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145 results on '"Yuan, Youzhong"'

1. Plasmablastic Lymphoma: A Multi-institutional Study and Review of the Literature

Author

Choudhuri, Jui, Pan, Zenggang, Yuan, Ji, Chen, Mingyi, Wu, Xiaojun, Zheng, Gang, Zhao, Chen, Yuan, Youzhong, Agarwal, Beamon, Liu, John, Ma, Maxwell Y., Wang, Yanhua, and Shi, Yang

Subjects
Lymphomas -- Diagnosis, Proteoglycans -- Health aspects, Health
Abstract

Context.--Plasmablastic lymphoma (PBL) is a rare aggressive lymphoma, usually positive for CD138 and frequently occurring in the oral cavity of human immunodeficiency virus (HIV) patients. Up to 10% of cases are negative for CD138 and diagnostically very challenging. Objective.--To investigate the appropriate approach to diagnose [CD138.sup.-] plasmablastic lymphoma and avoid misdiagnosis. Design.--We studied 21 cases of [CD138.sup.-] PBL from multiple large institutes in the United States and 21 cases from the literature. Results.--[CD138.sup.-] PBLs were positive for different B/ plasma cell markers at various percentages: MUM1 (94.4%; 34 of 36), OCT2 (70.6%; 12 of 17), immunoglobulin light chains (68.8%; 22 of 32), CD38 (68.4%; 13 of 19), CD79a (34.2%; 13 of 38), and PAX5 (15.6%; 5 of 32), suggesting that MUM1, OCT2, immunoglobulin light chains, and CD38 are useful markers to help establish the lineage. A total of 83% of cases (30 of 36) were extraoral lesions. Extraoral lesions showed much lower Epstein-Barr virus (EBV) infection rates (16 of 30; 53.3%) and had worse prognosis. MYC was positive in 80% (8 of 10) of [EBV.sup.+] cases and 40% (2 of 5) [EBV.sup.-] cases, indicating the importance of MYC in pathogenesis, especially in [EBV.sup.+] cases. Conclusions.--Our study emphasizes that [CD138.sup.-] PBLs tend to be extraoral lesions, with much lower EBV infection rates, and diagnostically very challenging. Accurate diagnosis requires a thorough investigation and workup by using appropriate markers. (Arch Pathol Lab Med. 2023;147:643-654; doi: 10.5858/arpa.2021-0462-OA), Plasmablastic lymphoma (PBL) is a diagnostic challenge in pathology, with morphologic and immunophenotypical features lying within the spectrum of diffuse large B-cell lymphoma and plasma cell myeloma. PBL was classified [...]

Published
2023
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4. Flower isoforms promote competitive growth in cancer

Author

Madan, Esha, Pelham, Christopher J., Nagane, Masaki, Parker, Taylor M., Canas-Marques, Rita, Fazio, Kimberly, Shaik, Kranti, Yuan, Youzhong, Henriques, Vanessa, Galzerano, Antonio, Yamashita, Tadashi, Pinto, Miguel Alexandre Ferreira, Palma, Antonio M., Camacho, Denise, Vieira, Ana, Soldini, David, Nakshatri, Harikrishna, Post, Steven R., Rhiner, Christa, Yamashita, Hiroko, Accardi, Davide, Hansen, Laura A., Carvalho, Carlos, Beltran, Antonio L., Kuppusamy, Periannan, Gogna, Rajan, and Moreno, Eduardo

Published
2019
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6. CD138− Plasmablastic Lymphoma

Author

Choudhuri, Jui, primary, Pan, Zenggang, additional, Yuan, Ji, additional, Chen, Mingyi, additional, Wu, Xiaojun, additional, Zheng, Gang, additional, Zhao, Chen, additional, Yuan, Youzhong, additional, Agarwal, Beamon, additional, Liu, John, additional, Ma, Maxwell Y., additional, Wang, Yanhua, additional, and Shi, Yang, additional

Published
2022
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10. Hemorrhagic shock augments lung endothelial cell activation: role of temporal alterations of TLR4 and TLR2

Author

Li, Yuehua, Xiang, Meng, Yuan, Youzhong, Xiao, Guozhi, Zhang, Jian, Jiang, Yong, Vodovotz, Yoram, lliar, Timothy R., Wilson, Mark A., and Fan, Jie

