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94 results on '"Cai, Donghong"'

53. Energy-Efficient Design for a NOMA Assisted STAR-RIS Network With Deep Reinforcement Learning

Author

Guo, Yi, Fang, Fang, Cai, Donghong, and Ding, Zhiguo

Abstract

Simultaneous transmitting and reflecting reconfigurable intelligent surfaces (STAR-RISs) have been considered promising auxiliary devices to enhance the performance of the wireless network, where users located at different sides of the surfaces can be simultaneously served by the transmitting or reflecting signals. In this article, an energy efficiency (EE) optimization problem for non-orthogonal multiple access (NOMA) assisted STAR-RIS downlink network is investigated. Due to the fractional form of the objective function, it is challenging to solve the EE optimization problem using traditional convex optimization solutions. This article proposes a deep deterministic policy gradient (DDPG)-based algorithm to maximize the EE by jointly optimizing the transmission beamforming vectors at the base station and the coefficients matrices at the STAR-RIS. Simulation results demonstrate that the proposed algorithm can effectively maximize the system EE considering the time-varying channels.

Published
2023
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57. Three-dimensional facial-image analysis to predict heterogeneity of the human ageing rate and the impact of lifestyle

Author

Xia, Xian, primary, Chen, Xingwei, additional, Wu, Gang, additional, Li, Fang, additional, Wang, Yiyang, additional, Chen, Yang, additional, Chen, Mingxu, additional, Wang, Xinyu, additional, Chen, Weiyang, additional, Xian, Bo, additional, Chen, Weizhong, additional, Cao, Yaqiang, additional, Xu, Chi, additional, Gong, Wenxuan, additional, Chen, Guoyu, additional, Cai, Donghong, additional, Wei, Wenxin, additional, Yan, Yizhen, additional, Liu, Kangping, additional, Qiao, Nan, additional, Zhao, Xiaohui, additional, Jia, Jin, additional, Wang, Wei, additional, Kennedy, Brian K., additional, Zhang, Kang, additional, Cannistraci, Carlo V., additional, Zhou, Yong, additional, and Han, Jing-Dong J., additional

Published
2020
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65. Polyostotic Fibrous Dysplasia Mimicking Metastatic Disease Radiographically: A Case Report and Literature Review

Author

Gay, David, Philip, Joey, Ahmed, Shahida, Choe, Jin, and Cai, Donghong

Subjects
ossifying fibroma, metastatic malignancy, fibrous dysplasia, osteofibrous dysplasia, GNAS1 mutation
Abstract

Fibrous dysplasia is a benign intramedullary lesion characterized by an excessive proliferation of cellular fibrous tissue intermixed with irregular trabeculae. It involves any of the bones presenting as monostotic, polyostotic, or panostotic lesion. It is caused by mutation in the GNAS1 gene (20q13.2, encoding a G-protein) resulting in inhibition of intrinsic GTPase activity of Gs alpha protein. The timing of mutation in the developmental course determines the extent of the disease, in which an earlier mutational event leads to a wider distribution of mutant cells, and consequently a more severe course of the disease. We report a case of polyostotic fibrous dysplasia in a 58-year-old male with CT scan revealing multiple lucent and sclerotic areas in bilateral ribs and iliac bones. A metastatic process was suspected by radiologists. However, a bone marrow biopsy from left posterior iliac crest demonstrated a bland fibroblastic proliferation admixed with irregular metaplastic bone in a collagenized stroma. By pyrosequencing of alpha subunit of G-protein, a mutation in Arg201(p. R201H; c.602G>A) was detected. All the findings supported a diagnosis of polyostotic fibrous dysplasia. The present case highlights a rare clinical incidental disease with radiographic mimic of metastatic process. &nbsp

