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  1. Artikel ; Online: The landscape of SETBP1 gene expression and transcription factor activity across human tissues.

    Whitlock, Jordan H / Wilk, Elizabeth J / Howton, Timothy C / Clark, Amanda D / Lasseigne, Brittany N

    PloS one

    2024  Band 19, Heft 1, Seite(n) e0296328

    Abstract: The SET binding protein 1 (SETBP1) gene encodes a transcription factor (TF) involved in various cellular processes. Variants in SETBP1 can result in three different diseases determined by the introduction (germline vs. somatic) and location of the ... ...

    Abstract The SET binding protein 1 (SETBP1) gene encodes a transcription factor (TF) involved in various cellular processes. Variants in SETBP1 can result in three different diseases determined by the introduction (germline vs. somatic) and location of the variant. Germline variants cause the ultra-rare pediatric Schinzel Giedion Syndrome (SGS) and SETBP1 haploinsufficiency disorder (SETBP1-HD), characterized by severe multisystemic abnormalities with neurodegeneration or a less severe brain phenotype accompanied by hypotonia and strabismus, respectively. Somatic variants in SETBP1 are associated with hematological malignancies and cancer development in other tissues in adults. To better understand the tissue-specific mechanisms involving SETBP1, we analyzed publicly available RNA-sequencing (RNA-seq) data from the Genotype-Tissue Expression (GTEx) project. We found SETBP1 and its known target genes were widely expressed across 31 adult human tissues. K-means clustering identified three distinct expression patterns of SETBP1 targets across tissues. Functional enrichment analysis (FEA) of each cluster revealed gene sets related to transcriptional regulation, DNA binding, and mitochondrial function. TF activity analysis of SETBP1 and its target TFs revealed tissue-specific TF activity, underscoring the role of tissue context-driven regulation and suggesting its impact in SETBP1-associated disease. In addition to uncovering tissue-specific molecular signatures of SETBP1 expression and TF activity, we provide a Shiny web application to facilitate exploring TF activity across human tissues for 758 TFs. This study provides insight into the landscape of SETBP1 expression and TF activity across 31 non-diseased human tissues and reveals tissue-specific expression and activity of SETBP1 and its targets. In conjunction with the web application we constructed, our framework enables researchers to generate hypotheses related to the role tissue backgrounds play with respect to gene expression and TF activity in different disease contexts.
    Mesh-Begriff(e) Humans ; Abnormalities, Multiple/genetics ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Craniofacial Abnormalities/genetics ; Gene Expression ; Intellectual Disability/genetics ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemische Substanzen Carrier Proteins ; Nuclear Proteins ; SETBP1 protein, human ; Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2024-01-02
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0296328
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq.

    Soelter, Tabea M / Howton, Timothy C / Clark, Amanda D / Oza, Vishal H / Lasseigne, Brittany N

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Background: Alzheimer's disease is the most common cause of dementia and is characterized by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss. Although neuronal loss is a primary hallmark of Alzheimer's disease, it is known that non- ... ...

    Abstract Background: Alzheimer's disease is the most common cause of dementia and is characterized by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss. Although neuronal loss is a primary hallmark of Alzheimer's disease, it is known that non-neuronal cell populations are ultimately responsible for maintaining brain homeostasis and neuronal health through neuron-glia and glial cell crosstalk. Many signaling pathways have been proposed to be dysregulated in Alzheimer's disease, including WNT, TGFβ, p53, mTOR, NFkB, and Pi3k/Akt signaling. Here, we predict altered cell-cell communication between glia and neurons.
    Methods: Using public snRNA-sequencing data generated from postmortem human prefrontal cortex, we predicted altered cell-cell communication between glia (astrocytes, microglia, oligodendrocytes, and oligodendrocyte progenitor cells) and neurons (excitatory and inhibitory). We confirmed interactions in a second and third independent orthogonal dataset. We determined cell-type-specificity using Jaccard Similarity Index and investigated the downstream effects of altered interactions in inhibitory neurons through gene expression and transcription factor activity analyses of signaling mediators. Finally, we determined changes in pathway activity in inhibitory neurons.
    Results: Cell-cell communication between glia and neurons is altered in Alzheimer's disease in a cell-type-specific manner. As expected, ligands are more cell-type-specific than receptors and targets. We identified ligand-receptor pairs in three independent datasets and found involvement of the Alzheimer's disease risk genes
    Conclusions: Cell-cell communication between glia and neurons in Alzheimer's disease is altered in a cell-type-specific manner involving Alzheimer's disease risk genes. Signaling mediators had altered transcription factor activity suggesting altered glia-neuron interactions may dysregulate signaling pathways including WNT, p53, and NFkB in inhibitory neurons.
    Sprache Englisch
    Erscheinungsdatum 2024-05-10
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.11.29.569304
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Long-read RNA sequencing identifies region- and sex-specific C57BL/6J mouse brain mRNA isoform expression and usage.