Subjects
Acute respiratory distress syndrome -- Risk factors, Acute respiratory distress syndrome -- Research, Cell receptors -- Physiological aspects, Cell receptors -- Research, Epithelial cells -- Physiological aspects, Epithelial cells -- Research, Hemorrhagic shock -- Complications and side effects, Hemorrhagic shock -- Research, Biological sciences
Abstract

Li Y, Xiang M, Yuan Y, Xiao G, Zhang J, Jiang Y, Vodovotz Y, Billiar TR, Wilson MA, Fan J. Hemorrhagic shock augments lung endothelial cell activation: role of temporal alterations of TLR4 and TLR2. Am J Physiol Regul Integr Comp Physiol 297: R1670-R1680, 2009. First published October 14, 2009; doi: 10.1152/ajpregu.00445.2009.--Hemorrhagic shock (HS) due to major trauma predisposes the host to the development of acute lung inflammation and injury. The lung vascular endothelium is an active organ that plays a central role in the development of acute lung injury through generating reactive oxygen species and synthesizing and releasing of a number of inflammatory mediators, including leukocyte adhesion molecules that regulate neutrophils emigration. Previous study from our laboratory has demonstrated that in a setting of sepsis, Toll-like receptor-4 (TLR4) signaling can induce TLR2 expression in endothelial cells (ECs), thereby increasing the cells' response to TLR2 ligands. The present study tested the hypothesis that TLR4 activation by HS and the resultant increased TLR2 surface expression in ECs might contribute to the mechanism underlying HS-augmented activation of lung ECs. The results show that high-mobility group box 1 (HMGB1) through TLR4 signaling mediates HS-induced surface expression of TLR2 in the lung and mouse lung vascular endothelial cells (MLVECs). Furthermore, the results demonstrate that HMGB 1 induces activation of NAD(P)H oxidase and expression of ICAM-1 in the lung, and MLVECs sequentially depend on TLR4 in the early phase and on TLR2 in the late phase following HS. Finally, the data indicate an important role of the increased TLR2 surface expression in enhancing the activation of MLVECs and augmenting pulmonary neutrophil infiltration in response to TLR2 agonist peptidoglycan. Thus, induction of TLR2 surface expression in lung ECs, induced by HS and mediated by HMGB 1/TLR4 signaling, is an important mechanism responsible for endothelial cell-mediated inflammation and organ injury following trauma and hemorrhage. acute lung injury; neutrophil; Toll-like receptors doi: 10.1152/ajpregu.00445.2009

Published
2009

11. Preactivation of NKT cells with [alpha]-GalCer protects against hepatic ischemia-reperfusion injury in mouse by a mechanism involving IL-13 and adenosine [A.sub.2A] receptor

Author

Cao, Zongxian, Yuan, Youzhong, Jeyabalan, Geetha, Du, Qiang, Tsung, Allan, Geller, David A., and Billiar, Timothy R.

Subjects
Interleukins -- Health aspects, Interleukins -- Research, Liver diseases -- Genetic aspects, Liver diseases -- Physiological aspects, Liver diseases -- Prevention, Liver diseases -- Research, T cells -- Physiological aspects, T cells -- Research, Biological sciences
Abstract

Hepatic preconditioning has emerged as a promising strategy of activating natural pathways to augment tolerance to liver ischemia-reperfusion (IR) injury. Liver-resident natural killer T (NKT) cells play an important role in modulating the local immune and inflammatory responses. This work was aimed to investigate whether preactivation of NKT cells could provide a beneficial 'preconditioning' effect to ameliorate the subsequent hepatic IR injury. To selectively activate NKT cells, C57BL/6 mice were treated intraperitoneally with the glycolipid antigen a-galactosylceramide ([alpha]-GalCer) 1 h prior to hepatic ischemia. Significantly reduced liver IR injury was observed in mice pretreated with aGalCer, and this protective effect was specifically abrogated by a CD1d blocking antibody. Serum TNF-[alpha], IFN-[gamma] and IL-13 levels were markedly increased shortly after [alpha]-GalCer injection. Pretreatment with a neutralizing antibody against TNF-[alpha] or IFN-[gamma] did not influence the protective effect of [alpha]-GalCer preconditioning, whereas preadministration of an IL-13 neutralizing antibody completely abolished the effect. Treatment with [alpha]-GalCer also led to an increased expression of adenosine [A.sub.2A] receptor ([A.sub.2A]R) in the liver, and blockade of [A.sub.2A]R by SH58261 diminished [alpha]-GalCer pretreatment-mediated attenuation of liver IR injury. In contrast, administration of the selective [A.sub.2A]R agonist CGS21680 reversed the counteracting effect of the IL-13 neutralizing antibody on [alpha]-GalCer preconditioning. Additionally, [alpha]-GalCer pretreatment was associated with a decreased neutrophil accumulation in the ischemic liver. These findings provide the first evidence that hepatic preconditioning by prcactivation of NKT cells with [alpha]-GalCer protects the liver from IR injury via an IL-13 and adenosine [A.sub.2A]R-dependent mechanism. liver protection; natural killer T cells; glycolipid; Thl/Th2 cytokines; [alpha]-galactosylceramide

