scholarly journals Transcription Factor Erg Variants and Functional Diversification of Chondrocytes during Limb Long Bone Development

2000 ◽  
Vol 150 (1) ◽  
pp. 27-40 ◽  
Author(s):  
Masahiro Iwamoto ◽  
Yoshinobu Higuchi ◽  
Eiki Koyama ◽  
Motomi Enomoto-Iwamoto ◽  
Kojiro Kurisu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Limb Development ◽  
Matrix Protein ◽  
Molecular Mechanisms ◽  
Articular Chondrocytes ◽  
Bone Cells ◽  
Expression Patterns ◽  
Extracellular Matrix Protein ◽  
Long Bone ◽  
Chondrocyte Maturation

During limb development, chondrocytes located at the epiphyseal tip of long bone models give rise to articular tissue, whereas the more numerous chondrocytes in the shaft undergo maturation, hypertrophy, and mineralization and are replaced by bone cells. It is not understood how chondrocytes follow these alternative pathways to distinct fates and functions. In this study we describe the cloning of C-1-1, a novel variant of the ets transcription factor ch-ERG. C-1-1 lacks a short 27–amino acid segment located ∼80 amino acids upstream of the ets DNA binding domain. We found that in chick embryo long bone anlagen, C-1-1 expression characterizes developing articular chondrocytes, whereas ch-ERG expression is particularly prominent in prehypertrophic chondrocytes in the growth plate. To analyze the function of C-1-1 and ch-ERG, viral vectors were used to constitutively express each factor in developing chick leg buds and cultured chondrocytes. We found that virally driven expression of C-1-1 maintained chondrocytes in a stable and immature phenotype, blocked their maturation into hypertrophic cells, and prevented the replacement of cartilage with bone. It also induced synthesis of tenascin-C, an extracellular matrix protein that is a unique product of developing articular chondrocytes. In contrast, virally driven expression of ch-ERG significantly stimulated chondrocyte maturation in culture, as indicated by increases in alkaline phosphatase activity and deposition of a mineralized matrix; however, it had modest effects in vivo. The data show that C-1-1 and ch-ERG have diverse biological properties and distinct expression patterns during skeletogenesis, and are part of molecular mechanisms by which limb chondrocytes follow alternative developmental pathways. C-1-1 is the first transcription factor identified to date that appears to be instrumental in the genesis and function of epiphyseal articular chondrocytes.

scholarly journals Direct observation of structure and dynamics during phase separation of an elastomeric protein

2017 ◽  
Vol 114 (22) ◽  
pp. E4408-E4415 ◽  
Author(s):  
Sean E. Reichheld ◽  
Lisa D. Muiznieks ◽  
Fred W. Keeley ◽  
Simon Sharpe
Keyword(s):  
Phase Separation ◽  
Matrix Protein ◽  
Molecular Mechanisms ◽  
Bulk Water ◽  
Extracellular Matrix Protein ◽  
Elastic Fibers ◽  
Cross Linking ◽  
Structure And Dynamics ◽  
Chemical Cross Linking

Despite its growing importance in biology and in biomaterials development, liquid–liquid phase separation of proteins remains poorly understood. In particular, the molecular mechanisms underlying simple coacervation of proteins, such as the extracellular matrix protein elastin, have not been reported. Coacervation of the elastin monomer, tropoelastin, in response to heat and salt is a critical step in the assembly of elastic fibers in vivo, preceding chemical cross-linking. Elastin-like polypeptides (ELPs) derived from the tropoelastin sequence have been shown to undergo a similar phase separation, allowing formation of biomaterials that closely mimic the material properties of native elastin. We have used NMR spectroscopy to obtain site-specific structure and dynamics of a self-assembling elastin-like polypeptide along its entire self-assembly pathway, from monomer through coacervation and into a cross-linked elastic material. Our data reveal that elastin-like hydrophobic domains are composed of transient β-turns in a highly dynamic and disordered chain, and that this disorder is retained both after phase separation and in elastic materials. Cross-linking domains are also highly disordered in monomeric and coacervated ELP3 and form stable helices only after chemical cross-linking. Detailed structural analysis combined with dynamic measurements from NMR relaxation and diffusion data provides direct evidence for an entropy-driven mechanism of simple coacervation of a protein in which transient and nonspecific intermolecular hydrophobic contacts are formed by disordered chains, whereas bulk water and salt are excluded.

