Relevant bibliographies by topics / PECAM1

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Academic literature on the topic 'PECAM1'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "PECAM1"

1

Jamroziak, Krzysztof, Zofia Szemraj, Janusz Szemraj, Olga Grzybowska-Izydorczyk, Katarzyna Oszajca, Grazyna Janiszewska, Ewa Balcerczak, Marek Mirowski, Halina Urbanska-Rys, and Tadeusz Robak. "Polymorphisms in CD31/PECAM-1 and CD38 Genes Are Associated with Susceptibility to Multiple Myeloma." Blood 112, no. 11 (November 16, 2008): 5113. http://dx.doi.org/10.1182/blood.v112.11.5113.5113.

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Abstract Interactions with bone marrow microenvironment play a major role in the control of multiple myeloma (MM) growth and survival. MM clonal plasma cells co-express high levels of a signaling receptor CD38 and its ligand, the platelet endothelial adhesion molecule-1, CD31//PECAM-1. Homotypic and heterotypic interactions through these adhesion molecules (CD31/CD31, CD38/CD31 and CD38/hyaluronate interactions) may be involved in the pathogenesis of MM. The objective of this study was to investigate whether inherited variants in CD31/PECAM-1 and CD38 genes influence on susceptibility to MM. A total of 189 Caucasian patients with MM and 209 healthy controls were genotyped with the use of PCR-based methods. Genotyping was performed to assess allelic frequencies of three non-synonymous single nucleotide polymorphisms (SNPs) in CD31/PECAM1 gene including 373C>G (Leu 125Val), 1688G>A (Ser563Asn) and 2008A>G (Arg670Gly) as well as two SNPs in CD38 gene including 184C>G in intron 1 and non-synonymous 418C>T (Arg140Trp) in exon 3. Analyzing the prevalence of investigated genetic variants, we found that allelic frequencies of two SNPs in CD31/PECAM-1 gene and intron 1 184C>G SNP in CD38 gene differed significantly between MM patients and controls. Concerning CD31/PECAM-1 SNPs, the carriership of 373G allele was associated with the relative risk of MM of 4.5 (p=8×10−10), while in carriers of 1688A allele the relative risk of MM reached 3.0 (p=2×10−6). Regarding CD38 gene, compared to wild-type 184C-allele carriers, the carriers of variant 184G-allele had 3.4-fold increased risk of MM (p=1×1−9). In conclusion, the results of this study suggest that inherited variants in ligand-receptor CD31/PECAM1 - CD38 system contribute to the genetic susceptibility to MM in Caucasians.
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Cramer, EM, G. Berger, and MC Berndt. "Platelet alpha-granule and plasma membrane share two new components: CD9 and PECAM-1." Blood 84, no. 6 (September 15, 1994): 1722–30. http://dx.doi.org/10.1182/blood.v84.6.1722.1722.

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Abstract CD9 (p24) and PECAM1 (CD31) antigens are well-defined components of the platelet plasma membrane. Both are integral glycoproteins (GPs) implicated in the adhesive and aggregative properties of human platelets. In the present report, we have investigated their subcellular localization using immunoelectron microscopy. The monospecificity of the two polyclonal antibodies used was confirmed by immunoblotting. On normal resting platelets, immunolabeling for CD9 and PECAM1 was found lining the plasma membrane and the luminal face of the open canalicular system. Some labeling was also consistently found on the alpha-granule limiting membrane. This was confirmed by double labeling experiments in which fibrinogen and von Willebrand factor (vWF) were used as alpha-granule markers. CD9 and PECAM-1 were found lining the membrane of the same granules that contained fibrinogen and vWF in their matrix. CD9 and PECAM-1 thus appear to have an intracellular distribution identical to GPIIb-IIIa, a major aggregation platelet receptor. To rule out a cross-reactivity of the two polyclonal antibodies with GPIIb/IIIa, we studied PECAM1 and CD9 expression on the platelets from a patient with type I Glanzmann's thrombasthenia whose platelets are devoid of GPIIb/IIIa. The same pattern of labeling was observed for both antigens as for normal platelets. Normal platelets were further observed after stimulation by agonists that either fail to induce (ADP) or induce granule secretion (thrombin). After treatment with ADP, platelets changed shape and centralized their granules; the plasma membrane immunolabeling remained unchanged; and gold particles were still found decorating the periphery of the centralized alpha- granules. After thrombin treatment, alpha-granules fused with the platelet membrane and secretion occurred. A significant increase of labeling was then observed on the platelet surface. From these results we conclude that the alpha-granule membrane contains two additional receptors in common with the plasma membrane. This suggests that alpha- granule membrane receptors may originate from a dual mechanism: direct targeting from the Golgi complex in megakaryocytes (for alpha-granule- specific receptors such as P-selectin) or by endocytosis from the plasma membrane (for proteins distributed in the two compartments).
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3

Cramer, EM, G. Berger, and MC Berndt. "Platelet alpha-granule and plasma membrane share two new components: CD9 and PECAM-1." Blood 84, no. 6 (September 15, 1994): 1722–30. http://dx.doi.org/10.1182/blood.v84.6.1722.bloodjournal8461722.

