Database : MEDLINE
Search on : Neuronal and Migration and Disorders [Words]
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[PMID]: 29447953
[Au] Autor:Sokolov AM; Seluzicki CM; Morton MC; Feliciano DM
[Ad] Address:Department of Biological Sciences, Clemson University, Clemson, SC 29634-0314, USA. Electronic address: amsokol@clemson.edu.
[Ti] Title:Dendrite growth and the effect of ectopic Rheb expression on cortical neurons.
[So] Source:Neurosci Lett;671:140-147, 2018 Feb 12.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Ras homology enriched in brain (Rheb) is a GTPase that activates the protein kinase mammalian Target of Rapamycin (mTOR). Rheb mutations cause intellectual delay and megalencephaly. mTOR hyperactivation causes a constellation of neurodevelopmental disorders called "mTOR-opathies" that are frequently accompanied by hyperexcitable cortical malformations. Cortical malformations within the anterior cingulate cortex (ACC) and somatosensory cortex (SSC) frequently colocalize with hyperexcitability. Although Rheb and mTOR are implicated in the formation of cortical lesions, seizure activity, and defects in neuronal migration, the contribution of Rheb to changes in neuron size and dendrite morphology is not well established. Here, in utero electroporation of the developing embryonic brain was used to assess soma and dendrite growth in ACC and SCC layer II/III neurons. We found that between P0 and P21, neuronal soma size increased by 50 and 122 percent in the ACC and SSC, respectively. The increased size was accompanied by an increase in the number of basal dendrites and enhanced dendrite complexity. As an indicator of the involvement of the mTOR pathway in neuron maturation, phosphorylation of the mammalian target of rapamycin (mTOR) substrate S6 was identified in migrating cortical neuroblasts and maturing neurons. Notably, ectopic expression of Rheb caused cortical malformations comprised of ectopically positioned cytomegalic neurons with dendrite hypertrophy. This study provides a direct comparison of neuron maturation across two cortical regions during development, provides evidence for mTOR pathway activity during neuron maturation, and demonstrates that ectopic Rheb expression without mutation is sufficient to induce cortical malformations with cytomegaly and dendrite hypertrophy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher

  2 / 2193 MEDLINE  
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[PMID]: 28453628
[Au] Autor:Svetoni F; De Paola E; La Rosa P; Mercatelli N; Caporossi D; Sette C; Paronetto MP
[Ad] Address:Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", 00135 Rome, Italy.
[Ti] Title:Post-transcriptional regulation of FUS and EWS protein expression by miR-141 during neural differentiation.
[So] Source:Hum Mol Genet;26(14):2732-2746, 2017 07 15.
[Is] ISSN:1460-2083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Brain development involves proliferation, migration and specification of neural progenitor cells, culminating in neuronal circuit formation. Mounting evidence indicates that improper regulation of RNA binding proteins (RBPs), including members of the FET (FUS, EWS, TAF15) family, results in defective cortical development and/or neurodegenerative disorders. However, in spite of their physiological relevance, the precise pattern of FET protein expression in developing neurons is largely unknown. Herein, we found that FUS, EWS and TAF15 expression is differentially regulated during brain development, both in time and in space. In particular, our study identifies a fine-tuned regulation of FUS and EWS during neuronal differentiation, whereas TAF15 appears to be more constitutively expressed. Mechanistically FUS and EWS protein expression is regulated at the post-transcriptional level during neuron differentiation and brain development. Moreover, we identified miR-141 as a key regulator of these FET proteins that modulate their expression levels in differentiating neuronal cells. Thus, our studies uncover a novel link between post-transcriptional regulation of FET proteins expression and neurogenesis.
[Mh] MeSH terms primary: MicroRNAs/metabolism
Neurons/physiology
RNA Processing, Post-Transcriptional
RNA-Binding Protein EWS/biosynthesis
RNA-Binding Protein FUS/biosynthesis
[Mh] MeSH terms secundary: Animals
Brain/cytology
Brain/embryology
Brain/metabolism
Cell Differentiation/physiology
Humans
Mice
Mice, Inbred C57BL
MicroRNAs/genetics
Neurogenesis/physiology
Neurons/cytology
Neurons/metabolism
Protein Processing, Post-Translational
RNA-Binding Protein EWS/genetics
RNA-Binding Protein EWS/metabolism
RNA-Binding Protein FUS/genetics
RNA-Binding Protein FUS/metabolism
RNA-Binding Proteins/metabolism
TATA-Binding Protein Associated Factors/biosynthesis
TATA-Binding Protein Associated Factors/genetics
TATA-Binding Protein Associated Factors/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (EWSR1 protein, human); 0 (FUS protein, human); 0 (FUS protein, mouse); 0 (MIRN141 microRNA, human); 0 (MicroRNAs); 0 (Mirn141 microRNA, mouse); 0 (RNA-Binding Protein EWS); 0 (RNA-Binding Protein FUS); 0 (RNA-Binding Proteins); 0 (TAF15 protein, human); 0 (TAF15 protein, mouse); 0 (TATA-Binding Protein Associated Factors)
[Em] Entry month:1801
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx160