Published
2017

84. Contributors

Author

Abraham, Naif Z., Jr., Aoyagi, Katsumi, Ashihara, Yoshihiro, Banki, Katalin, Beavis, Kathleen G., Bem, Sylva, Bluth, Martin H., Bock, Jay L., Borowitz, Michael J., Bowne, Wilbur B., Brandt-Rauf, Paul W., Briefel, Gary, Cai, Donghong, Caragher, Timothy E., Carty, Robert P., Chan, Edward K.L., Charnot-Katsikas, Angella, Chen, Xueying, Cherian, Sindu, Clapp, William L., Collinsworth, Amy L., Cooling, Laura, Costello, Michael, Davenport, Robertson, DeCresce, Robert, Delgado, Julio C., Downs, Theresa, Elghetany, M. Tarek, Elkins, Matthew, Fagoaga, Omar Roberto, Farag, Amal F., Fritsche, Thomas Richard, Fritzler, Marvin J., Gabali, Ali, Gleeson, Elizabeth, Graham, Susan S., Greco, Nicholas J., Grody, Wayne W., Guber, Helena A., Hall, Geraldine S., Hamilton, Robert G., Harris, Neil S., Hilbert, Tim, Hill, Charles E., Hirschhorn, Julie Woolworth, Homburger, Henry A., Huber, Sally A., Hussain, M. Mahmood, Hutchison, Robert E., Iwen, Peter C., Jain, Shilpa, Jeelani, Roohi, Jennette, J. Charles, Jenny, Nancy S., Jhang, Jeffrey S., Karcher, Donald S., Kasahara, Yasushi, Kessler, Craig M., Kidd, Jason, Klein, Michael J., Klemm, Katrin M., Kumánovics, Attila, Kurec, Anthony, LaDoulis, Charles, LaSala, P. Rocco, Lee, Peng, Lewis, Michael R., Li, Jing, Lifshitz, Mark S., Loeffelholz, Michael, Long, Patrick Michael, Massey, H. Davis, Mathur, Sharad C., Mazur, Lech J., McPherson, Richard A., McVoy, Lauren, Merkel, Kimberly L., Miller, Jonathan L., Miller, W. Greg, Mintz, Paul D., Mitsios, John V., Mohi, Golam, Nadkarni, Prashant, Napolitano, Mariasanta, Nolte, Frederick S., Oh, Man S., Olano, Juan P., Ortel, Thomas L., Patterson, Emily Rupp, Pincus, Matthew R., Piper, Margaret, Pritt, Bobbi S., Rand, Jacob H., Rao, A. Koneti, Riley, Roger S., Roby, Rhonda K., Rossi, Ralph, Salwen, Martin J., Sanford, Kimberly W., Sarafraz-Yazdi, Ehsan, Schexneider, Katherine I., Schmaier, Alvin H., Shaikh, Mohammad F., Siddiqi, Haseeb A., Stein, Constance K., Steinau, Martin, Tierno, Philip M., Jr., Tranchida, Paul, Unger, Elizabeth R., Vajpayee, Neerja, von Mühlen, Carlos Alberto, Walker, David H., Weimer, Eric T., Weindel, Michael, Weinstock, Ruth S., Winter, William E., Winters, Jeffrey L., Wood, Brent L., Woods, Gail L., Xu, Ruliang, Zhang, David Y., and Zhou, Liye

Published
2017
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89. The precursor of PI(3,4,5)P3 alleviates aging by activating daf-18(Pten) and independent of daf-16.

Author

Shi, Dawei, Xia, Xian, Cui, Aoyuan, Xiong, Zhongxiang, Yan, Yizhen, Luo, Jing, Chen, Guoyu, Zeng, Yingying, Cai, Donghong, Hou, Lei, McDermott, Joseph, Li, Yu, Zhang, Hong, and Han, Jing-Dong J.

Subjects
LIFE spans, TUMOR suppressor genes, SMALL molecules, CAENORHABDITIS elegans, DEGENERATION (Pathology)
Abstract

Aging is characterized by the loss of homeostasis and the general decline of physiological functions, accompanied by various degenerative diseases and increased rates of mortality. Aging targeting small molecule screens have been performed many times, however, few have focused on endogenous metabolic intermediates—metabolites. Here, using C. elegans lifespan assays, we conducted a worm metabolite screen and identified an eukaryotes conserved metabolite, myo-inositol (MI), to extend lifespan, increase mobility and reduce fat content. Genetic analysis of enzymes in MI metabolic pathway suggest that MI alleviates aging through its derivative PI(4,5)P2. MI and PI(4,5)P2 are precursors of PI(3,4,5)P3, which is negatively related to longevity. The longevity effect of MI is dependent on the tumor suppressor gene, daf-18 (homologous to mouse Pten), independent of its classical pathway downstream genes, akt or daf-16. Furthermore, we found MI effects on aging and lifespan act through mitophagy regulator PTEN induced kinase-1 (pink-1) and mitophagy. MI's anti-aging effect is also conserved in mouse, indicating a conserved mechanism in mammals. Phosphatidylinositol 3-kinase catalyzes the reaction from PI(4,5)P2 to PI(3,4,5)P3 and is encoded by the age-1 gene known to regulate lifespan. Here the researchers found that the metabolite myo-inositol, which can be converted to PI(3,4,5)P3 extends worm lifespan and alleviates worm as well as mouse health decline during aging. [ABSTRACT FROM AUTHOR]