Published
2009

18. Carbamate derivatives of colchicine show potent activity towards primary acute lymphoblastic leukemia and primary breast cancer cells—in vitro and ex vivo study

Author

Urbaniak, Alicja, primary, Jousheghany, Fariba, additional, Piña‐Oviedo, Sergio, additional, Yuan, Youzhong, additional, Majcher‐Uchańska, Urszula, additional, Klejborowska, Greta, additional, Moorjani, Anika, additional, Monzavi‐Karbassi, Behjatolah, additional, Huczyński, Adam, additional, and Chambers, Timothy C., additional

Published
2020
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19. Coactivation of NF-κB and Notch signaling is sufficient to induce B-cell transformation and enables B-myeloid conversion

Author

Xiu, Yan, primary, Dong, Qianze, additional, Fu, Lin, additional, Bossler, Aaron, additional, Tang, Xiaobing, additional, Boyce, Brendan, additional, Borcherding, Nicholas, additional, Leidinger, Mariah, additional, Sardina, José Luis, additional, Xue, Hai-hui, additional, Li, Qingchang, additional, Feldman, Andrew, additional, Aifantis, Iannis, additional, Boccalatte, Francesco, additional, Wang, Lili, additional, Jin, Meiling, additional, Khoury, Joseph, additional, Wang, Wei, additional, Hu, Shimin, additional, Yuan, Youzhong, additional, Wang, Endi, additional, Yuan, Ji, additional, Janz, Siegfried, additional, Colgan, John, additional, Habelhah, Hasem, additional, Waldschmidt, Thomas, additional, Müschen, Markus, additional, Bagg, Adam, additional, Darbro, Benjamin, additional, and Zhao, Chen, additional

Published
2020
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23. Carbamate Derivatives of Colchicine Show Potent Activity toward Primary Acute Lymphoblastic Leukemia and Primary Breast Cancer Cells: In Vitro and Ex Vivo Study

Author

Urbaniak, Alicja, primary, Jousheghany, Fariba, additional, Yuan, Youzhong, additional, Pina‐Oviedo, Segio, additional, Delgado, Magdalena, additional, Majcher, Urszula, additional, Klejborowska, Greta, additional, Huczyński, Adam, additional, Monzavi‐Karbassi, Behjatolah, additional, Kieber‐Emmons, Thomas, additional, and Chambers, Timothy C., additional

Published
2019
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29. Coactivation of NF-?B and Notch signaling is sufficient to induce B-cell transformation and enables B-myeloid conversion

Author

Xiu, Yan, Dong, Qianze, Fu, Lin, Bossler, Aaron, Tang, Xiaobing, Boyce, Brendan, Borcherding, Nicholas, Leidinger, Mariah, Sardina, José Luis, Xue, Hai-hui, Li, Qingchang, Feldman, Andrew, Aifantis, Iannis, Boccalatte, Francesco, Wang, Lili, Jin, Meiling, Khoury, Joseph, Wang, Wei, Hu, Shimin, Yuan, Youzhong, Wang, Endi, Yuan, Ji, Janz, Siegfried, Colgan, John, Habelhah, Hasem, Waldschmidt, Thomas, Müschen, Markus, Bagg, Adam, Darbro, Benjamin, and Zhao, Chen