  3 / 2193 MEDLINE  
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[PMID]: 29274387
[Au] Autor:Chen Z
[Ad] Address:Department of MCD Biology, University of Colorado Boulder, Boulder, CO 80309, USA. Electronic address: zhe.chen@colorado.edu.
[Ti] Title:Common cues wire the spinal cord: Axon guidance molecules in spinal neuron migration.
[So] Source:Semin Cell Dev Biol;, 2018 Feb 20.
[Is] ISSN:1096-3634
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Topographic arrangement of neuronal cell bodies and axonal tracts are crucial for proper wiring of the nervous system. This involves often-coordinated neuronal migration and axon guidance during development. Most neurons migrate from their birthplace to specific topographic coordinates as they adopt the final cell fates and extend axons. The axons follow temporospatial specific guidance cues to reach the appropriate targets. When neuronal or axonal migration or their coordination is disrupted, severe consequences including neurodevelopmental disorders and neurological diseases, can arise. Neuronal and axonal migration shares some molecular mechanisms, as genes originally identified as axon guidance molecules have been increasingly shown to direct both navigation processes. This review focuses on axon guidance pathways that are shown to also direct neuronal migration in the vertebrate spinal cord.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:Publisher

  4 / 2193 MEDLINE  
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[PMID]: 29386386
[Au] Autor:Pierce SB; Stewart MD; Gulsuner S; Walsh T; Dhall A; McClellan JM; Klevit RE; King MC
[Ad] Address:Department of Medicine, University of Washington, Seattle, WA 98195.
[Ti] Title:De novo mutation in with epigenetic effects on neurodevelopment.
[So] Source:Proc Natl Acad Sci U S A;115(7):1558-1563, 2018 Feb 13.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RING1 is an E3-ubiquitin ligase that is involved in epigenetic control of transcription during development. It is a component of the polycomb repressive complex 1, and its role in that complex is to ubiquitylate histone H2A. In a 13-year-old girl with syndromic neurodevelopmental disabilities, we identified a de novo mutation, RING1 p.R95Q, which alters a conserved arginine residue in the catalytic RING domain. In vitro assays demonstrated that the mutant RING1 retains capacity to catalyze ubiquitin chain formation, but is defective in its ability to ubiquitylate histone H2A in nucleosomes. Consistent with this in vitro effect, cells of the patient showed decreased monoubiquitylation of histone H2A. We modeled the mutant RING1 in by editing the comparable amino acid change into , the suggested ortholog. Animals with either the missense mutation or complete knockout of were defective in monoubiquitylation of histone H2A and had defects in neuronal migration and axon guidance. Relevant to our patient, animals heterozygous for either the missense or knockout allele also showed neuronal defects. Our results support three conclusions: mutation of is the likely cause of a human neurodevelopmental syndrome, mutation of can disrupt histone H2A ubiquitylation without disrupting RING1 catalytic activity, and the comparable mutation in both recapitulates the effects on histone H2A ubiquitylation and leads to neurodevelopmental abnormalities. This role for adds to our understanding of the importance of aberrant epigenetic effects as causes of human neurodevelopmental disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1721290115