    Jones, Emma F / Howton, Timothy C / Flanary, Victoria L / Clark, Amanda D / Lasseigne, Brittany N

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Alternative splicing (AS) contributes to the biological heterogeneity between species, sexes, tissues, and cell types. Many diseases are either caused by alterations in AS or by alterations to AS. Therefore, measuring AS accurately and efficiently is ... ...

    Abstract Alternative splicing (AS) contributes to the biological heterogeneity between species, sexes, tissues, and cell types. Many diseases are either caused by alterations in AS or by alterations to AS. Therefore, measuring AS accurately and efficiently is critical for assessing molecular phenotypes, including those associated with disease. Long-read sequencing enables more accurate quantification of differentially spliced isoform expression than short-read sequencing approaches, and third-generation platforms facilitate high-throughput experiments. To assess differences in AS across the cerebellum, cortex, hippocampus, and striatum by sex, we generated and analyzed Oxford Nanopore Technologies (ONT) long-read RNA sequencing (lrRNA-Seq) C57BL/6J mouse brain cDNA libraries. From >85 million reads that passed quality control metrics, we calculated differential gene expression (DGE), differential transcript expression (DTE), and differential transcript usage (DTU) across brain regions and by sex. We found significant DGE, DTE, and DTU across brain regions and that the cerebellum had the most differences compared to the other three regions. Additionally, we found region-specific differential splicing between sexes, with the most sex differences in DTU in the cortex and no DTU in the hippocampus. We also report on two distinct patterns of sex DTU we observed, sex-divergent and sex-specific, that could potentially help explain sex differences in the prevalence and prognosis of various neurological and psychiatric disorders in future studies. Finally, we built a Shiny web application for researchers to explore the data further. Our study provides a resource for the community; it underscores the importance of AS in biological heterogeneity and the utility of long-read sequencing to better understand AS in the brain.
    Sprache Englisch
    Erscheinungsdatum 2024-01-11
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.01.11.575219
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Altered glia-neuron communication in Alzheimer's Disease affects WNT, p53, and NFkB Signaling determined by snRNA-seq.

    Soelter, Tabea M / Howton, Timothy C / Clark, Amanda D / Oza, Vishal H / Lasseigne, Brittany N

    Cell communication and signaling : CCS

    2024  Band 22, Heft 1, Seite(n) 317

    Abstract: Background: Alzheimer's disease is the most common cause of dementia and is characterized by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss. Although neuronal loss is a primary hallmark of Alzheimer's disease, it is known that non- ... ...

