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12 results on '"Zhang, Dongji"'

1. Transfer Learning for Computational Chaos System Based on Pool

Author

Lu, Ruiting, Zhang, Dongji, Cui, Yingying, Zhang, Yongping, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, 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, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Panigrahi, Bijaya Ketan, 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, Zamboni, Walter, Series Editor, Zhang, Junjie James, Series Editor, Tan, Kay Chen, Series Editor, S. Shmaliy, Yuriy, editor, and Nayyar, Anand, editor

Published
2023
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3. Subpallial Enhancer Transgenic Lines: a Data and Tool Resource to Study Transcriptional Regulation of GABAergic Cell Fate

Author

Silberberg, Shanni N, Taher, Leila, Lindtner, Susan, Sandberg, Magnus, Nord, Alex S, Vogt, Daniel, Mckinsey, Gabriel L, Hoch, Renee, Pattabiraman, Kartik, Zhang, Dongji, Ferran, Jose L, Rajkovic, Aleksandar, Golonzhka, Olga, Kim, Carol, Zeng, Hongkui, Puelles, Luis, Visel, Axel, and Rubenstein, John LR

Subjects
Biomedical and Clinical Sciences, Neurosciences, Genetics, 1.1 Normal biological development and functioning, Neurological, Generic health relevance, Animals, Basal Ganglia, Cell Differentiation, Enhancer Elements, Genetic, GABAergic Neurons, Gene Expression Regulation, Developmental, Homeodomain Proteins, LIM-Homeodomain Proteins, Mice, Mice, Transgenic, Nerve Tissue Proteins, Transcription Factors, Psychology, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Elucidating the transcriptional circuitry controlling forebrain development requires an understanding of enhancer activity and regulation. We generated stable transgenic mouse lines that express CreERT2 and GFP from ten different enhancer elements with activity in distinct domains within the embryonic basal ganglia. We used these unique tools to generate a comprehensive regional fate map of the mouse subpallium, including sources for specific subtypes of amygdala neurons. We then focused on deciphering transcriptional mechanisms that control enhancer activity. Using machine-learning computations, in vivo chromosomal occupancy of 13 transcription factors that regulate subpallial patterning and differentiation and analysis of enhancer activity in Dlx1/2 and Lhx6 mutants, we elucidated novel molecular mechanisms that regulate region-specific enhancer activity in the developing brain. Thus, these subpallial enhancer transgenic lines are data and tool resources to study transcriptional regulation of GABAergic cell fate.

Published
2016

4. Transcriptional Regulation of Enhancers Active in Protodomains of the Developing Cerebral Cortex

Author

Pattabiraman, Kartik, Golonzhka, Olga, Lindtner, Susan, Nord, Alex S, Taher, Leila, Hoch, Renee, Silberberg, Shanni N, Zhang, Dongji, Chen, Bin, Zeng, HongKui, Pennacchio, Len A, Puelles, Luis, Visel, Axel, and Rubenstein, John LR

Subjects
Biomedical and Clinical Sciences, Neurosciences, Genetics, 1.1 Normal biological development and functioning, Animals, Binding Sites, COUP Transcription Factor I, Cerebral Cortex, Enhancer Elements, Genetic, Eye Proteins, Gene Expression Regulation, Developmental, Hippocampus, Homeodomain Proteins, Humans, Mice, Mice, Transgenic, PAX6 Transcription Factor, Paired Box Transcription Factors, Pre-B-Cell Leukemia Transcription Factor 1, Repressor Proteins, Transcription Factors, Transcription, Genetic, COUP Transcription Factor I/metabolism, Cerebral Cortex/*embryology/*metabolism, *Enhancer Elements, Genetic, Eye Proteins/metabolism, *Gene Expression Regulation, Developmental, Hippocampus/embryology/metabolism, Homeodomain Proteins/metabolism, Paired Box Transcription Factors/metabolism, Repressor Proteins/metabolism, Transcription Factors/metabolism, *Transcription, Genetic, Psychology, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Elucidating the genetic control of cerebral cortical (pallial) development is essential for understanding function, evolution, and disorders of the brain. Transcription factors (TFs) that embryonically regulate pallial regionalization are expressed in gradients, raising the question of how discrete domains are generated. We provide evidence that small enhancer elements active in protodomains integrate broad transcriptional information. CreER(T2) and GFP expression from 14 different enhancer elements in stable transgenic mice allowed us to define a comprehensive regional fate map of the pallium. We explored transcriptional mechanisms that control the activity of the enhancers using informatics, in vivo occupancy by TFs that regulate cortical patterning (CoupTFI, Pax6, and Pbx1), and analysis of enhancer activity in Pax6 mutants. Overall, the results provide insights into how broadly expressed patterning TFs regulate the activity of small enhancer elements that drive gene expression in pallial protodomains that fate map to distinct cortical regions.