  5 / 2193 MEDLINE  
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[PMID]: 29305907
[Au] Autor:Lins MP; Silva ECO; Silva GR; Souza ST; Medeiros NC; Fonseca EJS; Smaniotto S
[Ad] Address:Laboratório de Biologia Celular, Instituto de Ciências Biológicas e da Saúde, Universidade Federal de Alagoas, 57072-970 Maceió, Alagoas, Brazil.
[Ti] Title:Association between biomechanical alterations and migratory ability of semaphorin-3A-treated thymocytes.
[So] Source:Biochim Biophys Acta;1862(4):816-824, 2018 Apr.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Class 3 semaphorins are soluble proteins involved in cell adhesion and migration. Semaphorin-3A (Sema3A) was initially shown to be involved in neuronal guidance, and it has also been reported to be associated with immune disorders. Both Sema3A and its receptors are expressed by most immune cells, including monocytes, macrophages, and lymphocytes, and these proteins regulate cell function. Here, we studied the correlation between Sema3A-induced changes in biophysical parameters of thymocytes, and the subsequent repercussions on cell function. METHODS: Thymocytes from mice were treated in vitro with Sema3A for 30min. Scanning electron microscopy was performed to assess cell morphology. Atomic force microscopy was performed to further evaluate cell morphology, membrane roughness, and elasticity. Flow cytometry and/or fluorescence microscopy were performed to assess the F-actin cytoskeleton and ROCK2. Cell adhesion to a bovine serum albumin substrate and transwell migration assays were used to assess cell migration. RESULTS: Sema3A induced filopodia formation in thymocytes, increased membrane stiffness and roughness, and caused a cortical distribution of the cytoskeleton without changes in F-actin levels. Sema3A-treated thymocytes showed reduced substrate adhesion and migratory ability, without changes in cell viability. In addition, Sema3A was able to down-regulate ROCK2. CONCLUSIONS: Sema3A promotes cytoskeletal rearrangement, leading to membrane modifications, including increased stiffness and roughness. This effect in turn affects the adhesion and migration of thymocytes, possibly due to a reduction in ROCK2 expression. GENERAL SIGNIFICANCE: Sema3A treatment impairs thymocyte migration due to biomechanical alterations in cell membranes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180219
[Lr] Last revision date:180219
[St] Status:In-Data-Review

  6 / 2193 MEDLINE  
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Barraviera, Benedito
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[PMID]: 28450050
[Au] Autor:Araújo MR; Kyrylenko S; Spejo AB; Castro MV; Ferreira Junior RS; Barraviera B; Oliveira ALR
[Ad] Address:Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Sao Paulo, Brazil.
[Ti] Title:Transgenic human embryonic stem cells overexpressing FGF2 stimulate neuroprotection following spinal cord ventral root avulsion.
[So] Source:Exp Neurol;294:45-57, 2017 08.
[Is] ISSN:1090-2430
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ventral root avulsion (VRA) triggers a strong glial reaction which contributes to neuronal loss, as well as to synaptic detachment. To overcome the degenerative effects of VRA, treatments with neurotrophic factors and stem cells have been proposed. Thus, we investigated neuroprotection elicited by human embryonic stem cells (hESC), modified to overexpress a human fibroblast growth factor 2 (FGF-2), on motoneurons subjected to VRA. Lewis rats were submitted to VRA (L4-L6) and hESC/FGF-2 were applied to the injury site using a fibrin scaffold. The spinal cords were processed to evaluate neuronal survival, synaptic stability, and glial reactivity two weeks post lesion. Then, qRT-PCR was used to assess gene expression of ß2-microglobulin (ß2m), TNFα, IL1ß, IL6 and IL10 in the spinal cord in vivo and FGF2 mRNA levels in hESC in vitro. The results indicate that hESC overexpressing FGF2 significantly rescued avulsed motoneurons, preserving synaptic covering and reducing astroglial reactivity. The cells were also shown to express BDNF and GDNF at the site of injury. Additionally, engraftment of hESC led to a significant reduction in mRNA levels of TNFα at the spinal cord ventral horn, indicating their immunomodulatory properties. Overall, the present data suggest that hESC overexpressing FGF2 are neuroprotective and can shift gene expression towards an anti-inflammatory environment.
[Mh] MeSH terms primary: Human Embryonic Stem Cells/transplantation
Radiculopathy/surgery
Spinal Nerve Roots/pathology
[Mh] MeSH terms secundary: Animals
Cell Movement
Cell Survival/drug effects
Cell Survival/genetics
Disease Models, Animal
Doxycycline/therapeutic use
Female
Fibrin Tissue Adhesive/toxicity
Fibroblast Growth Factor 2/genetics
Fibroblast Growth Factor 2/metabolism
Gene Expression Regulation/drug effects
Gene Expression Regulation/genetics
Genetic Vectors/physiology
Human Embryonic Stem Cells/metabolism
Humans
Motor Neurons/metabolism
Motor Neurons/pathology
Nerve Tissue Proteins/metabolism
Neuroglia/drug effects
Neuroglia/metabolism
Radiculopathy/chemically induced
Rats
Rats, Inbred Lew
Tissue Adhesives/toxicity
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Fibrin Tissue Adhesive); 0 (Nerve Tissue Proteins); 0 (Tissue Adhesives); 103107-01-3 (Fibroblast Growth Factor 2); N12000U13O (Doxycycline)
[Em] Entry month:1708
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE