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CD9 (p24) and PECAM1 (CD31) antigens are well-defined components of the platelet plasma membrane. Both are integral glycoproteins (GPs) implicated in the adhesive and aggregative properties of human platelets. In the present report, we have investigated their subcellular localization using immunoelectron microscopy. The monospecificity of the two polyclonal antibodies used was confirmed by immunoblotting. On normal resting platelets, immunolabeling for CD9 and PECAM1 was found lining the plasma membrane and the luminal face of the open canalicular system. Some labeling was also consistently found on the alpha-granule limiting membrane. This was confirmed by double labeling experiments in which fibrinogen and von Willebrand factor (vWF) were used as alpha-granule markers. CD9 and PECAM-1 were found lining the membrane of the same granules that contained fibrinogen and vWF in their matrix. CD9 and PECAM-1 thus appear to have an intracellular distribution identical to GPIIb-IIIa, a major aggregation platelet receptor. To rule out a cross-reactivity of the two polyclonal antibodies with GPIIb/IIIa, we studied PECAM1 and CD9 expression on the platelets from a patient with type I Glanzmann's thrombasthenia whose platelets are devoid of GPIIb/IIIa. The same pattern of labeling was observed for both antigens as for normal platelets. Normal platelets were further observed after stimulation by agonists that either fail to induce (ADP) or induce granule secretion (thrombin). After treatment with ADP, platelets changed shape and centralized their granules; the plasma membrane immunolabeling remained unchanged; and gold particles were still found decorating the periphery of the centralized alpha- granules. After thrombin treatment, alpha-granules fused with the platelet membrane and secretion occurred. A significant increase of labeling was then observed on the platelet surface. From these results we conclude that the alpha-granule membrane contains two additional receptors in common with the plasma membrane. This suggests that alpha- granule membrane receptors may originate from a dual mechanism: direct targeting from the Golgi complex in megakaryocytes (for alpha-granule- specific receptors such as P-selectin) or by endocytosis from the plasma membrane (for proteins distributed in the two compartments).
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4

Fei, Hongjun, Songchang Chen, and Chenming Xu. "Interactive Verification Analysis of Multiple Sequencing Data for Identifying Potential Biomarker of Lung Adenocarcinoma." BioMed Research International 2020 (October 1, 2020): 1–18. http://dx.doi.org/10.1155/2020/8931419.

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Background. Lung adenocarcinoma (LUAD) comprises around 40% of all lung cancers, and in about 70% of patients, it has spread locally or systemically when first detected leading to a worse prognosis. Methods. We filtered out differentially expressed genes (DEGs) based on the RNA sequencing data in the Gene Expression Omnibus database and verified and deeply analyzed screened DEGs using a combined bioinformatics approach. Results. Expressions of 11,143 genes in 694 nontumor lung tissues and LUAD cases from 8 independent laboratories were analyzed; 188 mRNAs were identified as differentially expressed genes (DEGs). A PPI network constructed with 188 DEGs screened out 8 hub DEGs (CDH5, PECAM1, VWF, CLDN5, COL1A1, MMP9, SPP1, and IL6) which highly interconnected with other nodes. The expression levels of 8 hub genes in LUAD and control were assessed in the Oncomine database, and the results were consistent. The survival curves of 8 hub genes showed that their expressions are significantly related to the prognosis of lung cancer and LUAD patients except for IL6. Since the expression of IL6 is nonspecific and highly sensitive, we choose the other 7 hub genes we had verified to do the next analysis. Mutual exclusivity or cooccurrence analysis of 7 hub genes identified a tendency towards cooccurrence between CDH5, PECAM1, and VWF in LUAD. The coexpression profiles of CDH5 in LUAD were identified, and we found that PECAM1 and VWF coexpressed with CDH5. Immunohistochemistry and RT-PCR analysis showed that higher levels of CDH5, PECAM1, and VWF were expressed in normal lung tissues but a low or undetectable level was found in LUAD tissues. Conclusions. Taken together, we speculate that CDH5, PECAM1, and VWF played an important role in LUAD.
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Chen, Zhengshan, Huimin Geng, Maike Buchner, Lars Klemm, Kaveh Hemati, Seyedmehdi Shojaee, Mak W. Tak, et al. "ITIM-Containing Inhibitory Receptors Are Required to Balance Oncogenic Signaling Strength in Ph+ ALL." Blood 120, no. 21 (November 16, 2012): 291. http://dx.doi.org/10.1182/blood.v120.21.291.291.