scholarly journals The Anchorage of Bone Cells onto an Yttria-Stabilized Zirconia Surface with Mild Nano-Micro Curved Profiles

2020 ◽  
Vol 8 (4) ◽  
pp. 127
Author(s):  
Susanne Staehlke ◽  
Armin Springer ◽  
Thomas Freitag ◽  
Jakob Brief ◽  
J. Barbara Nebe
Keyword(s):  
Matrix Protein ◽  
Bone Cells ◽  
Cell Attachment ◽  
Yttria Stabilized Zirconia ◽  
Extracellular Matrix Protein ◽  
Cell Phenotype ◽  
Ros Generation ◽  
Stabilized Zirconia ◽  
Dental Surgery

The high biocompatibility, good mechanical properties, and perfect esthetics of ceramic dental materials motivate investigation into their suitability as an endosseous implant. Osseointegration at the interface between bone and implant surface, which is a criterion for dental implant success, is dependent on surface chemistry and topography. We found out earlier that osteoblasts on sharp-edged micro-topographies revealed an impaired cell phenotype and function and the cells attempted to phagocytize these spiky elevations in vitro. Therefore, micro-structured implants used in dental surgery should avoid any spiky topography on their surface. The sandblasted, acid-etched, and heat-treated yttria-stabilized zirconia (cer.face®14) surface was characterized by scanning electron microscopy and energy dispersive X-ray. In vitro studies with human MG-63 osteoblasts focused on cell attachment and intracellular stress level. The cer.face 14 surface featured a landscape with nano-micro hills that was most sinusoidal-shaped. The mildly curved profile proved to be a suitable material for cell anchorage. MG-63 cells on cer.face 14 showed a very low reactive oxygen species (ROS) generation similar to that on the extracellular matrix protein collagen I (Col). Intracellular adenosine triphosphate (ATP) levels were comparable to Col. Ceramic cer.face 14, with its sinusoidal-shaped surface structure, facilitates cell anchorage and prevents cell stress.

scholarly journals Role and Molecular Mechanisms of Pericytes in Regulation of Leukocyte Diapedesis in Inflamed Tissues

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Paulina Rudziak ◽  
Christopher G. Ellis ◽  
Paulina M. Kowalewska
Keyword(s):  
Basement Membrane ◽  
Matrix Protein ◽  
Molecular Mechanisms ◽  
Leukocyte Recruitment ◽  
Extracellular Matrix Protein ◽  
Chemotactic Migration ◽  
Blood Vessel Formation ◽  
Vascular Basement Membrane ◽  
Leukocyte Extravasation

Leukocyte recruitment is a hallmark of the inflammatory response. Migrating leukocytes breach the endothelium along with the vascular basement membrane and associated pericytes. While much is known about leukocyte-endothelial cell interactions, the mechanisms and role of pericytes in extravasation are poorly understood and the classical paradigm of leukocyte recruitment in the microvasculature seldom adequately discusses the involvement of pericytes. Emerging evidence shows that pericytes are essential players in the regulation of leukocyte extravasation in addition to their functions in blood vessel formation and blood-brain barrier maintenance. Junctions between venular endothelial cells are closely aligned with extracellular matrix protein low expression regions (LERs) in the basement membrane, which in turn are aligned with gaps between pericytes. This forms preferential paths for leukocyte extravasation. Breaching of the layer formed by pericytes and the basement membrane entails remodelling of LERs, leukocyte-pericyte adhesion, crawling of leukocytes on pericyte processes, and enlargement of gaps between pericytes to form channels for migrating leukocytes. Furthermore, inflamed arteriolar and capillary pericytes induce chemotactic migration of leukocytes that exit postcapillary venules, and through direct pericyte-leukocyte contact, they induce efficient interstitial migration to enhance the immunosurveillance capacity of leukocytes. Given their role as regulators of leukocyte extravasation, proper pericyte function is imperative in inflammatory disease contexts such as diabetic retinopathy and sepsis. This review summarizes research on the molecular mechanisms by which pericytes mediate leukocyte diapedesis in inflamed tissues.