Published
2020
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90. Three-dimensional facial-image analysis to predict heterogeneity of the human ageing rate and the impact of lifestyle

Author

Xia, Xian, Chen, Xingwei, Wu, Gang, Li, Fang, Wang, Yiyang, Chen, Yang, Chen, Mingxu, Wang, Xinyu, Chen, Weiyang, Xian, Bo, Chen, Weizhong, Cao, Yaqiang, Xu, Chi, Gong, Wenxuan, Chen, Guoyu, Cai, Donghong, Wei, Wenxin, Yan, Yizhen, Liu, Kangping, Qiao, Nan, Zhao, Xiaohui, Jia, Jin, Wang, Wei, Kennedy, Brian K., Zhang, Kang, Cannistraci, Carlo V., Zhou, Yong, Han, Jing Dong J., Xia, Xian, Chen, Xingwei, Wu, Gang, Li, Fang, Wang, Yiyang, Chen, Yang, Chen, Mingxu, Wang, Xinyu, Chen, Weiyang, Xian, Bo, Chen, Weizhong, Cao, Yaqiang, Xu, Chi, Gong, Wenxuan, Chen, Guoyu, Cai, Donghong, Wei, Wenxin, Yan, Yizhen, Liu, Kangping, Qiao, Nan, Zhao, Xiaohui, Jia, Jin, Wang, Wei, Kennedy, Brian K., Zhang, Kang, Cannistraci, Carlo V., Zhou, Yong, and Han, Jing Dong J.

Abstract

Xia, X., Chen, X., Wu, G., Li, F., Wang, Y., Chen, Y., ... & Han, J-D. (2020). Three-dimensional facial-image analysis to predict heterogeneity of the human ageing rate and the impact of lifestyle. Nature Metabolism, 1-12. https://doi.org/10.1038/s42255-020-00270-x

92. Contributors

Author

Abraham, Naif Z., Jr., Ashihara, Yoshihiro, Banki, Katalin, Bem, Sylva, Ben-Ezra, Jonathan, Bluth, Martin H., Bock, Jay L., Borawski, Dorota, Borowitz, Michael J., Bowne, Wilbur B., Brandt-Rauf, Paul W., Bylund, David J., Cai, Donghong, Carty, Robert P., Cooling, Laura, Costello, Michael, Croft, Ann C., Czuchlewski, David R., Davenport, Robertson D., Delgado, Julio C., Dilts, Thomas J., Downs, Theresa, Elghetany, M. Tarek, Fagoaga, Omar R., Farag, Amal F., Fenelus, Maly, Ferreira-Gonzalez, Andrea, Fink, Louis M., Fritsche, Thomas R., Graham, Susan S., Gress, Frank G., Grody, Wayne W., Guber, Helena A., Hall, Geraldine S., Hill, Charles E., Homburger, Henry A., Hubbell, Charlene A., Hussain, M. Mahmood, Hutchison, Robert E., Iwen, Peter C., Jain, Shilpa, Jhang, Jeffrey S., Josekutty, Joby, Karcher, Donald S., Kasahara, Yasushi, Khan, Mukhtar I., Klein, Michael J., Klemm, Katrin M., Kratz, Alexander, Kurec, Anthony S., Larson, Richard S., LaSala, P. Rocco, Lee, Peng, Li, Jing, Lifshitz, Mark S., Mageau, Ronald, Marlar, Richard A., Massey, H. Davis, Mathur, Sharad C., McCallum, Rex M., McPherson, Richard A., Miller, W. Greg, Miller, Jonathan L., Mintz, Paul D., Nakamura, Robert M., Nolte, Frederick S., Oh, Man S., Pincus, Matthew R., Piper, Margaret A., Polesky, Herbert F., Rao, A. Koneti, Riley, Roger S., Roby, Rhonda K., Rosales, Lazaro, Roseff, Susan D., Rossi, Ralph, Sabatini, Linda M., Salwen, Martin J., Sanford, Kimberly W., Schexneider, Katherine I., Schmaier, Alvin H., Selvarangan, Rangaraj, Shah, Ankoor, Siddiqi, Haseeb A., Sireci, Anthony N., Smith, Michael B., Soh, James, Stein, Constance K., Steinau, Martin, Sunheimer, Robert L., Threatte, Gregory A., Tierno, Philip M., Jr., Tranchida, Paul, Unger, Elizabeth R., Vajpayee, Neerja, Viswanatha, David S., von Mühlen, Carlos Alberto, Walker, David H., Weinstock, Ruth S., Wilkinson, David S., Winters, Jeffrey L., Wood, Brent L., Woods, Gail L., Woolf, William, Xu, Ruliang, and Yungbluth, Margaret