    Abstract Background: Alzheimer's disease is the most common cause of dementia and is characterized by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss. Although neuronal loss is a primary hallmark of Alzheimer's disease, it is known that non-neuronal cell populations are ultimately responsible for maintaining brain homeostasis and neuronal health through neuron-glia and glial cell crosstalk. Many signaling pathways have been proposed to be dysregulated in Alzheimer's disease, including WNT, TGFβ, p53, mTOR, NFkB, and Pi3k/Akt signaling. Here, we predict altered cell-cell communication between glia and neurons.
    Methods: Using public snRNA-sequencing data generated from postmortem human prefrontal cortex, we predicted altered cell-cell communication between glia (astrocytes, microglia, oligodendrocytes, and oligodendrocyte progenitor cells) and neurons (excitatory and inhibitory). We confirmed interactions in a second and third independent orthogonal dataset. We determined cell-type-specificity using Jaccard Similarity Index and investigated the downstream effects of altered interactions in inhibitory neurons through gene expression and transcription factor activity analyses of signaling mediators. Finally, we determined changes in pathway activity in inhibitory neurons.
    Results: Cell-cell communication between glia and neurons is altered in Alzheimer's disease in a cell-type-specific manner. As expected, ligands are more cell-type-specific than receptors and targets. We identified ligand-receptor pairs in three independent datasets and found involvement of the Alzheimer's disease risk genes APP and APOE across datasets. Most of the signaling mediators of these interactions were not significantly differentially expressed, however, the mediators that are also transcription factors had differential activity between AD and control. Namely, MYC and TP53, which are associated with WNT and p53 signaling, respectively, had decreased TF activity in Alzheimer's disease, along with decreased WNT and p53 pathway activity in inhibitory neurons. Additionally, inhibitory neurons had both increased NFkB signaling pathway activity and increased TF activity of NFIL3, an NFkB signaling-associated transcription factor.
    Conclusions: Cell-cell communication between glia and neurons in Alzheimer's disease is altered in a cell-type-specific manner involving Alzheimer's disease risk genes. Signaling mediators had altered transcription factor activity suggesting altered glia-neuron interactions may dysregulate signaling pathways including WNT, p53, and NFkB in inhibitory neurons.
    Mesh-Begriff(e) Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/genetics ; Humans ; Neurons/metabolism ; Neurons/pathology ; Neuroglia/metabolism ; Neuroglia/pathology ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Protein p53/genetics ; NF-kappa B/metabolism ; Signal Transduction ; Cell Communication/genetics ; Wnt Signaling Pathway
    Chemische Substanzen Tumor Suppressor Protein p53 ; NF-kappa B
    Sprache Englisch
    Erscheinungsdatum 2024-06-07
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-024-01686-8
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: The landscape of

    Whitlock, Jordan H / Wilk, Elizabeth J / Howton, Timothy C / Clark, Amanda D / Lasseigne, Brittany N

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Background: The SET binding protein 1 (: Results: To better understand the tissue-specific mechanisms involving : Conclusions: This study provides insight into the landscape ... ...

    Abstract Background: The SET binding protein 1 (
    Results: To better understand the tissue-specific mechanisms involving
    Conclusions: This study provides insight into the landscape of
    Sprache Englisch
    Erscheinungsdatum 2023-10-14
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.08.08.551337
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Computational Advancements in Cancer Combination Therapy Prediction.

    Flanary, Victoria L / Fisher, Jennifer L / Wilk, Elizabeth J / Howton, Timothy C / Lasseigne, Brittany N

    JCO precision oncology

    2023  Band 7, Seite(n) e2300261

    Abstract: Given the high attrition rate of de novo drug discovery and limited efficacy of single-agent therapies in cancer treatment, combination therapy prediction through in silico drug repurposing has risen as a time- and cost-effective alternative for ... ...

    Abstract Given the high attrition rate of de novo drug discovery and limited efficacy of single-agent therapies in cancer treatment, combination therapy prediction through in silico drug repurposing has risen as a time- and cost-effective alternative for identifying novel and potentially efficacious therapies for cancer. The purpose of this review is to provide an introduction to computational methods for cancer combination therapy prediction and to summarize recent studies that implement each of these methods. A systematic search of the PubMed database was performed, focusing on studies published within the past 10 years. Our search included reviews and articles of ongoing and retrospective studies. We prioritized articles with findings that suggest considerations for improving combination therapy prediction methods over providing a meta-analysis of all currently available cancer combination therapy prediction methods. Computational methods used for drug combination therapy prediction in cancer research include networks, regression-based machine learning, classifier machine learning models, and deep learning approaches. Each method class has its own advantages and disadvantages, so careful consideration is needed to determine the most suitable class when designing a combination therapy prediction method. Future directions to improve current combination therapy prediction technology include incorporation of disease pathobiology, drug characteristics, patient multiomics data, and drug-drug interactions to determine maximally efficacious and tolerable drug regimens for cancer. As computational methods improve in their capability to integrate patient, drug, and disease data, more comprehensive models can be developed to more accurately predict safe and efficacious combination drug therapies for cancer and other complex diseases.
    Mesh-Begriff(e) Humans ; Drug Discovery ; Machine Learning ; Meta-Analysis as Topic ; Neoplasms/drug therapy ; Retrospective Studies
    Sprache Englisch
    Erscheinungsdatum 2023-10-12
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2473-4284
    ISSN (online) 2473-4284
    DOI 10.1200/PO.23.00261
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Cell-type-specific gene expression and regulation in the cerebral cortex and kidney of atypical Setbp1

