Relevant bibliographies by topics / TGFGIp

Academic literature on the topic 'TGFGIp'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "TGFGIp"

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Anandalakshmi, Venkatraman, Guillaume Hochart, David Bonnel, Jonathan Stauber, Shigeto Shimmura, Rajamani Lakshminarayanan, Konstantin Pervushin, and Jodhbir S. Mehta. "Targeted Expression of TGFBIp Peptides in Mouse and Human Tissue by MALDI-Mass Spectrometry Imaging." Separations 8, no. 7 (July 3, 2021): 97. http://dx.doi.org/10.3390/separations8070097.

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Stromal corneal dystrophies are a group of hereditary disorders caused by mutations in the TGFBI gene. The mutant TGFBIp is prone to protein aggregation and the mutant protein gets deposited in the cornea, leading to severe visual impairment. The mutations lead to a corneal specific protein aggregation suggesting the involvement of tissue-specific factors. The exact molecular mechanism of the process of tissue-specific protein aggregation remains to be elucidated. Differential proteolysis of mutant TGFBIp is a critical component of the disease pathology. The differential proteolysis gives rise to shorter peptides that are highly aggregation-prone and initiate the aggregation cascade. Analyzing the proteolytic processing of the different TGFBIp mutant may provide insight to aid in understanding the amyloid aggregation mechanism. We developed a MALDI-MSI methodology to identify expression and spatial localization of TGFBIp peptides in the cornea. Corneal tissue samples were collected from both control and dystrophic patients (with 2 different mutations), embedded in OCT and sectioned. The sections were trypsin digested and subjected to mass spectrometry imaging using a targeted approach to detect TGFBIp. MALDI-MSI identified peptides from TGFBIp that co-localized with the amyloid corneal deposits. In addition to the relative abundance data, the specific location of the peptides across the corneal sections as molecular signatures was also identified. Spatial distribution and intensity of the TGFBIp peptides showed differences between diseased and control models but also between the two LCD phenotypes. The TGFBIp peptide with m/z of 787.474 and m/z of 1179.579 showed increased expression in both LCD mutants compared to the controls. The peptide with m/z of 929.5 showed increased expression in the LCD phenotype with H626R mutation while the peptide with m/z of 1315.802 was abundant in the sample with R124C mutation. This initial report of 2D spatial protein signature and localization of TGFBIp may be expanded to other mutations to understand the proteolytic patterns of TGFBIp in different mutations.
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Miyakawa, Ayumi A., Thais Girão-Silva, Jose E. Krieger, and Elazer R. Edelman. "Rapamycin activates TGF receptor independently of its ligand: implications for endothelial dysfunction." Clinical Science 132, no. 4 (February 16, 2018): 437–47. http://dx.doi.org/10.1042/cs20171457.

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Rapamycin, the macrolide immunosuppressant and active pharmaceutic in drug-eluting stents (DES), has a well-recognized antiproliferative action that involves inhibition of the mTOR pathway after binding to the cytosolic protein FKBP12. TGF receptor-type I (TGFRI) spontaneous activation is inhibited by the association with FKBP12. We hypothesized that rapamycin, in addition to inhibition of mTOR signaling, activates TGFRI independent of TGFβ. Human umbilical vein endothelial cells (HUVECs) were treated with rapamycin (10 nmol/l) and/or TGFβ RI kinase inhibitor (TGFRIi, 100 nmol/l) for 24 h. Rapamycin induced SMAD phosphorylation (SMAD1, SMAD2, and SMAD5) and PAI-1 up-regulation, which was specifically abrogated by SMAD2 knockdown. TGFRIi efficiently blocked phosphorylation of SMAD2, but not SMAD1/5. Interestingly, the inhibitor did not alter cell proliferation arrest induced by rapamycin. Active TGFβ secretion was not affected by the treatment. Neutralizing TGFβ experiments did not influence SMAD2 phosphorylation or PAI-1 expression indicating that activation of this pathway is independent of the ligand. In addition, rapamycin induction of endothelial-to-mesenchymal transition (EndMT) was potentiated by IL-1β and efficiently blocked by TGFRIi. In vivo, the prothrombogenic effects of rapamycin and up-regulation of PAI-1 in murine carotid arteries were reduced by TGFRIi treatment. In conclusion, we provide evidence that rapamycin activates TGF receptor independent of its ligand TGFβ, in concert with promotion of PAI-1 expression and changes in endothelial phenotype. These undesirable effects, the prothrombogenic state, and activation of EndMT are SMAD2-dependent and independent of the therapeutic rapamycin-induced cell proliferation arrest.
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Pereira, Marcelo de Souza Fernandes, Yasemin Sezgin, Aarohi Thakkar, and Dean Anthony Lee. "Tgfβ-Imprinting Decrease CD38 Expression and Lead to Metabolic Reprogramming on Primary NK Cell." Blood 136, Supplement 1 (November 5, 2020): 4. http://dx.doi.org/10.1182/blood-2020-143085.

