, Joel, Porten, Sima, Waldmann, Jens, Fassnacht, Martin, Asa, Sylvia L., Schadendorf, Dirk, Couce, Marta, Graefen, Markus, Huland, Hartwig, Sauter, Guido, Schlomm, Thorsten, Simon, Ronald, Tennstedt, Pierre, Olabode, Oluwole, Nelson, Mark, Bathe, Oliver, Carroll, Peter R., Chan, June M., Disaia, Philip, Glenn, Pat, Kelley, Robin K., Landen, Charles N., Phillips, Joanna, Prados, Michael, Simko, Jeffry, Smith-McCune, Karen, VandenBerg, Scott, Roggin, Kevin, Fehrenbach, Ashley, Kendler, Ady, Sifri, Suzanne, Steele, Ruth, Jimeno, Antonio, Carey, Francis, Forgie, Ian, Mannelli, Massimo, Carney, Michael, Hernandez, Brenda, Campos, Benito, Herold-Mende, Christel, Jungk, Christin, Unterberg, Andreas, von Deimling, Andreas, Bossler, Aaron, Galbraith, Joseph, Jacobus, Laura, Knudson, Michael, Knutson, Tina, Ma, Deqin, Milhem, Mohammed, Sigmund, Rita, Godwin, Andrew K., Madan, Rashna, Rosenthal, Howard G., Adebamowo, Clement, Adebamowo, Sally N., Boussioutas, Alex, Beer, David, Giordano, Thomas, Mes-Masson, Anne-Marie, Saad, Fred, Bocklage, Therese, Landrum, Lisa, Mannel, Robert, Moore, Kathleen, Moxley, Katherine, Postier, Russel, Walker, Joan, Zuna, Rosemary, Feldman, Michael, Valdivieso, Federico, Dhir, Rajiv, Luketich, James, Pinero, Edna M. Mora, Quintero-Aguilo, Mario, Carlotti, Carlos Gilberto, Jr., Dos Santos, Jose Sebastião, Kemp, Rafael, Sankarankuty, Ajith, Tirapelli, Daniela, Catto, James, Agnew, Kathy, Swisher, Elizabeth, Creaney, Jenette, Robinson, Bruce, Shelley, Carl Simon, Godwin, Eryn M., Kendall, Sara, Shipman, Cassaundra, Bradford, Carol, Carey, Thomas, Haddad, Andrea, Moyer, Jeffey, Peterson, Lisa, Prince, Mark, Rozek, Laura, Wolf, Gregory, Bowman, Rayleen, Fong, Kwun M., Yang, Ian, Korst, Robert, Rathmell, W. Kimryn, Fantacone-Campbell, J. Leigh, Hooke, Jeffrey A., Kovatich, Albert J., Shriver, Craig D., DiPersio, John, Drake, Bettina, Govindan, Ramaswamy, Heath, Sharon, Ley, Timothy, Van Tine, Brian, Westervelt, Peter, Rubin, Mark A., Lee, Jung Il, Aredes, Natália D., Mariamidze, Armaz, Jayasinghe, Reyka G., Cao, Song, Gao, Qingsong, Wendl, Michael C., Vo, Nam Sy, Reynolds, Sheila M., Zhao, Yanyan, Climente-González, Héctor, Chai, Shengjie, Wang, Fang, Varghese, Rajees, Huang, Mo, Liang, Wen-Wei, Wyczalkowski, Matthew A., Sengupta, Sohini, Li, Zhi, Payne, Samuel H., Fenyö, David, Miner, Jeffrey H., Walter, Matthew J., Vincent, Benjamin, Eyras, Eduardo, Chen, Ken, and Chen, Feng

Published
2018
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38. Identifying Fast-Flux Botnet With AGD Names at the Upper DNS Hierarchy

Author

Xiao-Dong Zang, Jian Gong, Shao-Huang Mo, Ahmad Jakalan, and De-Lin Ding

Subjects
AGD detection, fast-flux service networks, DNS, Botnet, network security, Electrical engineering. Electronics. Nuclear engineering, TK1-9971
Abstract

Modern botnets rely on a new DNS technique called fast-flux to organize compromised hosts into fast-flux service networks (FFSNs), which helps bot herds to hide their upstream servers. Given the prevalence of this mechanism, various approaches have been proposed to detect them by analyzing DNS traffic. However, these detection mechanisms either have low detection accuracy or long detection latency. Moreover, they cannot capture the behavioral regularity and other novel traits of the evolving behavior of each botnet which is being tracked. This paper proposes a new FFSNs detection scheme to solve the above-mentioned limitations. The proposed approach can recognize groups of domains generated by a domain generation algorithms or its variants that are representative of different botnets. In addition to that, it can also identify whether the algorithmically generated domain names in a cluster are using fast-flux technology or not by applying a double-stages detection mechanism. The proposed work is implemented in a real network (China Education and Research Network), and the DNS traffic is collected from backbone routers. Experimental results demonstrate that our algorithm has significantly increased the detection accuracy compared with similar works and reduced the computational complexity.

Published
2018
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49. A Level Shifter With Almost Full Immunity to Positive dv/dt for Buck Converters

Author

Yang, Y. (author), Huang, Mo (author), Du, S. (author), Martins, Rui P. (author), Lu, Yan (author), Yang, Y. (author), Huang, Mo (author), Du, S. (author), Martins, Rui P. (author), and Lu, Yan (author)

Abstract

High-frequency buck converters need a fast transition of switching nodes (high dv/dt). Such high dv/dt, especially the positive one, can cause malfunction of a conventional pulse-triggered active-coupled (PTAC) level shifter that is used to control the high-side NMOS switch. In this work, we first discuss the dv/dt immunity of conventional PTAC level shifters. Subsequently, we propose a new scheme to block the noise current during the dv/dt sequence, allowing an almost full immunity to the positive dv/dt. With this scheme, the maximum dv/dt is determined by how well the circuitry is protected from the overvoltage during the dv/dt sequence. We design a 20-V buck converter with this level shifter, fabricated in 180-nm BCD process. Experimental results show it works correctly under a 67-V/ns dv/dt., Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public., Electronic Instrumentation

Published
2023
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50. A Radio-Frequency Cross-Connected Rectifier With LC Source Degeneration

Author

Chen, Qiujin, Huang, Mo, Xia, Tian, Yin, Jun, Liu, Haiwen, Martins, Rui P., and Lu, Yan

Abstract

This paper proposes a radio-frequency (RF) cross-connected (CC) rectifier with LC source degeneration (CCLC). The LC network resonates at twice of the working RF frequency, shaping the drain-source and gate-source voltages of the rectifying transistors of the CC rectifier. As a result, the proposed scheme reduces the transistors’ reverse current and the shoot-through current, and thus the root mean square current of the switches, improving the power conversion efficiency (PCE). Meanwhile, it has a better input impedance matching over a wide input power range from the voltage reshaping. Subsequently, we implement the CCLC topology in both one-stage and two-stage CC rectifiers. To reduce the silicon area, we design coupled inductors for the two LC networks of the two-stage CCLC rectifier. We fabricated the rectifiers using a 65-nm CMOS process. The measured PCE of the one-stage and two-stage rectifiers are 67.6% and 61.2%, respectively. The proposed scheme has a wider dynamic range than previous works.

Published
2024
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