    Whitlock, Jordan H / Soelter, Tabea M / Howton, Timothy C / Wilk, Elizabeth J / Oza, Vishal H / Lasseigne, Brittany N

    Journal of cellular and molecular medicine

    2023  Band 27, Heft 22, Seite(n) 3565–3577

    Abstract: Schinzel Giedion Syndrome (SGS) is an ultra-rare autosomal dominant Mendelian disease presenting with abnormalities spanning multiple organ systems. The most notable phenotypes involve severe developmental delay, progressive brain atrophy, and drug- ... ...

    Abstract Schinzel Giedion Syndrome (SGS) is an ultra-rare autosomal dominant Mendelian disease presenting with abnormalities spanning multiple organ systems. The most notable phenotypes involve severe developmental delay, progressive brain atrophy, and drug-resistant seizures. SGS is caused by spontaneous variants in SETBP1, which encodes for the epigenetic hub SETBP1 transcription factor (TF). SETBP1 variants causing classical SGS cluster at the degron, disrupting SETBP1 protein degradation and resulting in toxic accumulation, while those located outside cause milder atypical SGS. Due to the multisystem phenotype, we evaluated gene expression and regulatory programs altered in atypical SGS by snRNA-seq of the cerebral cortex and kidney of Setbp1
    Mesh-Begriff(e) Humans ; Animals ; Mice ; Abnormalities, Multiple/genetics ; Abnormalities, Multiple/pathology ; Kidney/pathology ; Cerebral Cortex/pathology ; Gene Expression
    Sprache Englisch
    Erscheinungsdatum 2023-10-23
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.18001
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.

    Soelter, Tabea M / Howton, Timothy C / Wilk, Elizabeth J / Whitlock, Jordan H / Clark, Amanda D / Birnbaum, Allison / Patterson, Dalton C / Cortes, Constanza J / Lasseigne, Brittany N

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Alzheimer's disease (AD) is the most common form of dementia and is characterized by progressive memory loss and cognitive decline, affecting behavior, speech, and motor abilities. The neuropathology of AD includes the formation of extracellular amyloid- ... ...

    Abstract Alzheimer's disease (AD) is the most common form of dementia and is characterized by progressive memory loss and cognitive decline, affecting behavior, speech, and motor abilities. The neuropathology of AD includes the formation of extracellular amyloid-β plaque and intracellular neurofibrillary tangles of phosphorylated tau, along with neuronal loss. While neuronal loss is an AD hallmark, cell-cell communication between neuronal and non-neuronal cell populations maintains neuronal health and brain homeostasis. To study changes in cell-cell communication during disease progression, we performed snRNA-sequencing of the hippocampus from female 3xTg-AD and wild-type littermates at 6 and 12 months. We inferred differential cell-cell communication between 3xTg-AD and wild-type mice across time points and between senders (astrocytes, microglia, oligodendrocytes, and OPCs) and receivers (excitatory and inhibitory neurons) of interest. We also assessed the downstream effects of altered glia-neuron communication using pseudobulk differential gene expression, functional enrichment, and gene regulatory analyses. We found that glia-neuron communication is increasingly dysregulated in 12-month 3xTg-AD mice. We also identified 23 AD-associated ligand-receptor pairs that are upregulated in the 12-month-old 3xTg-AD hippocampus. Our results suggest increased AD association of interactions originating from microglia. Signaling mediators were not significantly differentially expressed but showed altered gene regulation and TF activity. Our findings indicate that altered glia-neuron communication is increasingly dysregulated and affects the gene regulatory mechanisms in neurons of 12-month-old 3xTg-AD mice.
    Sprache Englisch
    Erscheinungsdatum 2024-05-23
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.05.21.595199
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Signature reversion of three disease-associated gene signatures prioritizes cancer drug repurposing candidates.

