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1,039 results on '"Chen, Weina"'

5. Leveraging 'Flip,' a Video Discussion Platform, to Support the Needs of International ESL Pre-Service Teachers

Author

Chen, Weina L. and Wong, Kevin M.

Abstract

International students, particularly international English as a Second Language (ESL) students who come to the United States with relatively lower levels of English oral language proficiency, are often reluctant to participate in academic discussions. In a graduate-level TESOL program with a majority of international ESL students, a video recording, sharing, and discussion platform, "Flip," was utilized in the program's teaching innovation. "Flip" is widely adopted by educators of all grade levels worldwide, as it enables educators to create a less formal online space to meet the holistic needs of international ESL students, including both academic and social needs. The article explains the teaching context of the practice, four stages of course integration with "Flip," reasons for the integration, reflections, and future pedagogical directions. Incorporating "Flip" in this program promotes linguistic benefits, teacher identity and skill development, a community of belonging, and increased equity in assessment. Practical pedagogical considerations are also provided at the end of the article.

Published
2023
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11. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms

Author

Khoury, Joseph D, Solary, Eric, Abla, Oussama, Akkari, Yassmine, Alaggio, Rita, Apperley, Jane F, Bejar, Rafael, Berti, Emilio, Busque, Lambert, Chan, John KC, Chen, Weina, Chen, Xueyan, Chng, Wee-Joo, Choi, John K, Colmenero, Isabel, Coupland, Sarah E, Cross, Nicholas CP, De Jong, Daphne, Elghetany, M Tarek, Takahashi, Emiko, Emile, Jean-Francois, Ferry, Judith, Fogelstrand, Linda, Fontenay, Michaela, Germing, Ulrich, Gujral, Sumeet, Haferlach, Torsten, Harrison, Claire, Hodge, Jennelle C, Hu, Shimin, Jansen, Joop H, Kanagal-Shamanna, Rashmi, Kantarjian, Hagop M, Kratz, Christian P, Li, Xiao-Qiu, Lim, Megan S, Loeb, Keith, Loghavi, Sanam, Marcogliese, Andrea, Meshinchi, Soheil, Michaels, Phillip, Naresh, Kikkeri N, Natkunam, Yasodha, Nejati, Reza, Ott, German, Padron, Eric, Patel, Keyur P, Patkar, Nikhil, Picarsic, Jennifer, Platzbecker, Uwe, Roberts, Irene, Schuh, Anna, Sewell, William, Siebert, Reiner, Tembhare, Prashant, Tyner, Jeffrey, Verstovsek, Srdan, Wang, Wei, Wood, Brent, Xiao, Wenbin, Yeung, Cecilia, and Hochhaus, Andreas

Subjects
Genetics, Human Genome, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Hematologic Neoplasms, Histiocytosis, Humans, World Health Organization, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

The upcoming 5th edition of the World Health Organization (WHO) Classification of Haematolymphoid Tumours is part of an effort to hierarchically catalogue human cancers arising in various organ systems within a single relational database. This paper summarizes the new WHO classification scheme for myeloid and histiocytic/dendritic neoplasms and provides an overview of the principles and rationale underpinning changes from the prior edition. The definition and diagnosis of disease types continues to be based on multiple clinicopathologic parameters, but with refinement of diagnostic criteria and emphasis on therapeutically and/or prognostically actionable biomarkers. While a genetic basis for defining diseases is sought where possible, the classification strives to keep practical worldwide applicability in perspective. The result is an enhanced, contemporary, evidence-based classification of myeloid and histiocytic/dendritic neoplasms, rooted in molecular biology and an organizational structure that permits future scalability as new discoveries continue to inexorably inform future editions.

Published
2022

29. Multi-Level Transfer Alignment Method by Using the Inertial Network

Author

Chen, Weina, Yang, Zhong, Gu, Shanshan, Wang, Yizhi, 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, Martín, 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, Yan, Liang, editor, and Yu, Xiang, editor

Published
2022
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38. YAP activation in liver macrophages via depletion of MST1/MST2 enhances liver inflammation and fibrosis in MASLD.

Author

Zhang, Jinqiang, Chen, Weina, Song, Kyoungsub, Song, Kejing, Kolls, Jay, and Wu, Tong