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Abstract Abstract 291 Background: ITIM (immunoreceptor tyrosine-based inhibition motifs) motifs in the cytoplasmic tail of inhibitory receptors recruit inhibitory phosphatases. Upon ligation, these phosphatases inhibit signal transduction from tyrosine kinases including BCR-ABL1. ITIM-receptors are critical in the control of immune responses of B and T cells. Surprisingly, we found that a number of inhibitory ITIM-receptors are expressed at very high levels on the surface of patient-derived Ph+ acute lymphoblastic leukemia (ALL) cells compared to normal pre-B cells. In this study, three central ITIM-receptors were identified and analyzed for their function in Ph+ALL: PECAM1 (platelet/endothelial cell adhesion molecule 1/CD31), CD300A and LAIR1 (leukocyte-associated immunoglobulin-like receptor 1). Results: Microarray data showed mRNA levels of PECAM1, CD300A and LAIR1 were about 5-fold higher (p<0.005) in Ph+ ALL (n=15) than normal human pre-B cells (n=8). We confirmed this difference at the protein level by flow cytometry studying patient-derived Ph+ALL (n=11) and pre-B cells from normal bone marrow samples (n=2). These findings seem counterintuitive because signaling from these receptors would attenuate the signaling strength downstream of BCR-ABL1. Importantly, we found that high expression levels of ITIM-receptors are predictive of poor outcome in two clinical trials. In the COG trial (P9906; n=207) for children with high-risk ALL, we found that mRNA levels of PECAM1, CD300A and LAIR1 at diagnosis positively correlated with early minimal residual disease (MRD) findings on day 29 (p<0.0005), and negatively correlated with overall survival (OS) rate (p<0.02) or relapse free survival (RFS) rate (p<0.05). In ECOG trial E2993 for adults with ALL (n=215), we found that PECAM1 mRNA level in ALL patients negatively correlated with OS rate (p=0.0285). These results collectively indicate that inhibitory ITIM-receptors contribute to the course of human ALL disease. To study the role of PECAM1, CD300A and LAIR1 in Ph+ ALL in genetic experiments, we transformed pre-B cells from Pecam1−/−, Cd300a−/− and wildtype mice with BCR-ABL1. Compared to wildtype ALL cells, Pecam1−/− or Cd300a−/− ALL cells showed increased ROS levels. Consistent with higher levels of ROS, the Pecam1−/− and Cd300a−/− ALL cells accumulate p53, p21 and p27 protein, are prone to G0/G1cell cycle arrest and cellular senescence. Colony forming assays revealed that Pecam1- and cd300-deficient leukemia cells also formed 10-fold fewer colonies in methyl cellulose compared to wildtype ALL cells (p<0.0001). For Lair1, we performed genetic loss-of-function experiments by inducible activation of Cre in Lair1fl/fl leukemia cells. Inducible deletion of Lair1 resulted in drastic upregulation of ROS, accumulation of Arf, p53 and p21, cellular senescence and subsequent leukemia cell death. Transplanting Lair1fl/fl ALL cells into NOD-SCID mice, we found that Lair1 deletion resulted in rapid leukemia regression and prolonged survival of recipient mice. Leukemia cell death caused by Lair1 deletion could be rescued by overexpression of the inhibitory phosphatase Ptpn6 (SHP1) indicating that the protective effect of the Lair1 is indeed mediated by ITIM-based recruitment of inhibitory phosphatases. To test whether these findings are also relevant to other subtypes of ALL, we used a model for NRASG12D-driven ALL. BCR-ABL1 (∼25%) and NRAS lesions (∼30%) account for more than half of cases of ALL. Consistent with our findings with BCR-ABL1, NRASG12D Pecam1−/−, Cd300a−/−leukemia cells were prone to G0/G1 cell cycle arrest and cellular senescence (p<0.01). Conclusion: These results indicated that inhibitory ITIM-receptors are critical regulators of oncogenic signaling strength in BCR-ABL1 and NRAS-driven ALL. Deficiency of ITIM-receptor signaling can be rescued by overexpression of the PTPN6 phosphatase. These findings are of particular relevance, because they identify ITIM-receptors and inhibitory phosphatases as members of a fundamentally novel class of therapeutic targets. The concept of pharmacological perturbance of oncogenic signaling equilibrium in leukemia cells by inhibition (e.g. TKI-treatment) or exaggeration of signaling strength (e.g. blockade of ITIM-receptors) may lead to the discovery of multiple additional therapeutic targets and broaden our repertoire of currently available pathways for therapeutic intervention. Disclosures: No relevant conflicts of interest to declare.
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Wang, Xinyu, Jiaojiao Yang, and Xueren Gao. "Identification of key genes associated with lung adenocarcinoma by bioinformatics analysis." Science Progress 104, no. 1 (January 2021): 003685042199727. http://dx.doi.org/10.1177/0036850421997276.