    Fisher, Jennifer L / Wilk, Elizabeth J / Oza, Vishal H / Gary, Sam E / Howton, Timothy C / Flanary, Victoria L / Clark, Amanda D / Hjelmeland, Anita B / Lasseigne, Brittany N

    FEBS open bio

    2024  Band 14, Heft 5, Seite(n) 803–830

    Abstract: Drug repurposing is promising because approving a drug for a new indication requires fewer resources than approving a new drug. Signature reversion detects drug perturbations most inversely related to the disease-associated gene signature to identify ... ...

    Abstract Drug repurposing is promising because approving a drug for a new indication requires fewer resources than approving a new drug. Signature reversion detects drug perturbations most inversely related to the disease-associated gene signature to identify drugs that may reverse that signature. We assessed the performance and biological relevance of three approaches for constructing disease-associated gene signatures (i.e., limma, DESeq2, and MultiPLIER) and prioritized the resulting drug repurposing candidates for four low-survival human cancers. Our results were enriched for candidates that had been used in clinical trials or performed well in the PRISM drug screen. Additionally, we found that pamidronate and nimodipine, drugs predicted to be efficacious against the brain tumor glioblastoma (GBM), inhibited the growth of a GBM cell line and cells isolated from a patient-derived xenograft (PDX). Our results demonstrate that by applying multiple disease-associated gene signature methods, we prioritized several drug repurposing candidates for low-survival cancers.
    Mesh-Begriff(e) Drug Repositioning/methods ; Humans ; Antineoplastic Agents/pharmacology ; Animals ; Cell Line, Tumor ; Mice ; Glioblastoma/genetics ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Gene Expression Profiling ; Xenograft Model Antitumor Assays ; Gene Expression Regulation, Neoplastic/drug effects ; Brain Neoplasms/genetics ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Neoplasms/genetics ; Neoplasms/drug therapy ; Transcriptome/genetics ; Transcriptome/drug effects
    Chemische Substanzen Antineoplastic Agents
    Sprache Englisch
    Erscheinungsdatum 2024-03-26
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13796
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Ten simple rules for using public biological data for your research.

    Oza, Vishal H / Whitlock, Jordan H / Wilk, Elizabeth J / Uno-Antonison, Angelina / Wilk, Brandon / Gajapathy, Manavalan / Howton, Timothy C / Trull, Austyn / Ianov, Lara / Worthey, Elizabeth A / Lasseigne, Brittany N

    PLoS computational biology

    2023  Band 19, Heft 1, Seite(n) e1010749

    Abstract: With an increasing amount of biological data available publicly, there is a need for a guide on how to successfully download and use this data. The 10 simple rules for using public biological data are: (1) use public data purposefully in your research; ( ... ...

    Abstract With an increasing amount of biological data available publicly, there is a need for a guide on how to successfully download and use this data. The 10 simple rules for using public biological data are: (1) use public data purposefully in your research; (2) evaluate data for your use case; (3) check data reuse requirements and embargoes; (4) be aware of ethics for data reuse; (5) plan for data storage and compute requirements; (6) know what you are downloading; (7) download programmatically and verify integrity; (8) properly cite data; (9) make reprocessed data and models Findable, Accessible, Interoperable, and Reusable (FAIR) and share; and (10) make pipelines and code FAIR and share. These rules are intended as a guide for researchers wanting to make use of available data and to increase data reuse and reproducibility.
    Mesh-Begriff(e) Reproducibility of Results ; Information Storage and Retrieval
    Sprache Englisch
    Erscheinungsdatum 2023-01-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2193340-6
    ISSN 1553-7358 ; 1553-734X
    ISSN (online) 1553-7358
    ISSN 1553-734X
    DOI 10.1371/journal.pcbi.1010749
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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