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93. Langerhans Cell Sarcoma Arising from Chronic Lymphocytic Lymphoma/Small Lymphocytic Leukemia: Lineage Analysis and BRAF V600E Mutation Study.

Author

Chen W, Jaffe R, Zhang L, Hill C, Block AM, Sait S, Song B, Liu Y, and Cai D

Abstract

Background: the phenomenon that histiocytic/dendritic cell sarcomas may be transformed from lymphoproliferative diseases is dubbed 'transdifferentiation'. Langerhans cell sarcoma (LCS) transdifferentiated from chronic lymphocytic leukemia/small cell lymphoma (CLL/SLL) is extremely rare. The underlying mechanisms of LCS tumorogenesis and its transdifferentiation from CLL/SLL are largely unknown., Aims: the authors strive to further characterize LCS, to understand the potential molecular changes in LCS and the underlying mechanisms of CLL/SLL transformation to LCS., Materials and Methods: a progressively enlarging right inguinal lymph node from a 68-year-old female patient with a history of CLL was biopsied and submitted for flow cytometry analysis, routine hematoxylin, and eosin (H and E) stain and immunohistochemical study. Furthermore, clonality study (fluorescent in situ hybridization (FISH) analysis with a CLL panel probes) and BRAF V600E mutation study (pyrosequencing and immunostain) were performed., Results: two different neoplasms, LCS and CLL/SLL, were discovered to occur simultaneously in the same lymph node. These two entities were shown to be clonally related. More importantly, for the first time, BRAF V600E mutation was detected in LCS., Conclusions: LCS can be transdifferentiated from CLL/SLL and BRAF V600E mutation may provide the foundation for alternative therapy of LCS.

Published
2013
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94. Dysmegakaryocytopoiesis and maintaining platelet count in patients with plasma cell neoplasm.

Author

Mair Y, Zheng Y, and Cai D

Abstract

Background: Dysmegakaryocytopoiesis in patients with the plasma cell neoplasm (PCN) is rarely discussed in the literature. The puzzling phenomenon, which PCN patients maintaining normal platelet count even when the marrow is mostly replaced by plasma cells, is hardly explored., Aim: This study was aimed to determine the frequency of dysmegakaryocytopoiesis in PCN and the relationships between bone marrow (BM) plasma cell percentage, plasma cell immunomarkers, the severity of dysmegakaryocytopoiesis, and peripheral blood platelet count in PCN., Materials and Methods: We randomly selected 16 cases of PCN, among which 4 were with monoclonal gammopathy of undetermined significance and 12 were with plasma cell myeloma., Results: OUR STUDY SHOWED THAT: (1) Dysmegakaryocytopoiesis was present in all the selected cases of PCN and its severity was not correlated with the percentage of the plasma cells in BM; (2) almost all patients maintained normal platelet count even when BM was mostly replaced by plasma cells; (3) immunomarkers of the neoplastic plasma cells were not associated with dysmegakaryocytopoiesis or maintaining of platelet count. The possible mechanisms behind dysmegakaryocytopoiesis and maintaining of platelet count were also discussed., Conclusion: Despite the universal presence of dysmegakaryocytopoiesis in PCN, the platelet count is maintained at normal range.

Published
2013
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