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Transforming growth factor-β (TGF-β) plays an essential role in regulating immune responses through its immunossupressive effect on adaptive and innate immune cells. In addition, we and others have shown that alterations in cell-intrinsic metabolism profiles can significantly impact the function of immune cells. Previously, our group demonstrated that TGFβ-imprinting (TGFβi) decreases NK cell sensitivity to TGFβ through SMAD3 suppression and enhances a pro-inflammatory phenotype with hypersecretion of IFN-γ, TNF-α, and GM-CSF, which appeared to be mediated by an epigenetic mechanism. To evaluate this process, we conducted RNA-seq and ATAC-seq to evaluate the impact of chromosomal remodeling on gene expression. In addition to confirming low SMAD3 transcription, this data showed that TGFβi NK cells have decreased CD38 expression, which we confirmed at the protein level. Since CD38 is an ectoenzyme that regulates nicotinamide adenine dinucleotide (NAD+), a critical component of OXPHOS in both T and NK cells, we examined the effect of TGFβi on NK cell metabolism. TGFβi primary NK cells were generated from peripheral blood of healthy donors as previously described, and using a mitochondrial stress test assay, we observed higher oxygen consumption rates (OCR). However, in the glycolysis stress test assay we observed comparable extracellular acidification rates (ECAR) between Standard expanded and TGFbi NK cells, resulting in higher OCR/ECAR ratios in TGFbi NK cells. Since TGFβ has been shown to induce fragmented mitochondria, and inhibition of mitochondrial fragmentation improved mitochondrial metabolism, we evaluated subcellular structure of TGFβi NK cellsby transmission electron microscopy (TEM). We found no difference in mitochondrial fragmentation between STD and TGFβi NK cells. Together, these results show that TGFβi induces epigenetic reprograming of NK cells that results in increased OXPHOS through CD38 suppression. Moreover, the decreases CD38 expression in TGFβi NK cells could be a promising non-genetic alternative to generating CD38-negative NK cells to avoid fratricide in combination with DARA Figure Disclosures Lee: Kiadis Pharma Netherlands B.V: Consultancy, Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.
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Lee, In-Chul, and Jong-Sup Bae. "Suppressive Effects of Sulforaphane on TGFBIp-mediated Sepsis." Natural Product Communications 12, no. 10 (October 2017): 1934578X1701201. http://dx.doi.org/10.1177/1934578x1701201026.

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Sulforaphane (SFN) is produced when the enzyme myrosinase transforms glucoraphanin upon damage to the plant such as from chewing and effective in preventing carcinogenesis, diabetes, and inflammatory responses. Transforming growth factor β-induced protein (TGFBIp) is an extracellular matrix protein whose expression in several cell types is greatly increased by TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. We hypothesized that SFN could reduce TGFBIp-mediated severe inflammatory responses in human endothelial cells and mice. Here, we investigated the anti-septic effects and underlying mechanisms of SFN against TGFBIp-mediated septic responses. SFN effectively inhibited lipopolysaccharide-induced release of TGFBIp and suppressed TGFBIp-mediated septic responses. In addition, SFN suppressed cecal ligation and puncture (CLP)-induced sepsis lethality and pulmonary injury. In conclusion, SFN suppressed TGFBIp-mediated and CLP-induced septic responses. Therefore, SFN could be a potential therapeutic agent for treatment of various severe vascular inflammatory diseases via inhibition of the TGFBIp signaling pathway.
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Kim, Ha-Jeong, Suyeon Rhe, and Haeuk Jung. "Platelet TGFBIp induces foam cell formation after platelet phagocytosis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 206.26. http://dx.doi.org/10.4049/jimmunol.198.supp.206.26.

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Abstract Foam cells play a critical role in the atherosclerosis development. It is reported that platelets phagocytosis induces foam cell formation by producing more inflammatory cytokines. However, platelet induced foam cell formation mechanism is not clear. TGFBIp is a secreted extracellular matrix protein that is consisted by 4 fasciclin-1 domains. TGFBIp is produced by several cells include macrophages and works as chemoattractant to monocytes. TGFBIp is also in the platelet granule and it is secreted and bound on platelets when platelets are activated. Platelets are removed by macrophages when they are activated. However, the role of TGFBIp on activated platelets is not clear. In this report, we used TGFBIp lacking platelets to investigate the role of TGFBIp in platelets. When macrophages uptake TGFBIp lacking platelets, foam cell formation is less than WT platelets are uptaken.
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Kim, Ha-Jeong, Pan-Kyung Kim, Sang Mun Bae, Hye-Nam Son, Debraj Singh Thoudam, Jung-Eun Kim, Byung-Heon Lee, Rang-Woon Park, and In-San Kim. "Transforming growth factor-β–induced protein (TGFBIp/β ig-h3) activates platelets and promotes thrombogenesis." Blood 114, no. 25 (December 10, 2009): 5206–15. http://dx.doi.org/10.1182/blood-2009-03-212415.