scholarly journals Investigation of Tenascin Expression in Endometriosis

2012 ◽  
Vol 2012 ◽  
pp. 1-5
Author(s):  
Zehra Sema Ozkan ◽  
Hasan Cilgin ◽  
Remzi Atilgan ◽  
Mehmet Simsek ◽  
Bengu Cobanoglu ◽  
...  
Keyword(s):  
Matrix Protein ◽  
Expression Patterns ◽  
Serum Levels ◽  
Extracellular Matrix Protein ◽  
Secretory Phase ◽  
Tissue Samples ◽  
Intense Staining ◽  
Tissue Levels ◽  
Significant Difference ◽  
Ectopic Endometrium

Objective. To evaluate the serum and tissue levels and local expression pattern of tenascin, a high molecular weight extracellular matrix protein, in eutopic and ectopic endometrium from patients with and without endometriosis and to compare the proliferative and secretory phase differences. Materials and Methods. Thirty women with endometriosis and fifteen women without endometriosis undergoing surgery for benign indications were included in the study. Serum and tissue levels and proliferative and secretory phase expression patterns of tenascin in the ectopic and eutopic endometrium were analyzed with immunohistochemistry and immunoassays. The results were compared with Mann-Whitney U test. P values <0.05 were considered as statistically significant. Results. Tenascin expression was detected in both of eutopic and ectopic endometrium of women with and without endometriosis. In immunohistochemical staining, intense staining of tenascin was observed in glandular cells of eutopic and ectopic endometrial tissue samples of both groups during secretory phase (P<0.01). Eutopic and ectopic tissue levels of tenascin were higher than serum tenascin levels only secretory phase (P=0.02). There was no significant difference between groups for tissue and serum levels of tenascin during cycle phases. Conclusion. Tenascin expression showed cyclic change on eutopic and ectopic endometrium.

scholarly journals Transcriptome analysis identifies genes involved in the somatic embryogenesis of Eucalyptus

2020 ◽  
Author(s):  
Yufei Xiao ◽  
Junji Li ◽  
Ye Zhang ◽  
Xiaoning Zhang ◽  
Hailong Liu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Somatic Embryogenesis ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Zinc Finger Protein ◽  
Expression Patterns ◽  
Late Embryogenesis Abundant ◽  
Arabinogalactan Protein ◽  
Late Embryogenesis Abundant Protein ◽  
Eucalyptus Species

Abstract Background: Eucalyptus, a highly diverse genus of the Myrtaceae family, is the most widely planted hardwood in the world due to its increasing importance for fiber and energy. Somatic embryogenesis (SE) is one large-scale method to provide commercial use of the vegetative propagation of Eucalyptus and dedifferentiation is a key step for plant cells to become meristematic. However, little is known about the molecular changes during the Eucalyptus SE.Results: We compared the transcriptome profiles of the differentiated and dedifferentiated tissues of two Eucalyptus species – E. camaldulensis (high embryogenetic potential) and E. grandis x urophylla (low embryogenetic potential). Initially, we identified 18,777 to 20,240 genes in all samples. Compared to the differentiated tissues, we identified 9,229 and 8,989 differentially expressed genes (DEGs) in the dedifferentiated tissues of E. camaldulensis and E. grandis x urophylla, respectively, and 2,687 up-regulated and 2,581 down-regulated genes shared. Next, we identified 2,003 up-regulated and 1,958 down-regulated genes only in E. camaldulensis, including 6 somatic embryogenesis receptor kinase, 17 ethylene, 12 auxin, 83 ribosomal protein, 28 zinc finger protein, 10 heat shock protein, 9 histone, 122 cell wall related and 98 transcription factor genes. Genes from other families like ABA, arabinogalactan protein and late embryogenesis abundant protein were also found to be specifically dysregulated in the dedifferentiation process of E. camaldulensis. Further, we identified 48,447 variants (SNPs and small indels) specific to E. camaldulensis, including 13,434 exonic variants from 4,723 genes (e.g., annexin, GN, ARF and AP2-like ethylene-responsive transcription factor). qRT-PCR was used to confirm the gene expression patterns in both E. camaldulensis and E. grandis x urophylla. Conclusions: This is the first time to study the somatic embryogenesis of Eucalyptus using transcriptome sequencing. It will improve our understanding of the molecular mechanisms of somatic embryogenesis and dedifferentiation in Eucalyptus. Our results provide a valuable resource for future studies in the field of Eucalyptus and will benefit the Eucalyptus breeding program.

