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21 results on '"Wang, Xiao-min"'

1. Expanded phenotypic spectrum of neurodevelopmental and neurodegenerative disorder Bryant-Li-Bhoj syndrome with 38 additional individuals

Author

Layo-Carris, Dana E., Lubin, Emily E., Sangree, Annabel K., Clark, Kelly J., Durham, Emily L., Gonzalez, Elizabeth M., Smith, Sarina, Angireddy, Rajesh, Wang, Xiao Min, Weiss, Erin, Toutain, Annick, Mendoza-Londono, Roberto, Dupuis, Lucie, Damseh, Nadirah, Velasco, Danita, Valenzuela, Irene, Codina-Solà, Marta, Ziats, Catherine, Have, Jaclyn, Clarkson, Katie, Steel, Dora, Kurian, Manju, Barwick, Katy, Carrasco, Diana, Dagli, Aditi I., Nowaczyk, M. J. M., Hančárová, Miroslava, Bendová, Šárka, Prchalova, Darina, Sedláček, Zdeněk, Baxová, Alica, Nowak, Catherine Bearce, Douglas, Jessica, Chung, Wendy K., Longo, Nicola, Platzer, Konrad, Klöckner, Chiara, Averdunk, Luisa, Wieczorek, Dagmar, Krey, Ilona, Zweier, Christiane, Reis, Andre, Balci, Tugce, Simon, Marleen, Kroes, Hester Y., Wiesener, Antje, Vasileiou, Georgia, Marinakis, Nikolaos M., Veltra, Danai, Sofocleous, Christalena, Kosma, Konstantina, Traeger Synodinos, Joanne, Voudris, Konstantinos A., Vuillaume, Marie-Laure, Gueguen, Paul, Derive, Nicolas, Colin, Estelle, Battault, Clarisse, Au, Billie, Delatycki, Martin, Wallis, Mathew, Gallacher, Lyndon, Majdoub, Fatma, Smal, Noor, Weckhuysen, Sarah, Schoonjans, An-Sofie, Kooy, R. Frank, Meuwissen, Marije, Cocanougher, Benjamin T., Taylor, Kathryn, Pizoli, Carolyn E., McDonald, Marie T., James, Philip, Roeder, Elizabeth R., Littlejohn, Rebecca, Borja, Nicholas A., Thorson, Willa, King, Kristine, Stoeva, Radka, Suerink, Manon, Nibbeling, Esther, Baskin, Stephanie, L. E. Guyader, Gwenaël, Kaplan, Julie, Muss, Candace, Carere, Deanna Alexis, Bhoj, Elizabeth J. K., and Bryant, Laura M.

Published
2024
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4. Correction: Expanded phenotypic spectrum of neurodevelopmental and neurodegenerative disorder Bryant-Li-Bhoj syndrome with 38 additional individuals