Abstract

Macrophages have been recognized as pivotal players in the progression of MASLD/MASH. However, the molecular mechanisms underlying their multifaceted functions in the disease remain to be further clarified. In the current study, we developed a new mouse model with YAP activation in macrophages to delineate the effect and mechanism of YAP signaling in the pathogenesis of MASLD/MASH. Genetically modified mice, featuring specific depletion of both Mst1 and Mst2 in macrophages/monocytes, were generated and exposed to a high‐fat diet for 12 weeks to induce MASLD. Following this period, livers were collected for histopathological examination, and liver non‐parenchymal cells were isolated and subjected to various analyses, including single‐cell RNA‐sequencing, immunofluorescence and immunoblotting and qRT‐PCR to investigate the impact of YAP signaling on the progression of MASLD. Our data revealed that Mst1/2 depletion in liver macrophages enhanced liver inflammation and fibrosis in MASLD. Using single‐cell RNA‐sequencing, we showed that YAP activation via Mst1/2 depletion upregulated the expressions of both pro‐inflammatory genes and genes associated with resolution/tissue repair. We observed that YAP activation increases Kupffer cell populations (i.e., Kupffer‐2 and Kupffer‐3) which are importantly implicated in the pathogenesis of MASLD/MASH. Our data indicate that YAP activation via Mst1/2 deletion enhances both the pro‐inflammatory and tissue repairing functions of Kupffer‐1 and ‐2 cells at least in part through C1q. These YAP‐regulatory mechanisms control the plasticity of liver macrophages in the context of MASLD/MASH. Our findings provide important evidence supporting the critical regulatory role of YAP signaling in liver macrophage plasticity and the progression of MASLD. Therefore, targeting the Hippo‐YAP pathway may present a promising therapeutic strategy for the treatment of MASH. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Thrombocytosis and megakaryocyte changes associated with PRCA

Author

Abdallah, Joelle, primary, Williams, Robert George, additional, Awada, Hussein, additional, Raman, Ganesh, additional, Ozcan, Yusuf M, additional, Orland, Mark David, additional, Mete, Mutlu, additional, Chen, Weina, additional, Gurnari, Carmelo, additional, Maciejewski, Jaroslaw P., additional, and Bat, Taha, additional

Published
2024
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41. Ahemolytic PNH (white cell PNH): Clinical features and implications of a distinct phenotype of paroxysmal nocturnal haemoglobinuria

Author

Tombul, Zehra, primary, Bahaj, Waled, additional, Ozturk, Merve, additional, Patel, Bhavisha, additional, Toprak, Ahmet, additional, Ibrahim, Ibrahim, additional, Chen, Weina, additional, Fuda, Franklin, additional, Ogbue, Olisaemeka D., additional, Gurnari, Carmelo, additional, Parker, Charles, additional, Young, Neal S., additional, Maciejewski, Jaroslaw P., additional, Duran, Munevver, additional, and Bat, Taha, additional

Published
2024
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42. A Central Air Conditioning Control Strategy to Enhance Thermal Comfort in Library Buildings

Author

Zheng, Minglin, Dong, Zhenyuan, Xie, Qianjia, Wu, Xinyi, Lin, Zexi, Zhang, Ziyi, Liang, Weitang, Chen, Weina, Lam, Cho Kwong Charile, Hang, Jian, Förstner, Ulrich, Series Editor, Rulkens, Wim H., Series Editor, Salomons, Wim, Series Editor, Wang, Zhaojun, editor, Zhu, Yingxin, editor, Wang, Fang, editor, Wang, Peng, editor, Shen, Chao, editor, and Liu, Jing, editor

Published
2020
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44. The novel lnc-HZ12suppresses autophagy degradation of BBC3 by preventing its interactions with HSPA8 to induce trophoblast cell apoptosis

Author

Zhao, Jingsong, Xu, Zhongyan, Xie, Jiayu, Liang, Tingting, Wang, Rong, Chen, Weina, Mi, Chenyang, Tian, Peng, Guo, Jiarong, and Zhang, Huidong

Abstract

ABSTRACTAbnormal expression of long non-coding RNAs (lncRNAs) is associated with the dysfunctions of human trophoblast cells and the occurrence of miscarriage (abnormal early embryo loss). BBC3/PUMA (BCL2 binding component 3) plays significant roles in regulation of cell apoptosis. However, whether specific lncRNAs might regulate BBC3 in trophoblast cells and further induce apoptosis and miscarriage remains completely unclear. Through screening, we identified a novel lnc-HZ12, which was significantly highly expressed in villous tissues of recurrent miscarriage (RM) patients relative to their healthy control (HC) group. Lnc-HZ12suppressed chaperone-mediated autophagy (CMA) degradation of BBC3, promoted trophoblast cell apoptosis, and was associated with miscarriage. In mechanism, lnc-HZ12downregulated the expression levels of chaperone molecules HSPA8 and LAMP2A in trophoblast cells. Meanwhile, lnc-HZ12(mainly lnc-HZ12-SO2 region in F2 fragment) and HSPA8 competitively bound with the 169RVLYNL174patch on BBC3, which prevented BBC3 from interactions with HSPA8 and impaired the formation of BBC3-HSPA8-LAMP2A complex for CMA degradation of BBC3. Thus, lnc-HZ12upregulated the BBC3-CASP9-CASP3 pathway and induced trophoblast cell apoptosis. In villous tissues, lnc-HZ12was highly expressed, CMA degradation of BBC3 was suppressed, and the apoptosis levels were higher in RM vs HC villous tissues, all of which were associated with miscarriage. Interestingly, knockdown of murine Bbc3could efficiently suppress placental apoptosis and alleviate miscarriage in a mouse miscarriage model. Taken together, our results indicated that lnc-HZ12and BBC3 played important roles in trophoblast cell apoptosis and miscarriage and might act as attractive targets for miscarriage treatment.Abbreviation: 7-AAD: 7-aminoactinomycin D; BaP: benzopyrene; BBC3/PUMA: BCL2 binding component 3; ChIP: chromatin immunoprecipitation; CHX: cycloheximide; CMA: chaperone-mediated autophagy; CQ: chloroquine; DMSO: dimethyl sulfoxide; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HC: healthy control; HSPA8: heat shock protein family A (Hsp70) member 8; IP: immunoprecipitation; LAMP2A: lysosomal associated membrane protein 2; LncRNA: long non-coding RNA; mRNA: messenger RNA; MT: mutant-type; NC: negative control; NSO: nonspecific oligonucleotide; PARP1: poly(ADP-ribose) polymerase 1; RIP: RNA immunoprecipitation; RM: recurrent miscarriage; TBP: TATA-box binding protein; WT: wild-type.