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Abstract Transforming growth factor-β–induced protein (TGFBIp)/βig-h3 is a 68-kDa extracellular matrix protein that is functionally associated with the adhesion, migration, proliferation, and differentiation of various cells. The presence of TGFBIp in platelets led us to study the role of this protein in the regulation of platelet functions. Upon activation, platelet TGFBIp was released and associated with the platelets. TGFBIp mediates not only the adhesion and spread of platelets but also activates them, resulting in phosphatidylserine exposure, α-granule secretion, and increased integrin affinity. The fasciclin 1 domains of TGFBIp are mainly responsible for the activation of platelets. TGFBIp promotes thrombus formation on type I fibrillar collagen under flow conditions in vitro and induces pulmonary embolism in mice. Moreover, transgenic mice, which have approximately a 1.7-fold greater blood TGFBIp concentration, are significantly more susceptible to collagen- and epinephrine-induced pulmonary embolism than wild-type mice. These results suggest that TGFBIp, a human platelet protein, plays important roles in platelet activation and thrombus formation. Our findings will increase our understanding of the novel mechanism of platelet activation, contributing to a better understanding of thrombotic pathways and the development of new antithrombotic therapies.
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Jeong, Seongdo, Sae-Kwang Ku, and Jong-Sup Bae. "Anti-inflammatory effects of pelargonidin on TGFBIp-induced responses." Canadian Journal of Physiology and Pharmacology 95, no. 4 (April 2017): 372–81. http://dx.doi.org/10.1139/cjpp-2016-0322.

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Transforming growth factor β induced protein (TGFBIp) is an extracellular matrix protein expressed in several cell types in response to TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. This study was undertaken to investigate whether PEL can modulate TGFBIp-mediated inflammatory responses in HUVECs and in mice. The anti-inflammatory activities of PEL were determined by measuring permeability, leukocyte adhesion and migration, and activation of proinflammatory proteins in TGFBIp-activated HUVECs and mice. In addition, the beneficial effects of PEL on survival rate in a mouse sepsis model were tested. We found that PEL inhibited TGFBIp-induced barrier disruption, expression of cell adhesion molecules and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed TGFBIp-induced hyperpermeability and leukocyte migration in vivo. These results suggest that PEL possesses anti-inflammatory properties that result in inhibition of hyperpermeability, expression of cell adhesion molecules, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.
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Park, Hee Ho, Hong Nam Kim, Hyelim Kim, Youngbum Yoo, Hyosoo Shin, Eun Young Choi, Jong-Sup Bae, and Wonhwa Lee. "Acetylated K676 TGFBIp as a severity diagnostic blood biomarker for SARS-CoV-2 pneumonia." Science Advances 6, no. 31 (July 2020): eabc1564. http://dx.doi.org/10.1126/sciadv.abc1564.

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The outbreak of the highly contagious and deadly severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as coronavirus disease 2019 (COVID-19), has posed a serious threat to public health across the globe, calling for the development of effective diagnostic markers and therapeutics. Here, we report a highly reliable severity diagnostic biomarker, acetylated 676th lysine transforming growth factor–beta–induced protein (TGFBIp K676Ac). TGFBIp K676Ac was consistently elevated in the blood of patients with SARS-CoV-2 pneumonia (n = 113), especially in patients in the intensive care unit (ICU) compared to non-ICU patients. Patients’ blood samples showed increased cytokines and lymphopenia, which are exemplary indicators of SARS-CoV-2 pneumonia. Treatment with TGFBIp neutralizing antibodies suppressed the cytokine storm. The increased level of TGFBIp K676Ac in ICU patients suggests the promise of this protein as a reliable severity diagnostic biomarker for severe SARS-CoV-2 disease.
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Nam, Sang Min, Yong-Sun Maeng, Eung Kweon Kim, Kyoung Yul Seo, and Helen Lew. "Ex Vivo Expansion of Human Limbal Epithelial Cells Using Human Placenta-Derived and Umbilical Cord-Derived Mesenchymal Stem Cells." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4206187.

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Ex vivo culture of human limbal epithelial cells (LECs) is used to treat limbal stem cell (LSC) deficiency, a vision loss condition, and suitable culture systems using feeder cells or serum without animal elements have been developed. This study evaluated the use of human umbilical cord or placenta mesenchymal stem cells (C-MSCs or P-MSCs, resp.) as feeder cells in an animal/serum-free coculture system with human LECs. C-/P-MSCs stimulated LEC colony formation of the stem cell markers (p63, ABCG2) and secreted known LEC clonal growth factors (keratinocyte growth factor, β-nerve growth factor). Transforming growth factor-β-induced protein (TGFBIp), an extracellular matrix (ECM) protein, was produced by C-/P-MSCs and resulted in an increase in p63+ ABCG2+ LEC colonies. TGFBIp-activated integrin signaling molecules (FAK, Src, and ERK) were expressed in LECs, and TGFBIp-induced LEC proliferation was effectively blocked by a FAK inhibitor. In conclusion, C-/P-MSCs enhanced LEC culture by increasing growth of the LSC population by secreting growth factors and the ECM protein TGFBIp, which is suggested to be a novel factor for promoting the growth of LECs in culture. C-/P-MSCs may be useful for the generation of animal-free culture systems for the treatment of LSC deficiency.
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Sørensen, Charlotte S., Kasper Runager, Carsten Scavenius, Morten M. Jensen, Nadia S. Nielsen, Gunna Christiansen, Steen V. Petersen, Henrik Karring, Kristian W. Sanggaard, and Jan J. Enghild. "Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp." Biochemistry 54, no. 19 (May 6, 2015): 2943–56. http://dx.doi.org/10.1021/acs.biochem.5b00292.