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Lung adenocarcinoma (LUAD) is the most common histological type of lung cancer, comprising around 40% of all lung cancer. Until now, the pathogenesis of LUAD has not been fully elucidated. In the current study, we comprehensively analyzed the dysregulated genes in lung adenocarcinoma by mining public datasets. Two sets of gene expression datasets were obtained from the Gene Expression Omnibus (GEO) database. The dysregulated genes were identified by using the GEO2R online tool, and analyzed by R packages, Cytoscape software, STRING, and GPEIA online tools. A total of 275 common dysregulated genes were identified in two independent datasets, including 54 common up-regulated and 221 common down-regulated genes in LUAD. Gene Ontology (GO) enrichment analysis showed that these dysregulated genes were significantly enriched in 258 biological processes (BPs), 27 cellular components (CCs), and 21 molecular functions (MFs). Furthermore, protein-protein interaction (PPI) network analysis showed that PECAM1, ENG, KLF4, CDH5, and VWF were key genes. Survival analysis indicated that the low expression of ENG was associated with poor overall survival (OS) of LUAD patients. The low expression of PECAM1 was associated with poor OS and recurrence-free survival of LUAD patients. The cox regression model developed based on age, tumor stage, ENG, PECAM1 could effectively predict 5-year survival of LUAD patients. This study revealed some key genes, BPs, CCs, and MFs involved in LUAD, which would provide new insights into understanding the pathogenesis of LUAD. In addition, ENG and PECAM1 might serve as promising prognostic markers in LUAD.
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Minchenko, Dmytro O., D. O. Tsymbal, O. P. Yavorovsky, N. V. Solokha, and O. H. Minchenko. "Expression of genes encoding IGFBPs, SNARK, CD36, and PECAM1 in the liver of mice treated with chromium disilicide and titanium nitride nanoparticles." Endocrine Regulations 51, no. 2 (April 25, 2017): 84–95. http://dx.doi.org/10.1515/enr-2017-0008.

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AbstractObjective. The aim of the present study was to examine the effect of chromium disilicide and titanium nitride nanoparticles on the expression level of genes encoding important regulatory factors (IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK/NUAK2, CD36, and PECAM1/CD31) in mouse liver for evaluation of possible toxic effects of these nanoparticles.Methods. Male mice received 20 mg chromium disilicide nanoparticles (45 nm) and titanium nitride nanoparticles (20 nm) with food every working day for 2 months. The expression of IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver was studied by quantitative polymerase chain reaction.Results. Treatment of mice with chromium disilicide nanoparticles led to down-regulation of the expression of IGFBP2, IGFBP5, PECAM1, and SNARK genes in the liver in comparison with control mice, with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3 and CD36 genes was increased in mouse liver upon treatment with chromium disilicide nanoparticles. We have also shown that treatment with titanium nitride nanoparticles resulted in down-regulation of the expression of IGFBP2 and SNARK genes in the liver with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3, IGFBP4, and CD36 genes was increased in the liver of mice treated with titanium nitride nanoparticles. Furthermore, the effect of chromium disilicide nanoparticles on IGFBP2 and CD36 genes expression was significantly stronger as compared to titanium nitride nanoparticles.Conclusions. The results of this study demonstrate that chromium disilicide and titanium nitride nanoparticles have variable effects on the expression of IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver, which may reflect the genotoxic activities of the studied nanoparticles.
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Gumina, Richard J., Nancy E. Kirschbaum, P. Nagesh Rao, Peter vanTuinen, and Peter J. Newman. "The Human PECAM1 Gene Maps to 17q23." Genomics 34, no. 2 (June 1996): 229–32. http://dx.doi.org/10.1006/geno.1996.0272.

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Leclerc, Michel. "Platelets, Pecam1 Gene, Thromboxane Genes, in Invertebrates." International Journal of Research Studies in Medical and Health Sciences 5, no. 4 (2020): 12–14. http://dx.doi.org/10.22259/ijrsmhs.0504004.

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Корытина, Г. Ф., Ю. Г. Азнабаева, М. Ю. Темнов, Ш. Р. Зулькарнеев, Л. З. Ахмадишина, О. В. Кочетова, Ш. З. Загидуллин, and Т. В. Викторова. "Molecular mechanisms of phenotypic heterogeneity of chronic obstructive pulmonary disease: the role of JAK / STAT-, NFKB1-signaling pathway and inflammatory response molecules." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 8(217) (August 31, 2020): 100–104. http://dx.doi.org/10.25557/2073-7998.2020.08.100-104.