Abstract

NF-?B and Notch signaling can be simultaneously activated in a variety of B-cell lymphomas. Patients with B-cell lymphoma occasionally develop clonally related myeloid tumors with poor prognosis. Whether concurrent activation of both pathways is sufficient to induce B-cell transformation and whether the signaling initiates B-myeloid conversion in a pathological context are largely unknown. Here, we provide genetic evidence that concurrent activation of NF-?B and Notch signaling in committed B cells is sufficient to induce B-cell lymphomatous transformation and primes common progenitor cells to convert to myeloid lineage through dedifferentiation, not transdifferentiation. Intriguingly, the converted myeloid cells can further transform, albeit at low frequency, into myeloid leukemia. Mechanistically, coactivation of NF-?B and Notch signaling endows committed B cells with the ability to self renew. Downregulation of BACH2, a lymphoma and myeloid gene suppressor, but not upregulation of CEBPa and/or downregulation of B-cell transcription factors, is an early event in both B-cell transformation and myeloid conversion. Interestingly, a DNA hypomethylating drug not only effectively eliminated the converted myeloid leukemia cells, but also restored the expression of green fluorescent protein, which had been lost in converted myeloid leukemia cells. Collectively, our results suggest that targeting NF-?B and Notch signaling will not only improve lymphoma treatment, but also prevent the lymphoma-to-myeloid tumor conversion. Importantly, DNA hypomethylating drugs might efficiently treat these converted myeloid neoplasms.

Published
2020
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30. Protein ISGylation modulates the JAK-STAT signaling pathway

Author

Malakhova, Oxana A., Yan, Ming, Malakhov, Michael P., Yuan, Youzhong, Ritchie, Kenneth J., Kim, Keun Il, Peterson, Luke F., Shuai, Ke, and Zhang, Dong-Er

Subjects
Genetic research -- Analysis, Proteins -- Genetic aspects, Genetic regulation -- Analysis, Cells -- Genetic aspects, Interferon -- Physiological aspects, Proteases -- Genetic aspects, Biological sciences
Abstract

Research has been conducted on protease removing ISG15 from ISGylated proteins. The authors demonstrate that the mice lacking this protease are hypersensitive to type I interferon.

Published
2003

31. The response of phyllodes tumor of the breast to anticancer therapy: An in vitro and ex vivo study.

Author

Urbaniak, Alicja, Jousheghany, Fariba, Yuan, Youzhong, Piña-Oviedo, Sergio, Huczyński, Adam, Delgado, Magdalena, Kieber-Emmons, Thomas, Monzavi-Karbassi, Behjatolah, and Chambers, Timothy C.

Subjects
BREAST tumors, PHYLLODES tumors, EPITHELIAL cells, CELL death, CELL culture, PRIMARY cell culture
Abstract

Phyllodes tumors of the breast (PTB) are uncommon stromal-epithelial neoplasms, with the main recommended treatment being surgical removal. However, even with adequate resection, the risk of recurrence in the malignant form remains as high as 40%, and there is no recognized consensus on the most effective drugs for PTB. In the present study, an ex vivo model of malignant phyllodes and derived primary cell cultures were used to evaluate the effectiveness of a panel of different drugs, including the Bcl-2/Bcl-xL inhibitor ABT-263, salinomycin (SAL), doxorubicin (DOX), paclitaxel (TAX), vincristine (VCR), colchicine (COL) and cisplatin (CIS). ABT-263, SAL and DOX were highly effective towards phyllodes spindle cells when assessed in the ex vivo model, contributing to ~98% tumor cell death. Furthermore, ABT-263 was highly selective for tumor cells in this system, and exhibited little toxic effect on adjacent normal epithelial cells. Furthermore, consistent with findings in the ex vivo model, ABT-263 was significantly less toxic towards MCF 10A non-tumorigenic breast epithelial cells compared with SAL and DOX. A conditional reprogramming strategy was subsequently used, involving Rho kinase inhibition, to successfully generate primary phyllodes tumor cells that could be cultured for several passages. The primary cells were sensitive to DOX with an IC50 of 0.40±0.07 µM in a standard viability assay and the preliminary results were obtained indicating sensitivity to ABT-263 and SAL. The present study demonstrated the feasibility of using explants and primary cells for drug discovery, selectively targeting PTB cells. [ABSTRACT FROM AUTHOR]