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Dissertations / Theses on the topic "TGFGIp"

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Wang, Feng. "The role of TGFBI in development and cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610043.

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Schwanekamp, Jennifer A. "Dissecting the Roles of Periostin and TGFBI in Cardiovascular Disease." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504803264229101.

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Dixon, James Edward. "Arkadia Family Ubiquitin-Ligases in TGFp Signalling." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486282.

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During vertebrate development and in human pathology the regulation of the level and duration of TGFp signalling is important in controlling cell plasticity, migration, proliferation and apoptosis. My work has focused on Arkadia (Akd) which is a nuclear RING-H2 domain E3 ubiquitin-ligase that enhances Smad2/3-mediated TGFp sign!llling and is essential in mammalian development. Akd has recently been shown to destroy inhibitory (I)-Smads, sensitising cells to TGFp ligands. Here I describe data that demonstrates a second more important mechanism by which Akd enhances and terminates Smad2/3 signalling in which phosphorylated(P)Smad2 and Smad3 are the targets for Akd. I have employed reporter' analyses to investigate the Akd protein domains required for ubiquitination, and highlight�· the requirement ofP-Smad2/3-interaction to activate Smad2/3-mediated signalling. This has lead to the hypothesis that the primary pathway of Akd is through ubiquitination of PSmad2/ 3s, which many co-operate with the function of Akd to destroy I-Smads. Furthermore, I have isolated a second Akd gene (Akd2) in mouse and human, and shown its function is complementary to enhance Smad2/3 signalling in reporter analyses. Moreover, I confirmed the importance of Akd in TGFp signalling by isolating a functional Akd homologue in the invertebrate drosophila melanogaster (termed dAkd). Akd and certain isoforms of Akd2 are ubiquitpusly expressed. I have employed reporter analyses to address the regulation of Akd genes post-transcriptionally and engineered tools to analyse these mechanisms in the�· embryo. My data strongly implicates post-translational regulation of Akd genes to fine-tune TGFp signalling in vivo. My study confirms the central role of the Akd family in regulation of TGFpsignals and highlights the importance of post-transcriptional control ofAkd genes. These data will be important in understanding how the alternate cellular interpretation of TGFp ligands is achieved in many important biological processes.
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Ruiz, Maxime. "Le TGFβI dans la physiopathologie de l'arthrose et son rôle dans l'effet thérapeutique des cellules souches mésenchymateuses." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT008/document.

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L’arthrose est une maladie ostéoarticulaire fréquente et sans traitement curatif. Elle se manifeste par une dégénérescence du cartilage, associée à une altération des autres tissus de l’articulation. Dans ce contexte, les cellules souches mésenchymateuses (CSM) démontrent un effet thérapeutique. Afin d’identifier de nouveaux médiateurs de l’homéostasie articulaire, nous avons analysé le secrétome des CSM en nous focalisant sur les membres de la famille du facteur de croissance transformant β (TGFβ), une voie centrale dérégulée dans l’arthrose.Cette approche nous a permis d’identifier la protéine induite par le TGFβ (TGFβI ou βIGH3), pour laquelle nous avons évalué le rôle dans la différenciation des CSM et comparé l’expression dans les tissus articulaires de patients arthrosiques et de sujets sains.Nous montrons l’importance du TGFβI dans la régulation des processus de différenciation osseuse et chondrogénique des CSM. Nous mettons également en évidence une dérégulation au niveau transcriptionnel et protéique de ce facteur dans le cartilage, l’os sous-chondral ainsi que les CSM de patients arthrosiques. En testant son implication dans l’effet thérapeutique des CSM sur des modèles d’arthrose in vitro et in vivo, nous montrons que la diminution de son expression dans les CSM annule leur effet thérapeutique dans les modèles d’arthrose. Cet effet chondroprotecteur du TGFβI est associé à une inhibition du remodelage osseux et de la calcification des tissus mous articulaires.L’ensemble de nos résultats démontrent l’importance de la régulation de la voie TGFβ, et plus particulièrement du TGFβI, dans l’homéostasie articulaire. En parallèle, nos travaux illustrent le rôle de ce facteur dans l’effet thérapeutique des CSM, et suggèrent que l’altération de son expression dans les CSM de patients arthrosiques soit à l’origine d’une diminution de leur potentiel régénératif
Osteoarthritis (OA) is the most common form of joint diseases without curative treatments. The disease is mainly characterized by the degradation of articular cartilage which is associated with other pathological changes in joint tissues. In this context, mesenchymal stem cells (MSC) have demonstrated a therapeutic effect. In order to identify new mediators involved in articular homeostasis, we analyzed MSC secretome, focusing on the transforming growth factor β (TGFβ) members, a central pathway dysregulated in OA.This approach allows us to identify the TGFβ induced protein (TGFβI or βIGH3). In the present study, we evaluated its role in the differentiation of MSC and compared its expression in articular tissues from OA patients and healthy donors.We highlight the importance of TGFβI in the regulation of differentiation of MSC towards bone and cartilage. We also demonstrate its dysregulation at both transcript and protein level in cartilage, bone and MSC from OA patients. We then evaluated its role in the therapeutic effect of MSC in vitro and in vivo and demonstrated that its decreased expression in MSC is associated with a loss of their therapeutic effect in OA models. The chondroprotective effect of TGFβI is associated with an inhibition of bone remodeling and calcification of soft articular tissues.Together, our results highlight the importance of the TGFβ pathway, and specially of TGFβI regulation, in joint homeostasis. Moreover, our work demonstrates its role in the therapeutic effect of MSC, suggesting that its dysregulation in OA MSC could lead to a decreased regenerative potential
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Touma, Dona. "Molecular differences in sporadic breast cancer in young women (≤ 35-year old) : analysis of TGFBI, DDB2 and MCM5." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9164.