scholarly journals Transcriptome analysis identifies genes involved in the somatic embryogenesis of Eucalyptus

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Yufei Xiao ◽  
Junji Li ◽  
Ye Zhang ◽  
Xiaoning Zhang ◽  
Hailong Liu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Somatic Embryogenesis ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Zinc Finger Protein ◽  
Expression Patterns ◽  
Late Embryogenesis Abundant ◽  
Arabinogalactan Protein ◽  
Late Embryogenesis Abundant Protein ◽  
Eucalyptus Species

Abstract Background Eucalyptus, a highly diverse genus of the Myrtaceae family, is the most widely planted hardwood in the world due to its increasing importance for fiber and energy. Somatic embryogenesis (SE) is one large-scale method to provide commercial use of the vegetative propagation of Eucalyptus and dedifferentiation is a key step for plant cells to become meristematic. However, little is known about the molecular changes during the Eucalyptus SE. Results We compared the transcriptome profiles of the differentiated and dedifferentiated tissues of two Eucalyptus species – E. camaldulensis (high embryogenetic potential) and E. grandis x urophylla (low embryogenetic potential). Initially, we identified 18,777 to 20,240 genes in all samples. Compared to the differentiated tissues, we identified 9229 and 8989 differentially expressed genes (DEGs) in the dedifferentiated tissues of E. camaldulensis and E. grandis x urophylla, respectively, and 2687 up-regulated and 2581 down-regulated genes shared. Next, we identified 2003 up-regulated and 1958 down-regulated genes only in E. camaldulensis, including 6 somatic embryogenesis receptor kinase, 17 ethylene, 12 auxin, 83 ribosomal protein, 28 zinc finger protein, 10 heat shock protein, 9 histone, 122 cell wall related and 98 transcription factor genes. Genes from other families like ABA, arabinogalactan protein and late embryogenesis abundant protein were also found to be specifically dysregulated in the dedifferentiation process of E. camaldulensis. Further, we identified 48,447 variants (SNPs and small indels) specific to E. camaldulensis, including 13,434 exonic variants from 4723 genes (e.g., annexin, GN, ARF and AP2-like ethylene-responsive transcription factor). qRT-PCR was used to confirm the gene expression patterns in both E. camaldulensis and E. grandis x urophylla. Conclusions This is the first time to study the somatic embryogenesis of Eucalyptus using transcriptome sequencing. It will improve our understanding of the molecular mechanisms of somatic embryogenesis and dedifferentiation in Eucalyptus. Our results provide a valuable resource for future studies in the field of Eucalyptus and will benefit the Eucalyptus breeding program.

Aspekty diagnostyczne i terapeutyczne zespołu Marfana w wieku rozwojowym

2018 ◽  
Vol 22 (2) ◽  
Author(s):  
Małgorzata Ludzia ◽  
Ewa Smereczyńska-Wierzbicka ◽  
Bożena Werner
Keyword(s):  
Marfan Syndrome ◽  
Aortic Root ◽  
Matrix Protein ◽  
Autosomal Dominant ◽  
De Novo ◽  
Enzyme Inhibitor ◽  
Angiotensin Receptor Blockers ◽  
Extracellular Matrix Protein ◽  
Long Bone ◽  
De Novo Mutations