Published
2019
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32. Small-molecule inhibitors targeting INK4 protein p18INK4C enhance ex vivo expansion of haematopoietic stem cells

Author

Gao, Yingdai, primary, Yang, Peng, additional, Shen, Hongmei, additional, Yu, Hui, additional, Song, Xianmin, additional, Zhang, Liyan, additional, Zhang, Peng, additional, Cheng, Haizi, additional, Xie, Zhaojun, additional, Hao, Sha, additional, Dong, Fang, additional, Ma, Shihui, additional, Ji, Qing, additional, Bartlow, Patrick, additional, Ding, Yahui, additional, Wang, Lirong, additional, Liu, Haibin, additional, Li, Yanxin, additional, Cheng, Hui, additional, Miao, Weimin, additional, Yuan, Weiping, additional, Yuan, Youzhong, additional, Cheng, Tao, additional, and Xie, Xiang-Qun, additional

Published
2015
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33. Interacting Neuro-endocrine, Innate, and Acquired Immune Pathways Regulate Neutrophil Mobilization from Bone Marrow following Hemorrhagic Shock 1

Author

Liu, Yujian, Yuan, Youzhong, Li, Yuehua, Zhang, Jian, Xiao, Guozhi, Vodovotz, Yoram, Billiar, Timothy R., Wilson, Mark A., and Fan, Jie

Subjects
Male, Mice, Inbred C3H, Epinephrine, Resuscitation, Bone Marrow Cells, Shock, Hemorrhagic, Interleukin-23, Neurosecretory Systems, Article, Immunity, Innate, Toll-Like Receptor 4, Autocrine Communication, Mice, Neutrophil Infiltration, Cell Movement, Macrophages, Alveolar, Receptors, Adrenergic, beta, Animals, HMGB1 Protein, Signal Transduction
Abstract

Polymorphonuclear neutrophils (PMN) are critical innate immune effector cells that either protect the host or exacerbate organ dysfunction by migrating to injured or inflamed tissues. Resuscitated hemorrhagic shock following major trauma promotes the development of organ inflammation by priming PMN migration and activation in response to a second, often trivial, stimulus (a so-called "two hit" phenomenon). PMN mobilization from bone marrow supports a sustained, hemorrhagic shock/resuscitation (HS/R)-primed migration of PMN. We addressed the role and mechanism of HS/R in regulating PMN egress from bone marrow. We demonstrate that HS/R through the alarmin HMGB1 induces IL-23 secretion from macrophages in an autocrine and TLR4 signaling-dependent manner. In turn IL-23, through an IL-17 G-CSF-mediated mechanism, induces PMN egress from bone marrow. We also show that beta-adrenergic receptor activation by catecholamine of macrophages mediates the HS/R-induced release of HMGB1. These data indicate that HS/R, a global ischemia/reperfusion stimulus, regulates PMN mobilization through a series of interacting pathways that include neuroendocrine and innate and acquired immune systems. Blocking this novel signaling axis may present a novel therapeutic target for posttrauma inflammation.

Published
2009

34. p18INK4C is an unique target for hematopoietic stem cell expansion with small molecule inhibitors

Author

Gao, Yingdai, primary, Shen, Hongmei, additional, Yang, Peng, additional, Yu, Hui, additional, Xie, Zhaojun, additional, Zhang, Liyan, additional, Bartlow, Patrick, additional, Ji, Qing, additional, Ding, Yahui, additional, Wang, Lirong, additional, Hao, Sha, additional, Ma, Shihui, additional, Dong, Fang, additional, Li, Yanxin, additional, Zhang, Peng, additional, Cheng, Haizi, additional, Miao, Weimin, additional, Yuan, Youzhong, additional, Cheng, Tao, additional, and Xie, Xiang-Qun, additional

Published
2013
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35. The p53–PUMA axis suppresses iPSC generation

Author

Li, Yanxin, primary, Feng, Haizhong, additional, Gu, Haihui, additional, Lewis, Dale W., additional, Yuan, Youzhong, additional, Zhang, Lei, additional, Yu, Hui, additional, Zhang, Peng, additional, Cheng, Haizi, additional, Miao, Weimin, additional, Yuan, Weiping, additional, Cheng, Shi-Yuan, additional, Gollin, Susanne M., additional, and Cheng, Tao, additional

Published
2013
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