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The aim of this study was to investigate mRNA and protein expression of three genes (Transforming Growth Factor Beta Induced (TGFBI), Damaged-Specific DNA Binding (DDB2) and Minichromosomal Maintenance-5 (MCM5)) in breast cancers. Q-RT-PCR (36 cancers, 8 normal/benign tissues and 9 organoid samples), western blotting (6 cell lines, 6 cancers and 4 normal/benign tissues) and immunohistochemistry (67 breast cancers) were performed, and for TGFBI functional assays (viability, apoptosis and invasion) were carried out in two cell lines (ZR-75-1 and MDA-MB-468) after transient transfection with recombinant TGFBI and vector controls. TGFBI showed reduced mRNA and protein expression in all cancer cell lines relative to HBL-100. The mRNA levels were also significantly lower in breast cancers compared to normal/benign tissues. Immunohistochemistry results showed that 46 / 67 breast cancers were negative or had <1% nuclear staining. There was a significant correlation between TGFBI mRNA levels and patient age; with lower levels expressed in younger women (p=0.04). Higher expression of DDB2 mRNA was observed in ER/PR positive (MCF-7, T47-D and ZR-75-1) compared to ER/PR negative (HBL-100, MDA-MB-231 and MDA-MB-468) cell lines. Higher DDB2 mRNA levels was significantly correlated with ER positive (p=0.04) and grade II (p=0.02) tumours; lower levels were associated with younger patient age (p=0.025). In addition, higher DDB2 protein expression was associated with ER (p=0.001) and PR (p=0.004). Elevated MCM5 mRNA and protein levels were observed in MCF-7 and MDA-MB-231. MCM5 immunoreactivity was significantly correlated with low grade (p=0.02) and ER/PR positive (ER p=0.04 and PR p=0.01) tumours. Transfection with TGFBI had no effect on viability, apoptosis and invasion of ZR-75-1 and MDA-MB-468 cells. In conclusion, the results fail to support the hypothesis of this study, namely that expression of TGFBI, DDB2 and MCM5 could contribute to the more aggressive features of sporadic breast cancers in younger women.
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Morazzo, Sofia Faes. "A potencial função do nodal na endometrose da égua." Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2017. http://hdl.handle.net/10400.5/14039.