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Хроническая обструктивная болезнь легких (ХОБЛ) - это многофакторное хроническое воспалительное заболевание респираторной системы. Одной из причин трудностей в идентификации маркеров ХОБЛ является фенотипическая гетерогенность. Цель - идентификация новых молекулярных маркеров патогенетических изменений, связанных с фенотипической гетерогеностью ХОБЛ на основе анализа профиля экспрессии генов вовлеченных в развитие иммунного ответа в мононуклеарных клетках периферической крови и анализа ассоциации полиморфных вариантов новых кандидатных генов с развитием ХОБЛ. Проведен сравнительный анализ профиля экспрессии панели 84 генов, кодирующих цитокины, хемокины в PBMC пациентов с различными фенотипами ХОБЛ: с частыми обострениями N=10 и редкими обострениями N=10 и контрольной группе N=10. Для анализа ассоциации использовали образцы ДНК больных ХОБЛ (N=601) и контроля (N=617), методом ПЦР в реальном времени проведен анализ 56 полиморфных локусов генов JAK/STAT-, NFKB1-сигнального путей, кодирующих белки, вовлеченные в реализацию реакций иммунного ответа и воспаления. Выявлены значимые изменения профиля экспрессии ряда генов в группе больных ХОБЛ с частыми обострениями. Впервые получены данные по вкладу полиморфных локусов генов JAK1, JAK3, STAT3, ICAM1, PECAM1, SAA1, NFKB1, IL17A, CCR2, CCR6, CCL8, CRP, CX3CL1, CXCR2, CXCR1, TNFRSF1A, IL20, IL19, в развитие данного заболевания. Выявлены специфические генетические маркеры развития фенотипа с частыми обострениями: CXCR2, TNFRSF1B, CCR6, TNF, IL1B, IL10, JAK3, PECAM1. Установлена ассоциация полиморфных вариантов генов TNFRSF1B, TNFRSF1A, CCL23, CXCR2, JAK1, NFKB1, PECAM1, ICAM1, STAT1, LTA, CD14, CXCL12, CCL20, ADIPOR1 и CX3CR1 с показателями функции внешнего дыхания. Определена взаимосвязь аллельных вариантов генов: IL17A, JAK1, JAK3, NFKB1, CCL5, CCL11, CCL17, CXCL8, TNFRSF1A, CX3CL1, CCL8, CCR6, CXCR2, IL19, IL20 с индексом курения. Chronic obstructive pulmonary disease (COPD) is a multifactorial heterogeneous chronic inflammatory disease of the respiratory system predominantly affecting the lower respiratory pathways and the lung parenchyma. One of the reason for difficulties in identifying of COPD markers is phenotypic heterogeneity. The goal of the study is the identification of new molecular markers of pathogenetic changes associated with phenotypic heterogeneity of COPD based on the analysis of the expression profile of genes involved in the development of the immune response in peripheral blood mononuclear cells and analysis of the association of polymorphic variants of new candidate genes with COPD. Methods: to identify differential gene expression in COPD we performed expression profiling of 84 cytokines and chemokines genes in peripheral blood samples from COPD (N=10 with frequent exacerbation phenotype, N=10 rare exacerbation phenotype) and N=10 smoking controls. RNA was isolated from PBMCs, and gene expression was assessed using RT2 Profiler PCR Arrays «Human Cytokines & Chemokines PCR Array»» (Qiagen, Valencia, CA, USA). 56 SNPs of JAK / STAT-, NFKB1-signaling pathway and inflammatory response molecules genes were genotyped by the real-time polymerase chain reaction (TaqMan assays) in a case-control study (601 COPD patients and 617 controls). Results. Significant changes were revealed in the expression profile of several genes in “frequent exacerbator» COPD phenotype. The results indicate a down-regulation of inflammatory molecules in “frequent exacerbator» COPD phenotype. For the first time, we indicated the contribution of JAK1, JAK3, STAT3, ICAM1, PECAM1, SAA1, NFKB1, IL17A, CCR2, CCR6, CCL8, CRP, CX3CL1, CXCR2, CXCR1, TNFRSF1A, IL20, IL19 genes polymorphisms to COPD. Specific genetic markers of “frequent exacerbator” COPD phenotype have been identified, which are modifiers of COPD progression, including polymorphic loci of the CXCR2, TNFRSF1B, CCR6, TNF, IL1B, IL10, JAK3, PECAM1 genes. A significant genotype-dependent variation of lung function parameters was observed for CXCR2, JAK1, NFKB1, PECAM1, ICAM1, STAT1, LTA, CD14, CXCL12, CCL20, ADIPOR1 and CX3CR1 genes. The relationship of IL17A, JAK1, JAK3, NFKB1, CCL5, CCL11, CCL17, CXCL8, TNFRSF1A, CX3CL1, CCL8, CCR6, CXCR2, IL19, IL20 genes with smoking pack-years was found.
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Dissertations / Theses on the topic "PECAM1"

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Roberts, Samantha. "PECAM-1 expression by mesenchymal stromal cells is regulated by Notch signalling." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/pecam1-expression-by-mesenchymal-stromal-cells-is-regulated-by-notch-signalling(1259846d-df3b-43c3-8ce0-d25135ccdedd).html.

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Mesenchymal stromal cells (MSCs) reside within the perivascular niche and have been shown in vivo to facilitate vascular repair. Previous in vitro studies, have demonstrated the potential of MSCs to differentiate towards an endothelial lineage, when cultured at high cell density; but the characterisation of these cells and the mechanisms directing this important differentiation effect are ill-defined. To resemble a three-dimensional (3D) cellular environment, MSCs were cultured as spheroids and the endothelial characteristics of these cells determined. MSCs cultured as spheroids significantly increased their expression of the endothelial markers; PECAM-1, Tie2, VE-cadherin and vWF, when compared to MSCs cultured in close cell contact as a two-dimensional (2D) monolayer. In addition, MSCs cultured as 3D spheroids behaved as functional endothelial cells in vitro; including the ability to uptake low-density lipoproteins, secretion of nitric oxide and the ability to form network-like structures. MSC spheroids exhibited significantly increased levels of Notch signalling, compared to 2D MSCs in close cell contact, which caused a significant decrease in the endothelial characteristics when inhibited. Conversely, activation of Notch signalling caused a significant and specific increase in the expression of PECAM-1, which was regulated by the Notch ligands Jagged1 and DLL4. Thus, Notch signalling is a crucial pathway that controls PECAM-1 expression and regulates the angiogenic fate of MSCs within spheroids. This study has therefore identified an efficient culture model and key signalling mechanism which may be used to induce MSCs towards an angiogenic fate for vascular repair and regeneration therapies.
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Magnuson, Shelby M. "Descriptive analysis of pecan cultivars, a comparison of raw and roasted pecans, and how pecan flavor changes over time." Thesis, Kansas State University, 2015. http://hdl.handle.net/2097/20104.