Author

Layo-Carris, Dana E., Lubin, Emily E., Sangree, Annabel K., Clark, Kelly J., Durham, Emily L., Gonzalez, Elizabeth M., Smith, Sarina, Angireddy, Rajesh, Wang, Xiao Min, Weiss, Erin, Toutain, Annick, Mendoza-Londono, Roberto, Dupuis, Lucie, Damseh, Nadirah, Velasco, Danita, Valenzuela, Irene, Codina-Solà, Marta, Ziats, Catherine, Have, Jaclyn, Clarkson, Katie, Steel, Dora, Kurian, Manju, Barwick, Katy, Carrasco, Diana, Dagli, Aditi I., Nowaczyk, M. J. M., Hančárová, Miroslava, Bendová, Šárka, Prchalova, Darina, Sedláček, Zdeněk, Baxová, Alica, Nowak, Catherine Bearce, Douglas, Jessica, Chung, Wendy K., Longo, Nicola, Platzer, Konrad, Klöckner, Chiara, Averdunk, Luisa, Wieczorek, Dagmar, Krey, Ilona, Zweier, Christiane, Reis, Andre, Balci, Tugce, Simon, Marleen, Kroes, Hester Y., Wiesener, Antje, Vasileiou, Georgia, Marinakis, Nikolaos M., Veltra, Danai, Sofocleous, Christalena, Kosma, Konstantina, Synodinos, Joanne Traeger, Voudris, Konstantinos A., Vuillaume, Marie-Laure, Gueguen, Paul, Derive, Nicolas, Colin, Estelle, Battault, Clarisse, Au, Billie, Delatycki, Martin, Wallis, Mathew, Gallacher, Lyndon, Majdoub, Fatma, Smal, Noor, Weckhuysen, Sarah, Schoonjans, An-Sofie, Kooy, R. Frank, Meuwissen, Marije, Cocanougher, Benjamin T., Taylor, Kathryn, Pizoli, Carolyn E., McDonald, Marie T., James, Philip, Roeder, Elizabeth R., Littlejohn, Rebecca, Borja, Nicholas A., Thorson, Willa, King, Kristine, Stoeva, Radka, Suerink, Manon, Nibbeling, Esther, Baskin, Stephanie, Guyader, Gwenaël L. E., Kaplan, Julie, Muss, Candace, Carere, Deanna Alexis, Bhoj, Elizabeth J. K., and Bryant, Laura M.

Published
2024
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13. Overexpressed KCNK1 regulates potassium channels affecting molecular mechanisms and biological pathways in bladder cancer

Author

Zhang, Wei, primary, Chen, Xiao-Song, additional, Wei, Ying, additional, Wang, Xiao-Min, additional, Chen, Xian-Jin, additional, Chi, Bang-Teng, additional, Huang, Lin-Qing, additional, He, Rong-Quan, additional, Huang, Zhi-Guang, additional, Li, Qi, additional, Chen, Gang, additional, He, Juan, additional, and Wu, Mei, additional

Published
2024
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18. Correction: Overexpressed KCNK1 regulates potassium channels affecting molecular mechanisms and biological pathways in bladder cancer.

Author

Zhang, Wei, Chen, Xiao‑Song, Wei, Ying, Wang, Xiao‑Min, Chen, Xian‑Jin, Chi, Bang‑Teng, Huang, Lin‑Qing, He, Rong‑Quan, Huang, Zhi‑Guang, Li, Qi, Chen, Gang, He, Juan, and Wu, Mei

Subjects
POTASSIUM channels, BLADDER cancer
Abstract

This document is a correction notice for an article titled "Overexpressed KCNK1 regulates potassium channels affecting molecular mechanisms and biological pathways in bladder cancer" published in the European Journal of Medical Research. The correction states that Wei Zhang and Xiao-Song Chen should have been denoted as equally contributing authors. The original article has been corrected. The publisher, Springer Nature, remains neutral with regard to jurisdictional claims and institutional affiliations. The authors of the article are Wei Zhang, Xiao-Song Chen, Ying Wei, Xiao-Min Wang, Xian-Jin Chen, Bang-Teng Chi, Lin-Qing Huang, Rong-Quan He, Zhi-Guang Huang, Qi Li, Gang Chen, Juan He, and Mei Wu. [Extracted from the article]

Published
2024
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19. WITHDRAWN: Effect of acupuncture therapy on lung cancer patients with cancer-related fatigue during chemotherapy: Study protocol for a randomized controlled trial

Author

Wang, Huan, Yu, Ming Wei, Shi, Guang Xia, Zhang, Gan Lin, Li, Qi Wei, Zhang, Chen Xi, Han, Yan, Xu, Yong Mei, Zhang, Qing, Wang, Xiao Min, and Yang, Guo Wang

Abstract

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause.

Published
2024
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20. A novel iPSC model of Bryant-Li-Bhoj neurodevelopmental syndrome demonstrates the role of histone H3.3 in neuronal differentiation and maturation.