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Dissertação de Mestrado Integrado em Medicina Veterinária
Alguns membros da superfamília do TGFβ, tais como o Nodal e o TGFβ1, têm um papel importante na reprodução da égua, sendo que a sua disfunção pode contribuir para patologias uterinas. A endometrose é uma doença degenerativa em que o endométrio normal vai sendo substituído por tecido fibrótico. O objectivo deste estudo consistiu em avaliar: (i) como o Nodal pode influenciar o nível de mRNA dos recetores da PGE2 (EP2; EP4), do TGFβ1 (ALK5; TGFRII), e os próprios (ALK4; ALK7), e ainda, a secreção de prostaglandinas (PGs; PGE2; PGF2α) no endométrio equino; e (ii) como a fase do ciclo éstrico e grau de endometrose pode influenciar estas vias. Endométrios da fase folicular (FF; n=6) e da fase lútea (FL; n=6) foram classificados de acordo com o sistema de Kenney e Doig em categorias I e IIA (n=7), ou IIB e III (n=5). Os explantes foram incubados (24h; 37ºC, 5% CO2) com TNFα, ocitocina ou Nodal (0.1;1;10 ng/mL). A expressão de mRNA foi avaliada por qRT-PCR e a medição de prostaglandinas por ELISA. Em endométrios de categoria I/IIA, o Nodal inibiu a expressão génica de EP2, EP4 e ALK4 e estimulou a de TGFRII, em ambas as fases do ciclo éstrico; e estimulou também os níveis de mRNA de ALK5 e ALK7, apenas na FL. Em endométrios de categoria IIB/III, o Nodal estimulou os níveis de mRNA de EP2, EP4 e ALK5, na FF, e de ALK4 e ALK7, na FL, embora tenha inibido TGFRII e ALK4, na FF, e EP2, EP4, ALK5 e TGFRII na FL. O Nodal na concentração testada mais baixa (0.1ng/mL) estimulou a produção de PGE2 na FF e FL, enquanto que numa concentração superior a inibiu na FF (1ng/mL). A produção de PGF2α foi estimulada na FL com Nodal (0.1 e 10ng/mL). Concluindo, o Nodal parece estar envolvido na endometrose da égua, por afetar negativamente a sinalização da PGE2 anti-fibrótica e positivamente a da citocina pró-fibrótica TGFβ1 e a produção de PGF2α.
ABSTRACT - THE POTENCIAL ROLE OF NODAL IN MAR ENDOMETROSIS - Members of TGFβ superfamily, as Nodal and TGFβ1, have an important role in mare´s reproduction, and as such, their dysfunction may contribute for uterine pathologies. Endometrosis is a degenerative process with a switch of normal endometrium to fibrotic tissue. The aim of the study was to assess: (i) how Nodal may influence the receptors of PGE2 (EP2; EP4), TGFβ1 (ALK5; TGFRII), and its own (ALK4; ALK7) mRNA level and prostaglandin (PG) secretion in equine endometrium; and (ii) estrous cycle and endometrosis influence on these vias. Endometria from follicular (FP; n=6) and mid luteal phases (MLP; n=6) were classified in Kenney and Doig´s categories (cat) I and IIA (n=7), or IIB and III (n=5). Endometrium explants were incubated (24h; 37ºC, 5% CO2) with TNF, oxytocin or Nodal (0.1, 1; 10ng/mL). The mRNA expression was assessed by qRT-PCR and ELISA was used for PG measurement. In cat I/IIA endometria, Nodal down-regulated EP2, EP4 and ALK4 mRNA expression and up-regulated TGFRII in both FP and MLP; and ALK5 and ALK7 only in MLP. In cat IIB/III, Nodal up-regulated mRNA levels of EP2, EP4 and ALK5 in FP, and ALK4 and ALK7 in MLP, whereas it inhibited TGFRII and ALK4 in FP, and EP2, EP4, ALK5 and TGFRII in MLP. Nodal (0.1ng/mL) stimulated PGE2 production in both FF and FL, while at a higher concentration (1ng/mL) it decreased PGE2 in FP. The production of PGF2α increased in MLP with Nodal stimulation (at 0.1 and 10ng/mL). In conclusion, Nodal may be involved in endometrosis in the mare, by impairment of anti-fibrotic PGE2 and pro-fibrotic TGFβ1 signaling pathways and increasing PGF2α production.
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Ween, Miranda Peggy. "The biological role of extracellular matrix in ovarian cancer metastasis." Thesis, 2010. http://hdl.handle.net/2440/65056.

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Ovarian cancer metastasis is characterized by the shedding of malignant cells from the surface of the ovary and their implantation onto the peritoneal surface which lines the abdominal cavity. As the factors promoting this process are poorly understood, we investigated the ovarian cancer–peritoneal interaction by means of in vitro co-culture experiments with ovarian cancer (OVCAR-3, OVCAR-5, and SKOV-3) and peritoneal (LP-9) cells. In this system, we identified by mass spectrometry that levels of transforming growth factor β inducible protein (TGFBIp), periostin, fibronectin, plasminogen activator inhibitor-1, cytokeratins 1, 5, 6C, 9, 10, 14, and 16, transketolase, annexin A2, annexin A6, and elongation factor-2 were modulated as a result of direct contact between peritoneal and ovarian cancer cells or through interactions via shared media. We went on to investigate the functional role of the extracellular matrix (ECM) protein, TGFBIp in ovarian cancer. Immunohistochemistry showed high TGFBIp levels in normal surface ovarian epithelial and peritoneal cells whilst in comparison, TGFBIp levels in primary serous ovarian carcinomas and matching metastatic implants were greatly reduced. In functional in vitro experiments, rTGFBIp significantly increased the motility and invasion of OVCAR-5 and SKOV-3 cells and significantly increased ovarian cancer cell (OVCAR-5, OVCAR-3 and SKOV-3) adhesion to peritoneal (LP-9) cells which was reversed by addition of a neutralizing TGFBIp antibody. We also demonstrated that the increases in OVCAR-5 cell adhesion, motility, and invasion, were independent of the Arg-Gly-Asp (RGD) motif in the C-terminal domain of TGFBIp. We conclude that TGFBIp expressed by peritoneal cells increases the metastatic potential of ovarian cancer cells. TGFBIp is therefore a potential novel therapeutic target against ovarian cancer. Further investigation determined that secreted TGFBIp was processed at both the N- and C-terminal domains during ovarian cancer–peritoneal cell co-culture in the same amino acid range as that of TGFBIp cleaved by plasmin. Plasmin was found to be upregulated within 1 hr of co-culture and TGFBIp processing in the in vitro co-culture system could be blocked by a plasmin inhibitor, 6-aminocaproic acid (-ACA) and a broad spectrum protease inhibitor which inhibits plasmin but not matrix metalloproteinases (MMPs). Furthermore, the processing was not blocked by an MMP inhibitor, GM6001. We therefore conclude that TGFBIp is cleaved by plasmin and not an MMP during peritoneal-ovarian cancer co-culture. In summary, these studies have shown, that when peritoneal cells are allowed to interact with ovarian cancer cells, whether by direct contact or by shared growth media which occurs at different steps of ovarian cancer metastasis, a proteolytic response is triggered. We also investigated the expression of other ECM components in ovarian cancer; the proteoglycan versican, the polysaccharide hyaluronan (HA), and one of its receptors, CD44, in ovarian cancer tissues and their role in the metastatic behaviour of ovarian cancer cells. We found that a higher proportion of serous ovarian carcinoma had high stromal versican when compared with normal ovary and high stromal CD44 when compared with normal and benign serous tumours. Although high stromal versican was positively correlated with high stromal HA, stromal HA was not increased in serous ovarian carcinoma when compared with normal ovary or benign serous tumours. We determined that the assembly of a HA-versican pericellular sheath around ovarian cancer cells could promote the motility of metastatic CD44 expressing OVCAR-5 and SKOV-3 cells, but not by low-metastatic OVCAR-3 cells which lack CD44. The motility of OVCAR-5 and SKOV-3 cells was significantly increased in scratch wound and chemotaxis assays following treatment with recombinant versican. We demonstrated that small HA oligosaccharides (6-10) were able to significantly block formation of pericellular sheath, motility, and invasion of OVCAR-5 cells following treatment with versican. Treatment with exogenous HA increased ovarian cancer cell adhesion to peritoneal cells, and this increase was successfully blocked by the addition of HA oligosaccharides or treatment of the LP-9 monolayer with hyaluronidase. These novel findings indicate that the acquisition of a HA-versican pericellular sheath by ovarian cancer cells may aid their peritoneal dissemination and metastasis. Our results suggest that HA oligosaccharides may be effective at inhibiting the invasion of CD44 positive ovarian cancers and warrants further study as a potential therapy. Overall, the studies in this thesis indicate a very strong role for the tumour microenvironment, and in particular the proteolysis of proteins in the tumour microenvironment. Further investigation will increase our understanding of the mechanisms and pathways involved in the proteolytic cascade which is triggered during ovarian cancer metastasis.
Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproduction Health, 2010
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Peng, Bai-Jing, and 彭百竟. "Efficient Microwave-Assisted Palladium-Catalyzed Allylation of 2,3-Disubstituted Indoles with Allylic Alcohols." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/tgfg45.

