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10. Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death

Author

Falke, Lucas L, He, Nannan, Chuva de Sousa Lopes, Susana M, Broekhuizen, Roel, Lyons, Karen, Nguyen, Tri Q, and Goldschmeding, Roel

Subjects
Paediatrics, Biomedical and Clinical Sciences, Pediatric, Lung, Congenital Structural Anomalies, 2.1 Biological and endogenous factors, Aetiology, Respiratory, CCN2, CTGF, FoxD1, Hypoplasia, Skeletogenesis, Biochemistry and Cell Biology, Clinical Sciences, Oncology and Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in for example kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the fatal pulmonary hypoplasia resulting from selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells developed secondary to impaired breathing movements due to aberrant axial skeletogenesis.

Published
2020

11. FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death.

Author

Falke, Lucas L, He, Nannan, Chuva de Sousa Lopes, Susana M, Broekhuizen, Roel, Lyons, Karen, Nguyen, Tri Q, and Goldschmeding, Roel

Subjects
CCN2, CTGF, FoxD1, Hypoplasia, Lung, Skeletogenesis, Biochemistry and Cell Biology, Clinical Sciences, Oncology and Carcinogenesis
Abstract

Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in e.g. kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the development of fatal pulmonary hypoplasia caused by selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells was secondary to aberrant axial skeletogenesis.

Published
2020

12. FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death

Author

Falke, Lucas L, He, Nannan, Chuva de Sousa Lopes, Susana M, Broekhuizen, Roel, Lyons, Karen, Nguyen, Tri Q, and Goldschmeding, Roel

Subjects
Paediatrics, Biomedical and Clinical Sciences, Pediatric, Lung, Congenital Structural Anomalies, Aetiology, 2.1 Biological and endogenous factors, Respiratory, CCN2, CTGF, FoxD1, Hypoplasia, Skeletogenesis, Biochemistry and Cell Biology, Clinical Sciences, Oncology and Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in e.g. kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the development of fatal pulmonary hypoplasia caused by selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells was secondary to aberrant axial skeletogenesis.

Published
2019

24. Meta-cluster Based Consensus Clustering with Local Weighting and Random Walking

Author

He, Nannan, Huang, Dong, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Cui, Zhen, editor, Pan, Jinshan, editor, Zhang, Shanshan, editor, Xiao, Liang, editor, and Yang, Jian, editor

Published
2019
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36. Tightening Test Coverage Metrics: A Case Study in Equivalence Checking Using k-Induction

Author

Donaldson, Alastair F., He, Nannan, Kroening, Daniel, Rümmer, Philipp, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, Aichernig, Bernhard K., editor, de Boer, Frank S., editor, and Bonsangue, Marcello M., editor

Published
2012
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38. Mutation-Based Test Case Generation for Simulink Models

Author

Brillout, Angelo, He, Nannan, Mazzucchi, Michele, Kroening, Daniel, Purandare, Mitra, Rümmer, Philipp, Weissenbacher, Georg, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, de Boer, Frank S., editor, Bonsangue, Marcello M., editor, Hallerstede, Stefan, editor, and Leuschel, Michael, editor

Published
2010
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40. Towards a Model Level Debugger for the Cougaar Model Driven Architecture System

Author

George, Boby, Bohner, Shawn A, He, Nannan, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Dough, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, Carbonell, Jaime G., editor, Siekmann, Jörg, editor, Hinchey, Michael G., editor, Rago, Patricia, editor, Rash, James L., editor, Rouff, Christopher A., editor, Sterritt, Roy, editor, and Truszkowski, Walt, editor

Published
2006
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41. Identification of Immune-Related Key Genes as Potential Diagnostic Biomarkers of Sepsis in Children

Author

Wang,Huabin, Huang,Junbin, Yi,Wenfang, Li,Jiahong, He,Nannan, Kang,Liangliang, He,Zhijie, Chen,Chun, Wang,Huabin, Huang,Junbin, Yi,Wenfang, Li,Jiahong, He,Nannan, Kang,Liangliang, He,Zhijie, and Chen,Chun

Abstract

Huabin Wang,1,2,* Junbin Huang,1,2,* Wenfang Yi,1,2,* Jiahong Li,3 Nannan He,4 Liangliang Kang,4 Zhijie He,5 Chun Chen1,2 1Division of Hematology/Oncology, Department of Pediatrics, the Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, People’s Republic of China; 2Department of Pediatric Intensive Care Unit, the Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, People’s Republic of China; 3Department of Neonatal Intensive Care Unit, the Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, People’s Republic of China; 4Department of Pediatric Intensive Care Unit, Shenzhen Children’s Hospital, Shenzhen, 518000, People’s Republic of China; 5Department of Intensive Care Unit, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, 510000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhijie He; Chun Chen, Email hezhijie@mail.sysu.edu.cn; chenchun69@126.comObjective: The pathogenesis of sepsis is still unclear due to its complexity, especially in children. This study aimed to analyse the immune microenvironment and regulatory networks related to sepsis in children at the molecular level and to identify key immune-related genes to provide a new basis for the early diagnosis of sepsis.Methods: The GSE145227 and GSE26440 datasets were downloaded from the Gene Expression Omnibus. The analyses included differentially expressed genes (DEGs), functional enrichment, immune cell infiltration, the competing endogenous RNA (ceRNA) interaction network, weighted gene coexpression network analysis (WGCNA), protein–protein interaction (PPI) network, key gene screening, correlation of sepsis molecular subtypes/immune infiltration with key gene expression, the diagnostic capabilities of key genes, and networks describing the interaction of key genes with transcription factors and small-molecule compounds. Finally, real-time

Published
2022

48. Data Mining for Improving Health-Care Resource Deployment

Author

He, Nannan

Subjects
Information technology
Abstract

AbstractData Mining for Improving Health-Care Resource DeploymentNannan HeWhile the health care industry accounts for a significant large portion of the GDP, the health care system in the US are still relatively inefficient. Before cutting down unnecessary health care expenses, it is important to ensure that individuals who really need medical attention should receive it. For example, if we could predict the hospitalization period (in days) for a potential patient, then we could better predict and distribute health care resources.In this research, we apply data mining methods and tools to address the problem of predicting future hospitalization periods (in days) for patients from a given set of historical patient data. The data mining techniques that we explored were linear regression, random forest and gradient boosting. For each technique, we used different historical data sets. The combination of data mining techniques and historical datasets enabled us to compare access and choose the combination which provides the best prediction of hospitalization period of a set of patients. Based on the results of our work, the random forest technique provides the best prediction of patient hospitalization.

Published
2014

49. Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020)

Author

Pathologie Groep Goldschmeding, Utrecht Valorisatie Centrum, Pathologie Weefselfaciliteit en archief, Pathologie Pathologen staf, Circulatory Health, Falke, Lucas L, He, Nannan, Chuva de Sousa Lopes, Susana M, Broekhuizen, Roel, Lyons, Karen, Nguyen, Tri Q, Goldschmeding, Roel, Pathologie Groep Goldschmeding, Utrecht Valorisatie Centrum, Pathologie Weefselfaciliteit en archief, Pathologie Pathologen staf, Circulatory Health, Falke, Lucas L, He, Nannan, Chuva de Sousa Lopes, Susana M, Broekhuizen, Roel, Lyons, Karen, Nguyen, Tri Q, and Goldschmeding, Roel

Published
2020

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