Marfan’s syndrome (MFS) is a systemic, autosomal dominant connective tissue disease. It is caused mainly by the mutations in the FBN1 gene and is connected with extracellular matrix protein fibrillin-1. The incidence is about 2-3 per 10 000. About 70-75% of cases are inherited in an autosomal dominant fashion and the remaining are de-novo mutations. The most common findings involve cardiovascular, ocular and skeletal systems. The cardinal manifestations typically involving MFS are aortic root aneurysm/dissection and ectopia lentis. The other common manifestations are mitral valve prolapse, proximal aortic aneurysm, dolichocephaly, pectus carinatum deformity, enophthalmos, scoliosis, long-bone overgrowth. The manifestation in neonatal Marfan syndrome, in contrast to classical Marfan syndrome, is a rapidly progressing multi-valvular cardiac disease. The death connected with congestive heart failure happens mainly within the first year of life. Prognostic factors for life expectancy of patients with Marfan syndrome depend on the type of the MFS and in classical MFS – depend on the rate of aortic root dilatation, which leads to dissection or rupture. Pharmacological management includes beta blockers, angiotensin receptor blockers and angiotensin converting enzyme inhibitor as a preventive treatment to slow aortic root dilation.

Inflammation-dependent expression of SPARC during development of chronic pancreatitis in WBN/Kob rats and a microarray gene expression analysis

2009 ◽  
Vol 38 (2) ◽  
pp. 196-204 ◽  
Author(s):  
T. Reding ◽  
U. Wagner ◽  
A. B. Silva ◽  
L-K. Sun ◽  
M. Bain ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Pancreatitis ◽  
Chronic Inflammation ◽  
Wistar Rats ◽  
Matrix Protein ◽  
Expression Patterns ◽  
Acinar Cells ◽  
Extracellular Matrix Protein ◽  
Human Pancreas ◽  
Inflammatory Genes

The pathophysiology of human chronic pancreatitis is not well understood and difficult to follow on a molecular basis. Therefore, we used a rat model [Wistar-Bonn/Kobori (WBN/Kob)] that exhibits spontaneous chronic inflammation and fibrosis in the pancreas. Using microarrays we compared gene expression patterns in the pancreas during development of inflammation and fibrosis of WBN/Kob rats with age-matched healthy Wistar rats. The extracellular matrix protein SPARC (secreted protein, acidic, and rich in cysteines) and other transcripts of inflammatory genes were quantified by real-time PCR, and some were localized by immunohistochemistry. When pancreatic inflammation becomes obvious at the age of 16 wk, several hundred genes are increased between 3- and 50-fold in WBN/Kob rats compared with healthy Wistar rats. Proteins produced by acinar cells and characteristic for inflammation, e.g., pancreatitis-associated protein, are highly upregulated. Other proteins, derived from infiltrating inflammatory cells and from activated stellate cells (fibrosis) such as collagens and fibronectins are also significantly upregulated. SPARC was localized to acinar cells where it increased in the vicinity of inflammatory foci. However, acinar expression of SPARC was lost during destruction of acinar cells. In human pancreatic specimens with chronic pancreatitis, SPARC exhibited a similar expression profile. During chronic inflammation and fibrosis in the WBN/Kob rat, inflammatory genes, growth factors, and structural genes exhibit a high increase of expression. A temporal profile including pre- and postinflammatory phases indicates a concurrent activation of inflammatory and fibrotic changes. Inflammation dependent expression of SPARC appears to be lost during acinar-to-duct metaplasia both in rat and human pancreas.

FGF23, PHEX, and MEPE regulation of phosphate homeostasis and skeletal mineralization

2003 ◽  
Vol 285 (1) ◽  
pp. E1-E9 ◽  
Author(s):  
L. Darryl Quarles
Keyword(s):  
Extracellular Matrix ◽  
Matrix Protein ◽  
Molecular Mechanisms ◽  
Hypophosphatemic Rickets ◽  
Extracellular Matrix Protein ◽  
Phosphate Homeostasis ◽  
Genetic Studies ◽  
Autosomal Dominant Hypophosphatemic Rickets ◽  
Common Pathogenesis