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碩士
高雄醫學大學
藥學研究所
102
A principal goal of organometallic chemistry is the catalytic synthesis of organic compounds by using the chemistry of organic ligands covalently bound to transition metals. The palladium-catalyzed allylation of N-nucleophiles was an established and efficient method, which has been widely applied to organic chemistry. Utilizing the prevalence of indole nucleus in biologically active compounds, the direct C3-functionalization or N-functionalization of 2,3-disubstituted indoles represent an important problem. In this study, the palladium-catalyzed 2,3-disubstitued indoles with allylic alcohols in benzene was investigated under various conditions. Furthermore, microwave has been widely applied to shorten reaction time in organic synthesis. Herein, we develop a new highly selective method. This method provide particularly convenient, efficient, and selective.
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De, la Mare Jo-Anne, Tamarin Jurgens, and Adrienne Lesley Edkins. "Extracellular Hsp90 and TGFP regulate adhesion, migration and anchorage independent growth in a paired colon cancer cell line model." 2017. http://hdl.handle.net/10962/59920.

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Tumour metastasis remains the major cause of death in cancer patients and, to date, the mechanism and signalling pathways governing this process are not completely understood. The TGF-ß pathway is the most commonly mutated pathway in cancer, however its role in cancer progression is controversial as it can function as both a promoter and a suppressor of metastasis. Although previous studies have suggested a role for the molecular chaperone Hsp90 in regulating the TGF-ß pathway, the level at which this occurs as well as the consequences in terms of colon cancer metastasis are unknown.
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Book chapters on the topic "TGFGIp"

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Becker, Jürgen. "Pediatric Neuroblastoma: Role of TGFBI (Keratoepithelin)." In Pediatric Cancer, 229–36. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2418-1_23.

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Hei, Tom K., Yongliang Zhao, Hongning Zhou, and Vladimir Ivanov. "Mechanism of Radiation Carcinogenesis: Role of the TGFBI Gene and the Inflammatory Signaling Cascade." In Advances in Experimental Medicine and Biology, 163–70. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0254-1_13.

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Hinz, Steffen C., Adrian Elter, Julius Grzeschik, Jan Habermann, Bastian Becker, and Harald Kolmar. "Simplifying the Detection of Surface Presentation Levels in Yeast Surface Display by Intracellular tGFP Expression." In Methods in Molecular Biology, 211–22. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9853-1_12.

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Stenvang, Marcel, Maria Andreasen, Jan Johannes Enghild, and Daniel E. Otzen. "The Molecular Basis For TGFBIp-Related Corneal Dystrophies." In Bio-nanoimaging, 179–88. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-394431-3.00016-x.