Published
2014

5. Neutrophil histamine contributes to inflammation in mycoplasma pneumonia

Author

Xu, Xiang, Zhang, Dongji, Zhang, Hong, Wolters, Paul J, Killeen, Nigel P, Sullivan, Brandon M, Locksley, Richard M, Lowell, Clifford A, and Caughey, George H

Subjects
Biomedical and Clinical Sciences, Health Sciences, Pneumonia, Pneumonia & Influenza, Lung, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Animals, Antibodies, Monoclonal, Basophils, Bronchitis, Bronchoalveolar Lavage Fluid, Cell Count, Goblet Cells, Histamine, Histamine H1 Antagonists, Histidine Decarboxylase, Inflammation, Mast Cells, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mycoplasma pulmonis, Neutropenia, Neutrophils, Organ Size, Pneumonia, Mycoplasma, Proto-Oncogene Proteins c-kit, RNA, Messenger, Receptors, Chemokine, Time Factors, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Mycoplasmas cause chronic inflammation and are implicated in asthma. Mast cells defend against mycoplasma infection and worsen allergic inflammation, which is mediated partly by histamine. To address the hypothesis that mycoplasma provokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type and mast cell-deficient KitW-sh/KitW-sh (W-sh) mice. Low histamine levels in uninfected W-sh mice confirmed the conventional wisdom that mast cells are principal sources of airway and serum histamine. Although mycoplasma did not release histamine acutely in wild-type airways, levels rose up to 50-fold above baseline 1 week after infection in mice heavily burdened with neutrophils. Surprisingly, histamine levels also rose profoundly in infected W-sh lungs, increasing in parallel with neutrophils and declining with neutrophil depletion. Furthermore, neutrophils from infected airway were highly enriched in histamine compared with naive neutrophils. In vitro, mycoplasma directly stimulated histamine production by naive neutrophils and strongly upregulated mRNA encoding histidine decarboxylase, the rate-limiting enzyme in histamine synthesis. In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung weight and severity of pneumonia and tracheobronchitis in infected W-sh mice. These findings suggest that neutrophils, provoked by mycoplasma, greatly expand their capacity to synthesize histamine, thereby contributing to lung and airway inflammation.

Published
2006

11. Chlamydia trachomatisMouse Pneumonitis Lung Infection in IL-18 and IL-12 Knockout Mice: IL-12 Is Dominant over IL-18 for Protective Immunity

Author

Lu, Hang, Yang, Xi, Takeda, Kiyoshi, Zhang, Dongji, Fan, Yijun, Luo, Ma, Shen, Caixia, Wang, Shuhe, Akira, Shizuo, and Brunham, Robert C.

Abstract

Background: Interferon (IFN)-γis a key to protective immunity against a variety of intracellular bacterial infections, including Chlamydia trachomatis.Interleukin (IL)-18, a recently identified Th1 cytokine, together with IL-12 is a strong stimulator for IFN-γproduction. We investigated the relative roles of IL-18 and IL-12 in protective immunity to C. trachomatismouse pneumonitis (MoPn) infection using gene knockout (KO) and wild-type (WT) mice. Materials and Methods: Mice were intranasally infected with C. trachomatisMoPn and protective immunity was assessed among groups of mice by daily body weight changes, lung growth of MoPn, and histopathological appearances at day 10 postinfection. The corresponding immune responses for each group of mice at the same postinfection time point were evaluated by measuring antigen-specific antibody isotype responses and cytokine profiles. Results: Our results showed that IL-18 deficiency had little or no influence on clearance of MoPn from the lung, although KO mice exhibited slightly more severe inflammatory reactions in lung tissues, as well as reduced systemic and local IFN-γproduction, compared with WT mice. Results with IL-18 KO mice were in sharp contrast to those observed with IL-12 KO mice that showed substantially reduced clearance of MoPn from the lungs, substantial reductions of antigen-specific systemic and lung IFN-γproduction, decreased ratio of MoPn-specific immunoglobulin G (IgG)2a/IgG1, and severe pathological changes in the lung with extensive polymorphonuclear, instead of mononuclear, cell infiltration. Exogenous IL-12 or IL-18 was able to increase IFN-γproduction in IL-18 KO mice; whereas, only exogenous IL-12, but not IL-18, enhanced IFN-γproduction in IL-12 KO mice. Caspase-1 is the key protease for activation of IL-18 precursor into the bioactive form, and caspase-1 KO mice also displayed similar bacterial clearance and body weight loss to that in WT mice at early stages of MoPn infection. This further confirmed that IL-18 was not essential for host defense against chlamydia infection. Conclusions: These results suggest that IL-12, rather than IL-18, plays the dominant role in the development of protective immunity against chlamydia lung infection, although both cytokines are involved in the in vivo regulation of IFN-γproduction.

Published
2000
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12. Immunity to Chlamydia trachomatisMouse Pneumonitis Induced by Vaccination with Live Organisms Correlates with Early Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-12 Production and with Dendritic Cell-Like Maturation

Author

Zhang, Dongji, Yang, Xi, Lu, Hang, Zhong, Guangming, and Brunham, Robert C.

Abstract

ABSTRACTAs is true for other intracellular pathogens, immunization with live Chlamydia trachomatisgenerally induces stronger protective immunity than does immunization with inactivated organism. To investigate the basis for such a difference, we studied immune responses in BALB/c mice immunized with viable or UV-killed C. trachomatismouse pneumonitis (MoPn). Strong, acquired resistance to C. trachomatisinfection was elicited by immunization with viable but not dead organisms. Immunization with viable organisms induced high levels of antigen-specific delayed-type hypersensitivity (DTH), gamma interferon production, and immunoglobulin A (IgA) responses. Immunization with inactivated MoPn mainly induced interleukin-10 (IL-10) production and IgG1 antibody without IgA or DTH responses. Analysis of local early cytokine and cellular events at days 3, 5, and 7 after peritoneal cavity immunization showed that high levels of granulocyte-macrophage colony-stimulating factor and IL-12 were detected with viable but not inactivated organisms. Furthermore, enrichment of a dendritic cell (DC)-like population was detected in the peritoneal cavity only among mice immunized with viable organisms. The results suggest that early differences in inducing proinflammatory cytokines and activation and differentiation of DCs may be the key mechanism underlying the difference between viable and inactivated organisms in inducing active immunity to C. trachomatisinfection.

Published
1999
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