There is evidence for a hormone/enzyme/extracellular matrix protein cascade involving fibroblastic growth factor 23 (FGF23), a phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX), and a matrix extracellular phosphoglycoprotein (MEPE) that regulates systemic phosphate homeostasis and mineralization. Genetic studies of autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemia (XLH) identified the phosphaturic hormone FGF23 and the membrane metalloprotease PHEX, and investigations of tumor-induced osteomalacia (TIO) discovered the extracellular matrix protein MEPE. Similarities between ADHR, XLH, and TIO suggest a model to explain the common pathogenesis of renal phosphate wasting and defective mineralization in these disorders. In this model, increments in FGF23 and MEPE, respectively, cause renal phosphate wasting and intrinsic mineralization abnormalities. FGF23 elevations in ADHR are due to mutations of FGF23 that block its degradation, in XLH from indirect actions of inactivating mutations of PHEX to modify the expression and/or degradation of FGF23 and MEPE, and in TIO because of increased production of FGF23 and MEPE. Although this model is attractive, several aspects need to be validated. First, the enzymes responsible for metabolizing FGF23 and MEPE need to be established. Second, the physiologically relevant PHEX substrates and the mechanisms whereby PHEX controls FGF23 and MEPE metabolism need to be elucidated. Finally, additional studies are required to establish the molecular mechanisms of FGF23 and MEPE actions on kidney and bone, as well as to confirm the role of these and other potential “phosphatonins,” such as frizzled related protein-4, in the pathogenesis of the renal and skeletal phenotypes in XLH and TIO. Unraveling the components of this hormone/enzyme/extracellular matrix pathway will not only lead to a better understanding of phosphate homeostasis and mineralization but may also improve the diagnosis and treatment of hypo- and hyperphosphatemic disorders.

scholarly journals Molecular forms, binding functions, and developmental expression patterns of cytotactin and cytotactin-binding proteoglycan, an interactive pair of extracellular matrix molecules

1988 ◽  
Vol 106 (2) ◽  
pp. 519-532 ◽  
Author(s):  
S Hoffman ◽  
KL Crossin ◽  
GM Edelman
Keyword(s):  
Extracellular Matrix ◽  
Chondroitin Sulfate ◽  
Neural Development ◽  
Matrix Protein ◽  
Expression Patterns ◽  
Developmental Expression ◽  
Extracellular Matrix Protein ◽  
Molecular Forms ◽  
Biochemical Alterations ◽  
Extracellular Matrix Components

Cytotactin is an extracellular matrix protein that is found in a restricted distribution and is related to developmental patterning at a number of neural and non-neural sites. It has been shown to bind specifically to other extracellular matrix components including a chondroitin sulfate proteoglycan (cytotactin-binding [CTB] proteoglycan) and fibronectin. Cell binding experiments have revealed that cytotactin interacts with neurons and fibroblasts. When isolated from brain, both cytotactin and CTB proteoglycan contain the HNK-1 carbohydrate epitope. Here, specific antibodies prepared against highly purified cytotactin and CTB proteoglycan were used to correlate the biochemical alterations and modes of binding of these proteins with their differential tissue expression as a function of time and place during chicken embryo development. It was found that, during neural development, both the levels of expression of cytotactin and CTB proteoglycan and of the molecular forms of each molecule varied, following different time courses. In addition, a novel Mr 250,000 form of cytotactin was detected that contained chondroitin sulfate. The intermolecular binding of cytotactin and CTB proteoglycan and the binding of cytotactin to fibroblasts were characterized further and found to be inhibited by EDTA, consistent with a dependence on divalent cations. Unlike the molecules from neural tissue, cytotactin and CTB proteoglycan isolated from non-neural tissues such as fibroblasts lacked the HNK-1 epitope. Nevertheless, the intermolecular and cellular binding activities of cytotactin isolated from fibroblast culture medium were comparable to those of the molecule isolated from brain, suggesting that the HNK-1 epitope is not directly involved in binding. Binding experiments involving enzymatically altered molecules that lack chondroitin sulfate suggested that this glycosaminoglycan is also not directly involved in binding. Although they clearly formed a binding couple, the spatial distributions of cytotactin and CTB proteoglycan in the embryo were not always coincident. They were similar in tissue sections from the cerebellum, gizzard, and vascular smooth muscle. In contrast, CTB proteoglycan was present in cardiac muscle where no cytotactin is present, and it was seen in cartilage throughout development unlike cytotactin, which was present only in immature chondrocytes. Cell culture experiments were consistent with the previous conclusion that cytotactin was specifically synthesized by glia, whereas CTB proteoglycan was specifically synthesized by neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

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