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Röcken, C., A. Roessner, J. Rüschoff, and B. Stix. "Corneal Dystrophy Caused by a Novel Mutation of the TGFBI Gene." In Amyloid and Amyloidosis, 438–39. CRC Press, 2004. http://dx.doi.org/10.1201/9781420037494.ch150.

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"Corneal Dystrophies." In Medical Atlas of Cornea and External Diseases in Middle Eastern Populations, 251–64. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-6937-5.ch008.

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Corneal dystrophies have classically referred to inherited, bilateral disease without systemic findings, although there are several exceptions to this definition. Hereditary pattern is not present in most patients with epithelial basement membrane dystrophy (EBMD). Unilateral corneal changes may be found in some patients with posterior polymorphous corneal dystrophy (PPCD). TGFBI gene mutation (p.His572del) is associated with a unilateral, late-onset variant of lattice corneal dystrophy. Among all dystrophies, macular corneal dystrophy and posterior amorphous corneal dystrophy are associated with decreased corneal thickness. The International Committee for Classification of Corneal Dystrophies (IC3D) was created in 2005 to revise the corneal dystrophy nomenclature and create a current and accurate corneal dystrophy classification system. Evidential categories were created in the IC3D classification for reflecting the natural evolution of a corneal dystrophy and indicate the level of evidence supporting the existence of a given dystrophy.
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Stix, B., J. Rüschoff, A. Roessner, and C. Röcken. "Corneal Dystrophy Caused by a Novel Mutation of the TGFBI Gene: A Case Report." In Amyloid and Amyloidosis, 438–39. CRC Press, 2004. http://dx.doi.org/10.1201/9781420037494-156.

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Conference papers on the topic "TGFGIp"

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Seo, Jun-Young, Hae Uk Jung, Hye-Nam Son, Soyoun Kim, Eunsung Jun, Ju-Ock Nam, Jung-Eun Kim, and In-San Kim. "Abstract 11: Absence of TGFBI favors tumor angiogenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-11.

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Ruiz, Maxime, Marie Maumus, Karine Toupet, Guillaume Fonteneau, Yves-Marie Pers, Xavier Houard, Francis Berenbaum, Christian Jorgensen, and Danièle Noël. "04.03 Tgfβ-induced protein (tgfβi) is dysregulated in osteoarthritis." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211051.3.

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Nayeem, N. M., and J. E. Rice. "A New Approach to Online Testing of TGFSOP-based Ternary Toffoli Circuits." In 2012 IEEE 42nd International Symposium on Multiple-Valued Logic (ISMVL). IEEE, 2012. http://dx.doi.org/10.1109/ismvl.2012.57.

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Jiao, Yunjuan, Weixing Zhao, Xin Dong, Xiaoyu Yang, Zheying Zhang, Yongxia Wang, Jing Cui, Zhiqiang Qin, Wancai Yang, and Wancai Yang. "Abstract 4689: The alterations and significance of hMLH1 and TGFβII receptor expression during esophageal carcinogenesis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4689.

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Bragado, Paloma, Yeriel Estrada, Maria Soledad Sosa, Denis M. Schewe, Carla Capobianco, Kateri Moore, Hernan G. Farina, and Julio Aguirre-Ghiso. "Abstract 5234: Microenvironmental signals dictate disseminated tumor cells (DTCs) fate through regulation of TGFβII and p38α." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5234.

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Rudra-Ganguly, Nandini, Daulet Satpayev, Christine Lowe, Liping Hu, Bally Randhawa, Mi Sook Chang, Alla Verlinsky, et al. "Abstract 1086: Discoidin domain receptor 1 contributes to tumorigenesis through modulation of TGFBI expression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1086.

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Bissey, Pierre-Antoine, Jeff W. Bruce, Jacqueline Law, Kenneth W. Yip, and Fei-Fei Liu. "Abstract 5038: The repression of the extracellular matrix protein TGFBI induces chemoresistance in nasopharyngeal carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5038.

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Lee, Jong-Joo, Joo-Hong Park, Keunhee Park, Min-Ji Song, Wook-Jin Yang, and Hyoung-Pyo Kim. "Abstract 2211: Accessible chromatin structure permits factors Sp1 and Sp3 to regulate human TGFBI gene expression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2211.

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Liu, Yen-Nien, Wei-Yu Chen, Yuan-Chin Tsai, Hsiu-Lien Yeh, Florent Suau, and Jiaoti Huang. "Abstract A031: Androgen deprivation therapy-induced TGFBI signaling promotes EMT and bone metastasis of prostate cancer." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a031.

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Muramatsu, Tomoki, Taku Sato, Minoru Tanabe, and Johji Inazawa. "Abstract 163: Identification and characterization of TGFBI in circulating tumor cell subline from pancreatic cancer cell line." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-163.

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Reports on the topic "TGFGIp"

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Anderson, Ryan M. Functional Analysis of TGF-alpha/beta Regulated Protein (TGFRP) in Breast Cancer Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada412099.

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Xu, Mingna, Yaru Guo, and Song Yang. Prognostic and Clinicopathological Significance of TGFBI Expression in Cancer Patients: A Meta-Analysis and Bioinformatics Validation. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0089.

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