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Master of Science
Food Science Institute - Human Nutrition
Kadri Koppel
Pecan [Carya illinoinensis(Wangenh.) K. Koch] is a native North American nut tree that has progressed into a significant agricultural crop. Flavor characteristics were evaluated for sixteen pecan cultivars: ‘Giles’, ‘Hirschi’, ‘Maramec’, ‘Oswego’, ‘Lakota’, ‘Chetopa’, ‘Colby’, ‘Witte’, ‘Dooley’, ‘Kanza’, ‘Pawnee’, ‘Stuart’, ‘Chickasaw’, ‘Peruque’, ‘Major’, and ‘Henning’ using descriptive sensory analysis. A trained panel consisting of six panelists first developed a vocabulary for the raw pecans and scored the intensities of the samples for 20 flavor attributes. Results showed that the sixteen samples differed significantly (P ≤ 0.05) on 10 of the attributes. ‘Giles’, ‘Lakota’, and ‘Pawnee’ differed from the other 13 cultivars for the majority of the attributes. The remaining thirteen cultivars showed few differences in individual attribute ratings, but did show differences when mapped using multivariate techniques indicating as many as two clusters of pecan cultivars based on flavor. The same sixteen cultivars were then roasted and evaluated using descriptive sensory analysis by the same trained panel using the same 20 flavor attributes. Three texture attributes were also evaluated. These results were compared to the results from the raw pecans. Results showed that 4 attributes differed significantly across all cultivars when raw and roasted flavor was compared. Ten of the flavor attributes had higher intensities for the roasted pecans than for the raw pecans. Most of these attributes fell within the categories of ‘nutty’ and ‘sweet’. When pecans were roasted many flavor attributes were intensified, as compared to when they were raw. How the flavor of the sixteen cultivars changed over a 12 month period was then evaluated. Raw pecans were evaluated when fresh, at 3 months, 6 months, 9 months, and 12 months by descriptive sensory analysis. A trained six member panel evaluated four flavor attributes at all five time points. Results showed that bitter had the highest intensity scores for all 16 cultivars at all 5 time points. Rancidity increased over time and sweetness decreased over time for all attributes. The results from these studies can be used as a baseline for future pecan research.
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Hunter, Martha, Mette Petersen, Melinda McElween, and Michael Kilby. "Population Dynamics of Pecan Aphids and Their Green Lacewing Predators in Insecticide-Free Pecans." College of Agriculture, University of Arizona (Tucson, AZ), 2000. http://hdl.handle.net/10150/223847.

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Field surveys of aphids and their natural enemies were conducted in a 30 acre unsprayed block of 'Wichita' pecans in Southeastern Arizona (FICO, Sahuarita) during the growing seasons of 1997, 1998, and 1999. Each season showed a different pattern of aphid population development. In general, numbers of the more damaging black pecan aphid, Melanocallis caryaefoliae were always lower than those of the blackmargined pecan aphid Monellia caryella and no serious aphid damage by either species was observed. Two species of green lacewings were the dominant natural enemies in the orchard, and eggs could be found throughout the season.
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Kilby, Michael W. "Evaluation of Temik (aldicarb) for the Control of the Pecan Aphid Complex for Pecans Grown in Arizona." College of Agriculture, University of Arizona (Tucson, AZ), 2000. http://hdl.handle.net/10150/223856.

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This experiment was conducted to extend the label for Temik use in Arizona pecan orchards for aphid control. Spring application of Temik controlled both yellow and black aphids throughout the season and significantly increased yield.
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Walworth, James, Andrew Pond, and Michael W. Kilby. "Leaf Sampling Guide with Interpretation and Evaluation for Arizona Pecan Orchards." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2006. http://hdl.handle.net/10150/146970.

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Walworth, James L., Andrew P. Pond, and Michael W. Kilby. "Leaf Sampling Guide with Interpretation and Evaluation for Arizona Pecan Orchards." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2011. http://hdl.handle.net/10150/239608.

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Walworth, James, and Thomas L. Thompson. "Salinity Management and Soil Amendments for Southwestern Pecan Orchards." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2006. http://hdl.handle.net/10150/146654.

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Walworth, J. L. "Salinity Management and Soil Amendments for Southwestern Pecan Orchards." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2011. http://hdl.handle.net/10150/239609.

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Call, Rob, Rick Gibson, and Mike Kilby. "Pecan Production Guidelines for Small Orchards and Home Yards." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2006. http://hdl.handle.net/10150/144751.