  7 / 2193 MEDLINE  
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[PMID]: 29196536
[Au] Autor:Fontenot MR; Berto S; Liu Y; Werthmann G; Douglas C; Usui N; Gleason K; Tamminga CA; Takahashi JS; Konopka G
[Ad] Address:Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
[Ti] Title:Novel transcriptional networks regulated by CLOCK in human neurons.
[So] Source:Genes Dev;31(21):2121-2135, 2017 11 01.
[Is] ISSN:1549-5477
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The molecular mechanisms underlying human brain evolution are not fully understood; however, previous work suggested that expression of the transcription factor in the human cortex might be relevant to human cognition and disease. In this study, we investigated this novel transcriptional role for CLOCK in human neurons by performing chromatin immunoprecipitation sequencing for endogenous CLOCK in adult neocortices and RNA sequencing following CLOCK knockdown in differentiated human neurons in vitro. These data suggested that CLOCK regulates the expression of genes involved in neuronal migration, and a functional assay showed that CLOCK knockdown increased neuronal migratory distance. Furthermore, dysregulation of CLOCK disrupts coexpressed networks of genes implicated in neuropsychiatric disorders, and the expression of these networks is driven by hub genes with human-specific patterns of expression. These data support a role for CLOCK-regulated transcriptional cascades involved in human brain evolution and function.
[Mh] MeSH terms primary: CLOCK Proteins/genetics
CLOCK Proteins/metabolism
Gene Expression Regulation, Developmental/genetics
Gene Regulatory Networks/genetics
Neurons/physiology
[Mh] MeSH terms secundary: Cell Line
Cell Movement/genetics
Epigenesis, Genetic/genetics
Gene Knockdown Techniques
Humans
Neocortex/metabolism
Neurodevelopmental Disorders/genetics
Neurons/cytology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:EC 2.3.1.48 (CLOCK Proteins)
[Em] Entry month:1712
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[Js] Journal subset:IM
[Da] Date of entry for processing:171203
[St] Status:MEDLINE
[do] DOI:10.1101/gad.305813.117

  8 / 2193 MEDLINE  
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[PMID]: 29393650
[Au] Autor:Yun S; Shin TH; Lee JH; Cho MH; Kim IS; Kim JW; Jung K; Lee IS; Cheon J; Park KI
[Ad] Address:Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine , Seoul 03722, Korea.
[Ti] Title:Design of Magnetically Labeled Cells (Mag-Cells) for in Vivo Control of Stem Cell Migration and Differentiation.
[So] Source:Nano Lett;18(2):838-845, 2018 Feb 14.
[Is] ISSN:1530-6992
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cell-based therapies are attractive for treating various degenerative disorders and cancer but delivering functional cells to the region of interest in vivo remains difficult. The problem is exacerbated in dense biological matrices such as solid tissues because these environments impose significant steric hindrances for cell movement. Here, we show that neural stem cells transfected with zinc-doped ferrite magnetic nanoparticles (ZnMNPs) can be pulled by an external magnet to migrate to the desired location in the brain. These magnetically labeled cells (Mag-Cells) can migrate because ZnMNPs generate sufficiently strong mechanical forces to overcome steric hindrances in the brain tissues. Once at the site of lesion, Mag-Cells show enhanced neuronal differentiation and greater secretion of neurotrophic factors than unlabeled control stem cells. Our study shows that ZnMNPs activate zinc-mediated Wnt signaling to facilitate neuronal differentiation. When implemented in a rodent brain stroke model, Mag-Cells led to significant recovery of locomotor performance in the impaired limbs of the animals. Our findings provide a simple magnetic method for controlling migration of stem cells with high therapeutic functions, offering a valuable tool for other cell-based therapies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:In-Data-Review
[do] DOI:10.1021/acs.nanolett.7b04089