Author

Sangree AK, Angireddy R, Bryant LM, Layo-Carris DE, Lubin EE, Wang XM, Clark KJ, Durham EE, and Bhoj EJ

Abstract

Background: Bryant-Li-Bhoj neurodevelopmental syndrome (BLBS) is neurogenetic disorder caused by variants in H3-3A and H3-3B, the two genes that encode the histone H3.3 protein. Ninety-nine percent of individuals with BLBS show developmental delay/intellectual disability, but the mechanism by which variants in H3.3 result in these phenotypes is not yet understood. As a result, only palliative interventions are available to individuals living with BLBS., Methods: Here, we investigate how one BLBS-causative variant, H3-3B p.Leu48Arg (L48R), affects neurodevelopment using an induced pluripotent stem cell (iPSC) model differentiated to 2D neural progenitor cells (NPCs), 2D forebrain neurons (FBNs), and 3D dorsal forebrain organoids (DFBOs). We employ a multi-omic approach in the 2D models to quantify the resulting changes in gene expression and chromatin accessibility. We used immunofluorescence (IF) staining to define the identities of cells in the 3D DFBOs., Results: In the 2D systems, we found dysregulation of both gene expression and chromatin accessibility of genes important for neuronal fate, maturation, and function in H3.3 L48R compared to control. Our work in 3D organoids corroborates these findings, demonstrating altered proportions of radial glia and mature neuronal cells., Conclusions: These data provide the first mechanistic insights into the pathogenesis of BLBS from a human-derived model of neurodevelopment, which suggest that the L48R increases H3-3B expression, resulting in the hyper-deposition of H3.3 into the nucleosome which underlies changes in gene expression and chromatin accessibility. Functionally, this causes dysregulation of cell adhesion, neurotransmission, and the balance between excitatory and inhibitory signaling. These results are a crucial step towards preclinical development and testing of targeted therapies for this and related disorders.

Published
2024
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21. Crystal structural effects on up/down-conversion luminescence properties of GdInO 3 :Tm,Yb perovskite phosphors for effective dual-mode anti-counterfeit applications.

Author

Wang XM, Feng K, Shan L, Zou J, and Lu B

Abstract

Developing advanced luminescent materials that are recognizable under specified conditions provides better opportunity for reliable optical anti-counterfeiting techniques. In this work, to the best of our knowledge, novel GdInO 3 :Tm,Yb perovskite phosphors with ultrafine sizes and rounded morphologies were successfully synthesized by a facile chemical precipitation route. Two-type perovskites with orthorhombic and hexagonal structures could be obtained by calcining the precursor at 850 and 1100 °C, respectively. Under 980 nm excitation, the two phosphors exhibited cyan-bluish emission at ∼460-565 nm, red emission at 645-680 nm, and near-infrared emission at 770-825 nm arising from 1 G 4  +  1 D 2 → 3 H 5,6 , 3 F 2,3 → 3 H 6 , and 3 H 4 → 3 H 6 transitions of Tm 3+ , respectively, where the hexagonal perovskite phosphor had relatively strong and sharp red emission as well as red-shifted cyan-bluish emission via successive cross relaxations. The Yb 3+ sensitizer enhanced the upconversion luminescence via effective Yb 3+ →Tm 3+ energy transfer and the optimal Yb 3+ concentrations were 10 at.% for orthorhombic perovskite and 5 at.% for hexagonal one. The upconversion mechanism mainly ascribed to two-photon processes while three-photon was also present. Upon excitation at 254 nm, their down-conversion spectra exhibited broad multibands in the wavelength range of 400-500 nm deriving from combined effects of the defect-induced emission of GdInO 3 and the 1 D 2 → 3 F 4  +  4 G 4 → 3 H 6 emissions of Tm 3+ . The energy transfer from GdInO 3 defect level to Tm 3+ excitation state was observed for the first time. The unclonable security codes prepared by screen printing from those dual-mode emitting perovskite phosphors were almost invisible under natural light, which had promising potential for anti-counterfeiting application.

Published
2024
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