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Seidman, Michael Aaron. "An inconvenient truth : leukocyte transendothelial migration without pecam /." Access full-text from WCMC:, 2008. http://proquest.umi.com/pqdweb?did=1428864521&sid=12&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Books on the topic "PECAM1"

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Košir, Stanko. Pad peckame, cer s'm gor' rastu =: Pod peckami, kjer sem odrascal. Martuljek: K. Stanko, 1997.

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Pecado. Barcelona: Plaza & Janés Editores, 2000.

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Hamid, Rogayah A. Pecah-pecah ombak. Kuala Lumpur: Dewan Bahasa dan Pustaka, Kementerian Pelajaran Malaysia, 1986.

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D, Solomon J. A guide to the insect borers, pruners, and girdlers of pecan and hickory. New Orleans, La: U.S. Dept. of Agriculture, Forest Service, Southern Forest Experiment Station, 1986.

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Capão pecado. São Paulo, SP: Labortexto Editorial, 2000.

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Martin, Kat. Pecado perfecto. Madrid: Suma de Letras, 2003.

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Perroni, Maité. Mi pecado. Mexico]: Televisa Home Entertainment, 2011.

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Pineda, Mario R. Loarca. Pecado nefando. Casa Juan Pablos, Mexico: Universidad de Ciencias y Artes de Chiapas, 2006.

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Eliana, Pace, and Clair Janete 1925-1983, eds. Pecado capital. São Paulo, SP: Editora Globo, 2008.

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Pineda, Mario R. Loarca. Pecado nefando. Casa Juan Pablos, Mexico: Universidad de Ciencias y Artes de Chiapas, 2006.

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Book chapters on the topic "PECAM1"

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Kitazume, Shinobu. "PECAM." In Encyclopedia of Signaling Molecules, 3860–64. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101772.

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Kitazume, Shinobu. "PECAM." In Encyclopedia of Signaling Molecules, 1–4. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101772-1.

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Etzkorn, Girard. "John Pecham." In Encyclopedia of Medieval Philosophy, 1–4. Dordrecht: Springer Netherlands, 2019. http://dx.doi.org/10.1007/978-94-024-1151-5_277-2.

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Izbicki, Thomas M., Russell L. Friedman, R. W. Dyson, Vilém Herold, Ota Pavlíček, Harro Höpfl, Pekka Kärkkäinen, et al. "John Pecham." In Encyclopedia of Medieval Philosophy, 640–42. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-1-4020-9729-4_277.

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Knuuttila, Simo, David Piché, Pieter De Leemans, Stephen F. Brown, Fabrizio Amerini, Ian Wilks, Christopher Schabel, et al. "Pecham, John." In Encyclopedia of Medieval Philosophy, 931. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-1-4020-9729-4_375.

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Etzkorn, Girard J. "John Pecham." In A Companion to Philosophy in the Middle Ages, 384–87. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470996669.ch71.

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Etzkorn, Girard. "John Pecham." In Encyclopedia of Medieval Philosophy, 995–98. Dordrecht: Springer Netherlands, 2020. http://dx.doi.org/10.1007/978-94-024-1665-7_277.

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Thompson, Tommy E., and Patrick J. Conner. "Pecan." In Fruit Breeding, 771–801. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-0763-9_20.

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Gallegos-Infante, Jose Alberto, Nuria Elizabeth Rocha-Guzman, Ruben Francisco Gonzalez-Laredo, and Martha Rocio Moreno-Jimenez. "Pecans (Carya illinoinensis )." In Fruit and Vegetable Phytochemicals, 1137–44. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119158042.ch57.

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Santerre, Charles R. "Pecan Composition." In Pecan Technology, 98–110. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-010-9592-1_7.

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Conference papers on the topic "PECAM1"

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Wu, Hao, Xuejin Tian, Minghao Li, Yunxin Liu, Ganesh Ananthanarayanan, Fengyuan Xu, and Sheng Zhong. "PECAM." In ACM MobiCom '21: The 27th Annual International Conference on Mobile Computing and Networking. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3447993.3448618.

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Redwan, B., J. Kellermair, MK Renner, H. Panzenboeck, J. Jakowitsch, P. Petzelbauer, D. Bonderman, and IM Lang. "A Role for PECAM-1 in Venous Thrombus Resolution." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3336.

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Souto, João Vicente, Pedro Henrique Penna, Henrique Cota Freitas, and Márcio Castro. "Mecanismos de Comunicação entre Clusters para Lightweight Manycores no Nanvix OS." In Escola Regional de Alto Desempenho da Região Sul. Sociedade Brasileira de Computação - SBC, 2020. http://dx.doi.org/10.5753/eradrs.2020.10741.