  9 / 2193 MEDLINE  
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[PMID]: 29437173
[Au] Autor:Wang Y; Wang L; Zhu Y; Qin J
[Ad] Address:Division of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Dalian 116023, China. jhqin@dicp.ac.cn and University of Chinese Academy of Sciences, Beijing 100049, China and Key Laboratory of Separation Sciences for Analytical Chemistry, Dalian Ins
[Ti] Title:Human brain organoid-on-a-chip to model prenatal nicotine exposure.
[So] Source:Lab Chip;, 2018 Feb 13.
[Is] ISSN:1473-0189
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Nicotine has been recognized to trigger various neuronal disabilities in the fetal brain and long-lasting behavioral deficits in offspring. However, further understanding of fetal brain development under nicotine exposure is challenging due to the limitations of existing animal models. Here, we create a new brain organoid-on-a-chip system derived from human induced pluripotent stem cells (hiPSCs) that allows us to model neurodevelopmental disorders under prenatal nicotine exposure (PNE) at early stages. The brain organoid-on-a-chip system facilitates 3D culture, in situ neural differentiation, and self-organization of brain organoids under continuous perfused cultures in a controlled manner. The generated brain organoids displayed well-defined neural differentiation, regionalization, and cortical organization, which recapitulates the key features of the early stages of human brain development. The brain organoids exposed to nicotine exhibited premature neuronal differentiation with enhanced expression of the neuron marker TUJ1. Brain regionalization and cortical development were disrupted in the nicotine-treated organoids identified by the expressions of forebrain (PAX6 and FOXG1), hindbrain (PAX2 and KROX20) and cortical neural layer (preplate TBR1 and deep-layer CTIP2) markers. Moreover, the neurite outgrowth showed abnormal neuronal differentiation and migration in nicotine-treated brain organoids. These results suggest that nicotine exposure elicits impaired neurogenesis in early fetal brain development during gestation. The established brain organoid-on-a-chip system provides a promising platform to model neurodevelopmental disorders under environmental exposure, which can be extended for applications in brain disease studies and drug testing.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[St] Status:Publisher
[do] DOI:10.1039/c7lc01084b

  10 / 2193 MEDLINE  
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[PMID]: 29407440
[Au] Autor:Noda M
[Ad] Address:Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan. Electronic address: noda@phar.kyushu-u.ac.jp.
[Ti] Title:Thyroid Hormone in the CNS: Contribution of Neuron-Glia Interaction.
[So] Source:Vitam Horm;106:313-331, 2018.
[Is] ISSN:0083-6729
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The endocrine system and the central nervous system (CNS) are intimately linked. Among hormones closely related to the nervous system, thyroid hormones (THs) are critical for the regulation of development and differentiation of neurons and neuroglia and hence for development and function of the CNS. T3 (3,3',5-triiodothyronine), an active form of TH, is important not only for neuronal development but also for differentiation of astrocytes and oligodendrocytes, and for microglial development. In adult brain, T3 affects glial morphology with sex- and age-dependent manner and therefore may affect their function, leading to influence on neuron-glia interaction. T3 is an important signaling factor that affects microglial functions such as migration and phagocytosis via complex mechanisms. Therefore, dysfunction of THs may impair glial function as well as neuronal function and thus disturb the brain, which may cause mental disorders. Investigations on molecular and cellular basis of hyperthyroidism and hypothyroidism will help us to understand changes in neuron-glia interaction and therefore consequent psychiatric symptoms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:In-Data-Review


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