Published
2024
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47. T/myeloid mixed phenotype acute leukaemia harbouring TLX3::BCL11B with TLX3 activation.

Author

Botten, Giovanni A., Zhang, Yuannyu, Fuda, Franklin, Koduru, Prasad, Weinberg, Olga K., Slone, Tamra L., Zheng, Ruifang, Dickerson, Kathryn E., Gagan, Jeffrey R., and Chen, Weina

Subjects
ACUTE leukemia, EXTRAMEDULLARY diseases, GENE enhancers, NUCLEOTIDE sequencing, PHENOTYPES
Abstract

Summary: T/myeloid mixed phenotype acute leukaemia (MPAL) is a rare aggressive acute leukaemia with poorly understood pathogenesis. Herein, we report two cases of T/myeloid MPAL harbouring BCL11B‐associated structural variants that activate TLX3 (TLX3::BCL11B‐TLX3‐activation) by genome sequencing and transcriptomic analyses. Both patients were young males with extramedullary involvement. Cooperative gene alterations characteristic of T/myeloid MPAL and T‐lymphoblastic leukaemia (T‐ALL) were detected. Both patients achieved initial remission following lineage‐matched ALL‐based therapy with one patient requiring a lineage‐switched myeloid‐based therapy. Our study is the first to demonstrate the clinicopathological and genomic features of TLX3::BCL11B‐TLX3‐activated T/myeloid MPAL and provide insights into leukaemogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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48. Clinicopathologic features of relapsed CD19(−) B‐ALL in CD19‐targeted immunotherapy: Biological insights into relapse and LILRB1 as a novel B‐cell marker for CD19(−) B lymphoblasts.

Author

Chen, Dong, Fuda, Franklin, Rosado, Flavia, Saumell, Sílvia, John, Samuel, Chen, Mingyi, Koduru, Prasad, and Chen, Weina

Subjects
CYTOGENETICS, IMMUNOTHERAPY, TUMOR markers, DESCRIPTIVE statistics, ANTIGENS, IMMUNOLOGIC receptors, B cells, GENETIC profile, PHENOTYPES
Abstract

Introduction: The mechanism of relapsed CD19(−) B‐ALL after anti‐CD19 immunotherapy (Kymriah [CART‐19] and blinatumomab) is under active investigation. Our study aims to assess LILRB1 as a novel B‐cell marker for detecting CD19(−) B‐lymphoblasts and to analyze the clinicopathologic/genetic features of such disease to provide biological insight into relapse. Methods: Six patients (3 males/3 females, median age of 14 years) with relapsed CD19(−) B‐ALL were analyzed for cytogenetic/genetic profile and immunophenotype. Results: CD19(−) B‐ALL emerged after an interval of 5.8 months following anti‐CD19 therapy. Five of six patients had B‐cell aplasia, indicative of a persistent effect of CART or blinatumomab at relapse. Importantly, LILRB1 was variably expressed on CD19(−) and CD19(+) B lymphoblasts, strong on CD34(+) lymphoblasts and dim/partial on CD34(−) lymphoblasts. Three of six patients with paired B‐ALL samples (pre‐ and post‐anti‐CD19 therapy) carried complex and different cytogenetic abnormalities, either as completely different or sharing a subset of cytogenetic abnormalities. Conclusion: LILRB1 can be used as a novel B‐cell marker to identify CD19(−) B lymphoblasts. The emergence of CD19(−) B‐ALL appears to be associated with complex cytogenetic evolutions. The mechanism of CD19(−) B‐ALL relapse under anti‐CD19 immune pressure remains to be explored by comprehensive molecular studies. [ABSTRACT FROM AUTHOR]

Published
2024
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