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Ambientes de desenvolvimento para lightweight manycores pecam em prover uma boa relação entre programabilidade e portabilidade. Neste contexto, este artigo propõe mecanismos de comunicação entre clusters para um sistema operacional distribuído que sejam precisos, fáceis de usar, escalonáveis e facilmente portáveis. Os resultados mostram ser possível suportar algoritmos de comunicação colectiva de forma eficientemente.
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Kamaraj, Abishek Balsamy, Rachael Dyer, and Murali M. Sundaram. "Pulse Electrochemical Micromachining of Tungsten Carbide." In ASME 2012 International Manufacturing Science and Engineering Conference collocated with the 40th North American Manufacturing Research Conference and in participation with the International Conference on Tribology Materials and Processing. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/msec2012-7238.

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Pulse electrochemical micromachining (PECMM) is a non-conventional manufacturing method suitable for the production of micro-sized components on a wide range of conductive materials. PECMM improves dimensional accuracy and simplifies tool design in machining hard, high strength, and heat resistant materials into complex shapes. Extremely small interelectrode gaps are required in PECMM for better dimensional accuracy. However, excessively small interelectrode gaps may lead to complications like short-circuiting. This imposes the need for better control of the PECMM process. In this study a feedback controlled PECMM system was developed for the electrochemical micromachining of tungsten carbide. It was noticed that while, higher ratios of return velocity to feed rate is preferred as it reduces the number of current spikes, very high value of this ratio results in poor machining rates due to increased interelectrode gap. Therefore, this ratio of return velocity to feed rate may be used to optimize the PECMM process.
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Fuchs, Michael, Sven Geissler, Janine Mikutta, Georg N. Duda, Carsten Perka, Andrej Trampuz, and Andrea Sass. "Soluble Pecam-1 As Biomarker In Periprosthetic Joint Infections (PJI)." In Deutscher Kongress für Orthopädie und Unfallchirurgie. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1717359.

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Chaital P. Shah, Paul R. Weckler, and Niels O. Maness. "Detection of Pecan Weevil Larvae in Pecan Nutmeat using Multispectral Imaging." In 2006 Portland, Oregon, July 9-12, 2006. St. Joseph, MI: American Society of Agricultural and Biological Engineers, 2006. http://dx.doi.org/10.13031/2013.20881.

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Lishnevsky, Marta, Steven J. Woods, William A. Muller, David W. Riches, and Alan R. Schenkel. "Comparative Analysis Of Bleomycin In Pulmonary Disease Susceptible Pecam Deficient Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6001.

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Liapi, A., RG Herrera Gómez, B. Bisig, JP Brouland, F. Herrera, P. Mathevet, and A. Sarivalasis. "EP617 Second line treatment in metastatic uterine pecoma." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.674.

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"Message from the Chair of Malaysian Society of Information Retrieval and Knowledge Management (PECAMP)." In 2018 Fourth International Conference on Information Retrieval and Knowledge Management (CAMP). IEEE, 2018. http://dx.doi.org/10.1109/infrkm.2018.8464812.

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"Message from the Advisor of Malaysian Society of Information Retrieval and Knowledge Management (PECAMP)." In 2018 Fourth International Conference on Information Retrieval and Knowledge Management (CAMP). IEEE, 2018. http://dx.doi.org/10.1109/infrkm.2018.8464817.

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Reports on the topic "PECAM1"

1

DeLisser, Horace. PECAM-1 and Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, December 2009. http://dx.doi.org/10.21236/ada567787.

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Hochberg, Michael J. PECASE: New Directions for Silicon Integrated Optics. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada594983.

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Javaid, Asad, Turkan Aydogmus, and David M. Ford. Molecular simulations of MEMS and membrane coatings (PECASE). Office of Scientific and Technical Information (OSTI), March 2004. http://dx.doi.org/10.2172/918758.

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Adibi, Ali. PECASE: All-Optical Photonic Integrated Circuits in Silicon. Fort Belvoir, VA: Defense Technical Information Center, January 2011. http://dx.doi.org/10.21236/ada559908.

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Wood, Robert J. PECASE: Soaring Mechanisms for Flapping-Wing Micro Air Vehicles. Fort Belvoir, VA: Defense Technical Information Center, March 2015. http://dx.doi.org/10.21236/ada621719.

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McKeon, Beverley J. PECASE - Multi-Scale Experiments and Modeling in Wall Turbulence. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada619270.

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Zia, Rashid, and Jonathan A. Kurvits. PECASE: Resonantly-Enhanced Lanthanide Emitters for Subwavelength-Scale, Active Photonics. Fort Belvoir, VA: Defense Technical Information Center, March 2015. http://dx.doi.org/10.21236/ad1003197.

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Thompson, Aidan Patrick, Kunwoo Han, and David M. Ford. Molecular simulations of beta-amyloid protein near hydrated lipids (PECASE). Office of Scientific and Technical Information (OSTI), December 2005. http://dx.doi.org/10.2172/876519.

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Li, Ju. PECASE - First Principles Modeling of Mechanics and Chemistry of Materials. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada573756.

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Bulovic, Vladimir. PECASE: Nanostructure Hybrid Organic/Inorganic Materials for Active Opto-Electronic Devices. Fort Belvoir, VA: Defense Technical Information Center, January 2011. http://dx.doi.org/10.21236/ada547102.

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